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Abstract

Chronic corticosteroid therapy is widely used in the management of inflammatory, autoimmune, respiratory, and malignant conditions. Despite their clinical utility, prolonged exposure to glucocorticoids is associated with significant metabolic adverse effects, most notably weight gain and obesity. Steroid-induced obesity is characterized by increased body mass index, central fat redistribution, insulin resistance, and heightened cardiometabolic risk, resembling features of exogenous Cushing’s syndrome. This review summarizes current clinical evidence linking chronic corticosteroid use with obesity, elucidates underlying pathophysiological mechanisms, and discusses contemporary management strategies aimed at prevention and mitigation of this complication. Understanding these associations is critical for optimizing long-term outcomes in patients requiring sustained corticosteroid therapy.

Keywords

Obesity, corticosteroids, chronic steroid therapy, adipogenesis, insulin resistance, hyperphagia, visceral fat, cortisol, central obesity, leptin resistance, glucocorticoid metabolism, altered energy expenditure, hypothalamus, autoimmunity, steroids, clinical evidence, medical interventions, appetite, illness

Introduction

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Corticosteroids especially glucocorticoids such as prednisone, prednisolone and dexamethasone stay foundation treatments for a wide extend of incessant infections counting immune system disarranges inveterate respiratory ailments  bowel illness and malignancies their strong anti-inflammatory and immunosuppressive properties altogether move forward illness control and survival in numerous clinical settings in any case long-term corticosteroid treatment is related with various antagonistic impacts among which weight and metabolic dearrangements are among the most visit and clinically relevant steroid-induced obesity contributes considerably to expanded cardiovascular chance advancement of type 2 diabetes mellitus musculoskeletal complications and impairs quality of life with the developing predominance of unremitting inflammatory diseases requiring delayed steroid introduction, acknowledgment of weight gain as a major iatrogenic complication has picked up expanding significance in clinical practice [1]

2.Clinical Evidence Linking Corticosteroids to Obesity

2.1 Observational and Cohort Studies

solid clinical proves connecting persistent corticosteroid utilize to weight has developed from huge observational and cohort ponders conducted in real-world populaces not at all like randomized trials these ponders capture long-term introduction designs and metabolic results making them especially important for understanding corticosteroid-associated weight gain several population-based cohort considers have illustrated a clear affiliation between corticosteroid utilize and increments in body weight body mass list BMI and central adiposity one expansive longitudinal cohort taking after grown-ups over numerous a long time found

that people starting corticosteroid treatment experienced essentially more noteworthy weight pick up and abdomen circumference development compared with non-users critically these impacts were watched not as it were with systemic corticosteroids but moreover with locally managed shapes such as breathed in and intranasal corticosteroids proposing total systemic metabolic impacts indeed at lower measurements observational ponders encourage back these discoveries cross-sectional examinations comparing corticosteroid clients with non-users reliably report higher predominance of overweight and corpulence among corticosteroid-exposed people in a few cohorts hefty members were more likely to report later or constant corticosteroid utilize especially for incendiary and respiratory conditions these considers too famous patient-reported weight pick up taking after the start of corticosteroid treatment fortifying the clinical significance of this association sex-specific impacts have too been watched numerous cohort thinks about demonstrate that ladies utilizing corticosteroids are at a higher chance of weight pick up and central fat collection than men this may be related to sex contrasts in glucocorticoid affectability fat tissue dispersion and hormonal intelligent prove from disease-specific cohorts encourage reinforces the connect in long-term observational thinks about of patients with asthma rheumatoid joint pain and systemic immune system maladies delayed corticosteroid presentation was related with dynamic increments in BMI and higher rates of weight compared with patients getting steroid-sparing treatments a few thinks about illustrate a dose-response relationship with higher aggregate measurements relating with more prominent weight gain, cohort considers have moreover appeared fractional reversibility of corticosteroid-induced weight suspension or dosage lessening of corticosteroids was related with stabilization or diminishment of midriff circumference and body weight in a few population highlighting the causal nature [2]

2.2 Dose, Duration, and Route of Administration

Clinical demonstration dependably outlines that the chance and earnestness of corpulence related with corticosteroid treatment are decidedly affected by estimations length of introduction and course of organization these components choose the degree of systemic glucocorticoid development and ensuing metabolic unsettling impacts driving to weight choose up and central adiposity dose-related impacts observational and cohort considers have showed up a clear dose response relationship between corticosteroid introduction and weight choose up higher add up to doses of systemic glucocorticoids are related with more conspicuous increases in body mass record BMI and guts circumference patients getting moderate-to-high measurements of verbal corticosteroids for unremitting conditions such as rheumatoid joint torment asthma or combustible bowel ailment appear through and through higher rates of corpulence compared with those on low-dose or sporadic treatment undoubtedly in patients tolerating breathed in corticosteroids higher day by day measurements have been associated to energetic BMI increases appearing that metabolic impacts may happen in show disdain toward of limited systemic bioavailability length of treatment the length of corticosteroid utilize is a fundamental determinant of corpulence risk short-term corticosteroid treatment is more frequently than not related with worldly longing for prompting and insignificant weight choose up in separate long-term or diligent use defined as treatment intensifying past three months has been unequivocally related with kept up weight choose up and fat redistribution longitudinal cohort considers outline that individuals on drawn out corticosteroid treatment experience dynamic but decided increases in body weight with specific conglomeration of visceral fat basically cessation or dose reducing has been related with midway reversal of weight choose up supporting a causal relationship between long-term introduction and corpulence enhancement course of organization the course of corticosteroid organization inside and out impacts corpulence comes about systemic courses particularly verbal and intravenous organization are most decidedly related with corpulence due to ceaseless systemic presentation and arrange impacts on glucose assimilation framework insult resistance and adipocyte division in any case creating demonstrate illustrates that locally overseen corticosteroids tallying breathed in intranasal topical and intra-articular shapes may as well contribute to weight choose up when utilized chronically or at tall measurements tremendous population-based cohort considers have showed up increases in bmi and midriff circumference among long-term clients of breathed in corticosteroids proposing add up to systemic absorption over time. [3]

2.3 Vulnerable Populations

Clinical demonstrate illustrates that certain populaces are particularly frail to corpulence as a complication of deep rooted corticosteroid treatment these bunches association heightens metabolic impacts due to physiological hormonal or disease-related components that related with glucocorticoid exposure children and youthful individuals talk to a exceedingly feeble masses observational pediatric considers approximately have dependably showed up plan weight choose up and extended BMI percentiles in children tolerating long-term systemic corticosteroids for conditions such as asthma nephrotic clutter and juvenile idiopathic joint torment advancement concealment combined with extended adiposity leads to unfavorable body composition with long-term comes about growing into adulthood women especially post-menopausal women appear up more helpless to corticosteroid-induced corpulence sweeping cohort considers have point by point more conspicuous increases in body weight and guts circumference among female corticosteroid clients compared to folks hormonal contrasts changed fat movement plans and extended affectability of fat tissue to glucocorticoids may contribute to this divergence patients with pre-existing overweight or weight are additionally at expanded chance observational cohort data prescribe that corticosteroid presentation animates help weight choose up in these individuals progressing central adiposity and compounding insult resistance this makes a shocking cycle that increases the likelihood of metabolic clutter and cardiovascular complications individuals with unremitting provocative contaminations such as asthma rheumatoid joint torment systemic lupus erythematosus and provocative bowel disease habitually require drawn out corticosteroid treatment cohort considers approximately in these populaces outline total dose-dependent weight choose up particularly with long-term verbal or high-dose breathed in corticosteroids finally elderly patients are frail due to age-related metabolic abating lessened physical activity and comorbidities ceaseless corticosteroid utilize in more prepared grown-ups has been related with extended fat mass sarcopenic corpulence and utilitarian rot collectively these disclosures emphasize the require for centered on checking and preventive strategies in defenseless populaces getting diligent corticosteroid treatment. [4]

3. Pathophysiological Mechanisms of Steroid-Induced Obesity

3.1 Effects on Appetite and Energy Balance

One of the central pathophysiological instruments basic steroid-induced corpulence is the significant impact of constant corticosteroid presentation on craving control and vitality adjust glucocorticoids impact both central and fringe pathways that oversee starvation satiety caloric admissions and vitality consumption driving to a supported positive vitality adjust and dynamic weight pick up at the central apprehensive framework level corticosteroids act on the hypothalamus a key controller of craving and digestion system incessant glucocorticoid presentation upgrades the expression and movement of orexigenic neuropeptides especially neuropeptide Y (NPY) and agouti-related peptide agrp which invigorate starvation and nourishment admissions at the same time corticosteroids disable the anorexigenic signaling pathways including pro-opiomelanocortin pomc in this manner decreasing satiety this neurochemical awkwardness comes about in expanded craving visit snacking and inclination for energy-dense nourishments corticosteroids too disturb leptin and affront signaling hormones that regularly stifle craving and control vitality homeostasis long-term steroid treatment actuates leptin resistance lessening the hypothalamic reaction to circulating leptin in spite of expanded fat tissue mass in parallel corticosteroid-induced affront resistance debilitates insulins appetite-suppressing impacts inside the brain together these changes advance hyperphagia and diminish physiological criticism instruments that regularly restrain weight pick up past craving incitement corticosteroids antagonistically influence vitality consumption persistent introduction diminishes basal metabolic rate by disabling mitochondrial oxidative work and diminishing muscle protein blend steroids advance skeletal muscle catabolism diminishing incline body mass which is a major determinant of resting vitality use the misfortune of muscle mass brings down add up to day by day vitality utilization assist contributing to weight pick up indeed without intemperate caloric admissions furthermore corticosteroids impact behavioral and mental variables related to vitality adjust steroid-associated disposition changes weakness and rest unsettling influences may decrease physical movement levels whereas expanded stretch responsiveness advance opens up craving and nourishment utilization through enactment of the hypothalamic pituitary adrenal gland.[4,5]

3.2 Altered Adipose Tissue Distribution

One of the trademark highlights of steroid-induced weight is modified fat tissue dissemination characterized by particular fat aggregation in central and visceral stations or maybe than uniform weight pick up incessant presentation to glucocorticoids leads to a unmistakable phenotype regularly portrayed as cushingoid with expanded truncal weight facial fat testimony moon confront dorsocervical fat cushion buffalo bump and generally diminished fringe subcutaneous fat in the appendages these changes emerge from complex intelligent between glucocorticoids adipocytes and metabolic administrative pathways glucocorticoids apply site-specific impacts on fat tissue advancing lipid capacity in visceral fat whereas improving lipolysis in fringe fat terminals visceral fat tissue communicates higher levels of glucocorticoid receptors grs and expanded movement of 11-hydroxysteroid dehydrogenase sort 1 11-hsd1 an protein that changes over inert cortisone into dynamic cortisol locally this increases intracellular glucocorticoid activity inside visceral fat driving to adipocyte hypertrophy and hyperplasia in differentiate subcutaneous fat tissue appears generally lower glucocorticoid affectability contributing to territorial fat redistribution or maybe than generalized adiposity at the cellular level glucocorticoids fortify preadipocyte separation and adipogenesis especially in visceral fat terminals they upregulate translation variables such as peroxisome proliferator-activated receptor- ppar- and ccaatenhancer-binding proteins cebps which drive adipocyte development and lipid amassing moreover glucocorticoids increment the expression of lipogenic proteins whereas smothering vitality consumption assist favoring fat capacity in central locales steroid-induced affront resistance moreover plays a basic part in modified fat dissemination hyperinsulinemia improves triglyceride take-up into visceral adipocytes whereas glucocorticoids antagonize affront activity in muscle and fringe fat this metabolic awkwardness advances shunting of overabundance vitality toward visceral fat terminals compounding central weight moreover glucocorticoids impact adipokine emission by lessening adiponectin and expanding leptin resistance which disables craving direction and advances assist fat collection critically visceral fat is metabolically dynamic and discharges pro-inflammatory cytokines such as tumor corruption figure- and interleukin-6 their expanded generation in steroid-induced central corpulence contributes to unremitting low-grade aggravation and advance declines metabolic brokenness. [5,6]

3.3 Insulin Resistance and Metabolic Dysregulation

Insulin resistance and metabolic dysregulation are central pathophysiological components crucial steroid-induced weight particularly in the midst of consistent introduction to glucocorticoids glucocorticoids such as prednisone and dexamethasone altogether affect glucose and lipid absorption framework by antagonizing insult movement in periphery tissues checking skeletal muscle fat tissue and the liver at the hepatic level glucocorticoids strengthen gluconeogenesis by upregulating key proteins such as phosphoenolpyruvate carboxykinase and glucose-6-phosphatase driving to extended endogenous glucose era at the same time they obstruct insulin-mediated concealment of hepatic glucose abdicate coming almost in decided hyperglycemia in skeletal muscle glucocorticoids decrease glucose take-up by reducing insulin-stimulated translocation of glut-4 transporters help declining insult resistance in fat tissue unremitting glucocorticoid presentation propels lipolysis growing circulating free oily acids raised free oily acids interfered with attack signaling pathways through rebellious such as serine phosphorylation of insult receptor substrate proteins this not as it were compounds attack resistance but as well favors ectopic fat explanation in the liver and visceral fat terminals contributing to central corpulence too glucocorticoids progress adipocyte partition and lipid capacity particularly in visceral fat tissue which is metabolically energetic and unequivocally associated to cardiometabolic danger the coming around metabolic dysregulation is characterized by hyperinsulinemia dyslipidemia extended fat mass and decreased essentialness utilize collectively taking after highlights of metabolic clutter over time these changes make a shocking cycle in which insult resistance progresses energize fat conglomeration in this way reinforcing corpulence and extending the danger of Type 2 diabetes mellitus in patients tolerating long-term corticosteroid treatment. [6,7]

4. Clinical Features and Consequences

4.1 Phenotypic Characteristics      

Clinical highlights and results  phenotypic characteristics steroid-induced weight speaks to a particular clinical phenotype that contrasts from basic dietary or lifestyle-related weight it emerges essentially due to constant presentation to exogenous glucocorticoids which change fat digestion system dispersion and endocrine direction the phenotypic characteristics are generally driven by overabundance glucocorticoid movement mirroring highlights of cushings disorder body fat dissemination one of the trademark phenotypic highlights is central visceral weight patients ordinarily show unbalanced fat aggregation in the trunk guts confront neck and upper back whereas the appendages stay generally lean due to steroid-induced muscle catabolism this comes about in characteristic appearances such as moon confront buffalo bump and truncal weight the particular testimony of fat tissue in visceral warehouses is intervened by expanded lipogenesis and adipocyte separation beneath glucocorticoid impact changes in body composition steroid-induced weight is related with expanded fat mass and diminished incline muscle mass a condition regularly alluded to as sarcopenic corpulence unremitting glucocorticoid introduction advances protein breakdown in skeletal muscle and hinders protein amalgamation driving to muscle squandering shortcoming and diminished utilitarian capacity in spite of weight pick up this modified body composition contributes to diminished physical perseverance and expanded weakness cutaneous and physical highlights characteristic cutaneous appearances habitually go with steroid-induced weight these incorporate lean delicate skin simple bruising purple striae especially over the midriff and thighs and deferred wound recuperating facial adjusting and facial plenty assist complement the corpulent phenotype skin break out and hirsutism may moreover be show due to hormonal lopsidedness metabolic and endocrine phenotype patients regularly show highlights of metabolic disorder counting affront resistance hyperglycemia dyslipidemia and hypertension expanded craving and hyperphagia are common assist worsening weight pick up glucocorticoid-induced changes in leptin and affront signaling contribute to disabled satiety direction useful and psychosocial results the phenotypic changes are regularly related with diminished portability work out bigotry and mental trouble counting moo self-esteem and body picture disappointment these results can altogether disable quality of life and adherence to long-term treatment. [8,9]

4.2 Associated Comorbidities

Steroid-induced weight coming about fundamentally from drawn out systemic corticosteroid treatment is related with a wide run of metabolic cardiovascular endocrine musculoskeletal and mental comorbidities these complications emerge due to corticosteroid-mediated modifications in glucose digestion system lipid dissemination protein catabolism and neurohormonal direction altogether expanding dismalness and decreasing quality of life one of the most common comorbidities is affront resistance and steroid-induced diabetes mellitus corticosteroids antagonize affront activity by expanding hepatic gluconeogenesis and diminishing fringe glucose take-up especially in skeletal muscle and fat tissue corpulence assist worsens affront resistance through expanded free greasy corrosive discharge and fiery cytokines putting patients at a tall hazard of creating sort 2 diabetes mellitus cardiovascular comorbidities are too regularly watched steroid-induced weight contributes to hypertension dyslipidemia and quickened atherosclerosis corticosteroids advance sodium and water maintenance driving to expanded blood weight whereas central corpulence is related with hoisted triglycerides expanded low-density lipoprotein ldl cholesterol and diminished high-density lipoprotein hdl cholesterol together these components essentially lift the chance of coronary supply route malady and stroke another vital comorbidity is metabolic disorder characterized by stomach corpulence hyperglycemia hypertension and dyslipidemia incessant corticosteroid presentation advances visceral fat aggregation which is metabolically dynamic and secretes pro-inflammatory adipokines this low-grade persistent aggravation contributes to endothelial brokenness and expanded cardiometabolic chance musculoskeletal complications are common in patients with steroid-induced corpulence overabundance body weight places extra stretch on joints driving to osteoarthritis especially of the knees and hips corticosteroids too cause muscle protein breakdown coming about in steroid-induced myopathy which decreases physical action and assist compounds weight pick up furthermore long-term steroid utilize is related with osteoporosis and expanded break hazard compounding versatility confinements steroid-induced weight is moreover connected to respiratory complications counting obstructive rest apnea osa fat statement around the neck and upper aviation route increments aviation route resistance amid rest driving to discontinuous hypoxia daytime drowsiness and expanded cardiovascular hazard mental and neuropsychiatric comorbidities are habitually ignored but clinically noteworthy weight related with corticosteroid treatment can contribute to sadness uneasiness body-image disappointment and diminished self-esteem corticosteroids themselves may cause disposition unsettling influences sleep deprivation and cognitive changes encourage influencing quiet adherence and by and large well-being at last hepatic and gastrointestinal complications such as non-alcoholic fatty liver illness is progressively recognized in steroid-induced corpulence overabundance visceral fat and affront resistance advance hepatic lipid aggregation which may advance to steatohepatitis and fibrosis if cleared out unmanaged. [9,10]

5. Management Strategies

5.1 Optimization of Corticosteroid Therapy

Optimization of corticosteroid treatment is a establishment in the shirking and organization of steroid-induced corpulence since glucocorticoids are regularly imperative for controlling tireless combustible and safe framework clutters the objective is not add up to withdrawal but minimization of metabolic opposing impacts though keeping up therapeutic ampleness estimations minimization and term control one of the most compelling techniques is the utilize of the slightest fruitful estimations for the most brief conceivable term different clinical discernments appear that weight choose up and central adiposity are dose- and duration-dependent tall total introduction to systemic corticosteroids is unequivocally related with extended longing for fat redistribution and insult resistance in this way once disease control is finished clinicians should to immediately diminish corticosteroids or perhaps than continuing upkeep doses pointlessly standard reassessment of ailment activity makes a distinction maintain a strategic distance from drawn out presentation slant for neighborhood over systemic treatment at anything point clinically feasible locally acting corticosteroidssuch as breathed in topical intra-articular or intranasal preparationsshould be favored over systemic points of interest neighborhood medications donate centered on anti-inflammatory impacts with diminished systemic digestion in this way bringing down the risk of weight choose up and visceral fat collection in any case long-term or high-dose utilize of neighborhood corticosteroids can still contribute to metabolic impacts emphasizing the importance of cautious dosing and watching in fact with non-oral definitions alternate-day and timing procedures in chosen patients alternate-day dosing regimens may diminish concealment of the hypothalamic pituitary adrenal center and limit metabolic side impacts checking corpulence too controlling corticosteroids in the morning alters with the bodys ordinary cortisol cadence conceivably lessening longing for actuation and metabolic unsettling influence compared to evening dosing steroid-sparing pros the joining of steroid-sparing medicines is a key optimization technique immunomodulators biologics disease-modifying antirheumatic drugs dmards and centered on medications can diminish or arrange of the require for long-term corticosteroids in conditions such as rheumatoid joint torment red hot bowel ailment and asthma early begin of these pros has been showed up to basically lower total steroid presentation and in this way the chance of steroid-induced corpulence individualized treatment and risk stratification personalized corticosteroid regimens based on patient-specific chance factors such as standard BMI family history of weight diabetes chance and sex are principal individuals with pre-existing overweight or corpulence are particularly feeble to steroid-induced weight choose up and should to be supervised with expanded caution standard checking of body weight midsection circumference and metabolic parameters licenses early interventions and estimations modification. [10,11]

5.2 Lifestyle Interventions

Way of life modification remains the establishment of managing steroid-induced corpulence particularly in patients requiring long-term corticosteroid treatment for ingrained provocative or safe framework conditions since corticosteroids progress weight choose up through extended longing for attack resistance changed fat transport and diminished essentialness utilize centered on way of life trade are essential to check these impacts and diminish cardiometabolic risk dietary mediations dietary organization is the most fundamental way of life strategy in steroid-induced corpulence corticosteroids strengthen longing for and slant for calorie-dense nourishments in this way calorie-controlled nutrient-dense diets are recommended emphasis should to be put on high-protein confirmations to ensure slant body mass and overhaul satiety while obliging refined carbohydrates and doused fats that decline insult resistance a low-glycaemic-index check calories well off in aggregate grains vegetables vegetables and common items makes a distinction stabilize blood glucose levels and soothe steroid-induced hyperglycaemia reducing sodium confirmations is as well principal as corticosteroids progress sodium and water support contributing to weight choose up and hypertension palatable calcium and vitamin d affirmations should to be ensured to check steroid-induced bone mishap though supporting by and expansive metabolic prosperity physical activity and work out standard physical development plays a critical portion in foreseeing fat collection and moving forward attack affectability in patients getting corticosteroids oxygen devouring work out such as brisk walking cycling or swimming for at scarcest 150 minutes per week makes a contrast lessen include up to and visceral fat mass this is particularly imperative as corticosteroids uncommonly increase central adiposity which is decidedly related with metabolic syndrome resistance planning should to be joined at scarcest two to three times per week to secure muscle mass and check steroid-induced muscle wasting steroid myopathy upkeep of skeletal muscle advances basal metabolic rate and updates glucose utilization in this way diminishing the chance of corpulence and sort 2 diabetes behavioral and mental mediations behavioral methods are essential due to the appetite-stimulating and mood-altering impacts of corticosteroids organized dinner orchestrating allocate control and cautious eating methodologies offer help patients supervise extended starvation and eager eating self-monitoring of body weight food confirmations and physical activity has been showed up to make strides adherence and long-term weight control mental reinforce tallying cognitive-behavioral treatment may advantage patients experiencing steroid-induced personality changes thrust or rest unsettling impacts all of which can contribute to weight choose up tending to rest cleanliness is besides basic as dejected rest compounds hormonal dysregulation and longing for control understanding instruction and long-term adherence determined instruction is central to productive way of life intervention patients should to be taught around the obvious metabolic impacts of corticosteroids sensible weight-management destinations and the centrality of early way of life alteration at the begin of steroid treatment custom-made multidisciplinary approaches counting specialists dietitians and physiotherapists advance adherence. [12,13]

5.3 Pharmacological and Specialist Interventions

Steroid-induced corpulence is a challenging complication of long-term corticosteroid treatment, frequently characterized by central fat aggregation, affront resistance, and metabolic unsettling influences. Whereas way of life alteration remains the foundation of administration, pharmacological and specialist-led mediations play a significant part in patients who fall flat to accomplish satisfactory weight control or who create noteworthy metabolic complications. [14,15]

1.Pharmacological Interventions

Pharmacological administration points to check the metabolic impacts of corticosteroids, especially expanded craving, changed fat conveyance, and disabled glucose metabolism. [16]

a.Anti-obesity Medications

There are a types of anti-obesity medications that people can take for a long time. Medications like liraglutide and semaglutide are really good at helping people lose weight. These anti-obesity medications work in the brain to make people feel full so they eat slower. Take in fewer calories. Anti-obesity medications like liraglutide and semaglutide also help control blood sugar levels, which's great for patients with diabetes mellitus or people who have high blood sugar because of corticosteroid medications. Anti-obesity medications are an option, for people who need to lose weight and control their blood sugar levels at the same time. Clinical trials have demonstrated substantial and sustained weight loss with these agents, along with improvements in cardiometabolic risk factors.

Orlistat, a gastrointestinal lipase inhibitor, reduces dietary fat absorption by approximately 30%. It is especially useful in patients where systemic drug exposure must be minimized. However, gastrointestinal adverse effects such as steatorrhea and fat-soluble vitamin deficiencies may limit adherence. Despite these drawbacks, orlistat can contribute to modest weight loss and improvement in lipid profiles when combined with dietary modification.

Combination therapies, such as phentermine-topiramate and naltrexone-bupropion, target appetite regulation and reward pathways in the central nervous system. Phentermine suppresses appetite through sympathomimetic activity, while topiramate enhances satiety and reduces food cravings. Naltrexone-bupropion modulates hypothalamic appetite control and mesolimbic reward systems. These agents require careful patient selection due to potential cardiovascular, neuropsychiatric, and blood pressure-related adverse effects.

In corticosteroid-treated patients, close monitoring is essential to avoid drug interactions and exacerbation of underlying conditions. Anti-obesity medications should always be used as adjuncts to lifestyle modification rather than as standalone therapies. Long-term adherence, tolerability, and safety must be evaluated regularly. Overall, anti-obesity pharmacotherapy offers an effective tool for weight reduction and metabolic risk mitigation when appropriately prescribed and monitored.s or disabled glucose tolerance [17,18]

 b.Insulin-Sensitizing Agents

Insulin resistance is a central pathophysiological feature of corticosteroid-induced obesity, driven by increased hepatic gluconeogenesis, impaired peripheral glucose uptake, and altered adipokine secretion. Insulin-sensitising agents are therefore crucial in addressing both weight gain and metabolic complications associated with chronic corticosteroid therapy.Metformin is the most widely used insulin-sensitising agent and is often considered first-line therapy in patients with obesity and impaired glucose metabolism. It improves insulin sensitivity by reducing hepatic glucose production and enhancing peripheral glucose uptake. Additionally, metformin has modest weight-reducing or weight-neutral effects, which is advantageous in contrast to other antidiabetic agents that may promote weight gain. In corticosteroid-induced obesity, metformin helps counteract steroid-related hyperglycemia and may attenuate further weight gain.

Beyond glycemic control, metformin has been shown to reduce visceral adiposity and improve lipid profiles. Its favorable safety profile, low cost, and extensive clinical experience make it a valuable option. Gastrointestinal side effects are common but usually transient and can be minimized by dose titration or use of extended-release formulations.

Thiazolidinediones, such as pioglitazone, improve insulin sensitivity by activating peroxisome proliferator-activated receptor-gamma (PPAR-γ). While effective in improving insulin resistance, their use in obesity management is limited due to adverse effects including weight gain, fluid retention, and increased risk of heart failure. Consequently, thiazolidinediones are generally avoided in corticosteroid-induced obesity unless specific indications exist.

Emerging agents, including GLP-1 receptor agonists and dual incretin therapies, also demonstrate insulin-sensitising properties. These drugs improve pancreatic beta-cell function, reduce appetite, and promote weight loss, offering dual metabolic benefits. Their role is increasingly recognized in patients with steroid-induced diabetes or prediabetes.

Overall, insulin-sensitising agents form a cornerstone of pharmacological management in corticosteroid-induced obesity, particularly when metabolic derangements coexist. Careful selection based on patient comorbidities, renal function, and tolerance is essential to optimize outcomes. [18,19]

 c.Corticosteroid-Sparing Strategies

Corticosteroid-sparing strategies are essential in preventing and managing steroid-induced obesity, as chronic exposure to glucocorticoids is a primary driver of weight gain and metabolic dysfunction. These strategies aim to minimize cumulative steroid dose while maintaining adequate disease control.

One key approach involves dose optimization, using the lowest effective corticosteroid dose for the shortest possible duration. Tapering schedules should be individualized based on disease activity and patient response. Alternate-day dosing may reduce metabolic adverse effects in selected patients, although its applicability depends on the underlying condition.

The use of steroid-sparing immunosuppressive or anti-inflammatory agents is another critical strategy. Drugs such as methotrexate, azathioprine, mycophenolate mofetil, and biologic agents (e.g., TNF-α inhibitors, interleukin inhibitors) can reduce or eliminate the need for long-term corticosteroid therapy. These agents are particularly valuable in chronic inflammatory and autoimmune diseases.

Topical, inhaled, or localized corticosteroid formulations should be preferred over systemic therapy whenever feasible, as they are associated with reduced systemic absorption and fewer metabolic side effects. In conditions like asthma or inflammatory bowel disease, targeted delivery can significantly lower obesity risk.

Regular multidisciplinary monitoring is essential to ensure disease control while minimizing steroid exposure. Patients should be educated about potential adverse effects and involved in shared decision-making regarding treatment options. Overall, corticosteroid-sparing strategies represent a preventive and therapeutic cornerstone in managing steroid-induced obesity and its complications.

Pharmacological optimization of the fundamental malady is basic. Where conceivable, measurements lessening, alternate-day treatment, or exchanging to less strong corticosteroids may decrease weight pick up. In numerous constant fiery conditions, the presentation of steroid-sparing specialists such as methotrexate, azathioprine, or biologic treatments can essentially restrain long-term corticosteroid presentation and its obesogenic effects. [20,21]

 2. Specialist Interventions

Given the multifactorial nature of steroid-induced weight, multidisciplinary pro care is regularly required.

a.Endocrinologist Involvement:

 Endocrinologist involvement is crucial in the comprehensive management of corticosteroid-induced obesity, particularly when complex metabolic disturbances are present. Endocrinologists possess specialized expertise in hormonal regulation, metabolic disorders, and obesity-related comorbidities, enabling individualized and evidence-based care.

Patients on long-term corticosteroid therapy often develop endocrine complications such as insulin resistance, diabetes mellitus, dyslipidemia, and hypothalamic-pituitary-adrenal (HPA) axis suppression. An endocrinologist plays a key role in early identification and management of these conditions. Detailed metabolic evaluation, including assessment of glucose tolerance, lipid profile, and hormonal status, allows for timely intervention.

Endocrinologists also guide the selection and titration of pharmacological therapies, including anti-obesity medications and insulin-sensitising agents. They monitor treatment efficacy, manage adverse effects, and adjust therapy based on evolving clinical status. In complex cases, they coordinate corticosteroid tapering and advise on steroid-sparing alternatives in collaboration with the primary treating specialist.

Furthermore, endocrinologist involvement improves long-term outcomes through patient education, risk stratification, and prevention of complications. Their role is particularly important in patients with refractory obesity or multiple comorbidities, where specialized care is required.

Specialist dietitians give individualized sustenance plans centering on calorie control, low-glycemic-index nourishments, and diminished sodium admissions to counter steroid-induced liquid maintenance. Organized dietary counseling moves forward adherence and long-term outcomes. .[22]

b. Dietician-led nutrition therapy

Obesity is a problem that needs to be managed over a long time. To deal with obesity people need to make changes. One thing that really works is when a dietician helps someone, with their eating habits. Another option is a type of surgery called surgery. These two approaches are very different. They can also work well together especially for people who are very overweight or have other health issues because of their weight. Obesity is something that needs to be taken care of. People need to think about the best way to manage their obesity. Dietician-led nutrition therapy and bariatric surgery are two ways to manage obesity.

A dietician is very important when it comes to helping people with obesity. They help people eat better. This is the first thing doctors recommend. A registered dietician will work with each person to come up with a diet plan that's just right for them. This plan is based on the persons health and lifestyle. What they want to achieve. Dieticians are key to helping people with obesity because they can give them advice on food that's good for them and that they will like. This is what dieticians do. It is very important for people with obesity. They help people make changes to what they eat that they can stick to. A dietician will make sure the diet plan is right, for the persons metabolism and lifestyle and what they want to do to be healthy.

Medical nutrition therapy is about making a plan for eating that has a number of calories. This plan helps people lose weight slowly and in a way that lasts. It also helps keep the parts of your body strong and makes sure you get all the vitamins and minerals you need.

Some common ways to eat healthy include eating a diet that is low in calories eating foods that do not cause a big spike in blood sugar eating like people do in Mediterranean countries and eating a lot of protein. People who help you with your diet look at what you eat how you eat what foods you like and what might stop you from sticking to your plan. This helps them make a plan that's realistic and works for you. Medical nutrition therapy and the people who help with your diet make sure you have a plan that's just right, for you and your needs.

Dieticians do a kind of therapy that helps people change how they eat. They use things like setting goals and keeping track of what you eat to help you stick with it for a time. They also teach you how to eat and stop yourself from going back to old habits.

Dieticians talk to people about why they eat much or make bad food choices. Some people eat when they are stressed or bored. Others eat much food at one time. Dieticians help people with these problems because they are often linked to being overweight.

If you see a dietician regularly you will probably lose weight. Keep it off. This is better than trying to change what you eat on your own. Regular visits to a dietician really make a difference, in how weight you lose and whether you gain it back.

So nutrition therapy does a lot more than help with weight reduction. It also helps to improve your metabolic health. If you can lose an amount of weight like 5 to 10 percent through changing what you eat it can make a big difference. You will have insulin sensitivity your lipid profiles will be better your blood pressure will be lower and you will have fewer inflammatory markers.

Dieticians are also really helpful when it comes to managing conditions that are related to obesity, such as type 2 diabetes, non-alcoholic fatty liver disease and polycystic ovary syndrome. They use special nutrition plans to help with these conditions, which's really good news for people who are struggling with nutrition therapy and obesity. Nutrition therapy is very important for people who want to improve their metabolic health and manage obesity-related conditions like type 2 diabetes, non-alcoholic fatty liver disease and polycystic ovary syndrome, through nutrition therapy.

When it comes to people who're severely overweight like those with a body mass index of 40 kg/m² or more or 35 kg/m² or more with other health problems nutrition therapy led by a dietician may not be enough to help them lose weight. This is because their bodies have changed in ways that make it harder to lose weight, such as their bodies burning calories when they are resting and having more hormones that make them feel hungry. In these situations surgery might be the option to help with weight loss. The nutrition therapy led by a dietician is just not enough for people, with obesity so surgery is considered to help them lose weight and get healthier. [23,24]

c.Bariatric Surgery

Bariatric surgery is really good at helping people who're very overweight. It helps them lose a lot of weight and keep it off for a time. This type of surgery also helps with health problems that are related to being overweight. There are a few types of bariatric surgery that doctors can do. These include Roux-enY gastric bypass, sleeve gastrectomy and adjustable gastric banding. Now sleeve gastrectomy is the type of bariatric surgery that is done the most all around the world. Bariatric surgery, like sleeve gastrectomy is very effective. That is why it is used so much.

Bariatric surgery does a lot more than just limit the amount of food you can eat and reduce the amount of nutrients your body absorbs. When you have this type of surgery it can really change the way your body works. Your body starts to make amounts of certain hormones. For example it makes less of a hormone called ghrelin which's what makes you feel hungry. At the time it makes more of other hormones like glucagon-like peptide-1 and peptide YY, which help you feel full.

All of these changes can help you feel less hungry. They can also help your body deal with sugar and insulin better. Sometimes people who have surgery can even stop having type 2 diabetes and this can happen really quickly. The best part is that it is not just because they lost weight. Bariatric surgery can really help people with type 2 diabetes. It can do this even if they do not lose a lot of weight. Bariatric surgery and its effects on the body are really interesting. They can be very helpful, for people who are struggling with their weight and their health.

Bariatric surgery is really good at helping people lose weight. People who have this surgery usually lose fifty to seventy percent of their weight within two years. This weight loss is not just temporary it lasts for a time. Bariatric surgery also helps reduce the risk of heart problems and death. It even helps with health issues that are related to being overweight.

Bariatric surgery helps people feel better about themselves. It improves their overall quality of life. It also helps them move around easily and improves their mental health. Bariatric surgery is an option, for people who are struggling with their weight and related health issues.

Bariatric surgery is a way to lose weight but it has some problems. You can get infections where the doctor made the cut or the connection, between parts of your body can leak. Some people get dumping syndrome, which's very uncomfortable. Bariatric surgery can also cause you to not get iron, vitamin B12, calcium and other important vitamins like the fat-soluble vitamins. So you have to see a doctor about what you eat for your life and take extra vitamins to stay healthy. Bariatric surgery requires you to take care of your body and diet for the rest of your life because bariatric surgery can lead to these problems.

Dieticians are very important for people who are having surgery. Before the surgery the dieticians check what the patient is eating. If they have any bad eating habits. They also help the patients get ready for the changes they will have to make to what they eat after the surgery. When dieticians help patients lose weight before the surgery it can make the liver smaller. Make the surgery safer for the patients. Bariatric surgery is a deal and dieticians play a big role in it. Dieticians help patients, with surgery all the way through the process.

After the operation it is very important for people to get help from a dietician to make sure they are eating protein. This helps prevent them from not getting enough of the things their body needs. It also helps their body get used to the changes that were made to their system.

They need to start with liquids and then slowly move to foods. They also need to learn how to control the amount of food they eat.. They need to keep talking to the dietician about what they should be eating for a long time.

If people keep going to see the dietician they are more likely to keep the weight off and not have as many problems after the operation. Regular visits with the dietician and nutrition therapy from the dietician are really important, for nutrition therapy and for the dietician to help with weight and complications.

Bariatric surgery is not about losing weight it is also about changing your metabolism. It has an impact on your whole body. Studies that follow patients for a time show that many people keep the weight off for more than ten years. This is especially true for people who have Roux-en- gastric bypass or sleeve gastrectomy.

These types of Bariatric surgery work better than ways of treating obesity especially for people who are very overweight. Bariatric surgery is very good at helping people control their blood sugar levels. In fact many people, with type 2 diabetes are able to stop taking their medication or reduce the amount they take after having Bariatric surgery.

Bariatric surgery is having an effect on people who are obese. It helps with inflammation and the balance of bad bacteria in the gut. When people have this surgery the bacteria in their gut. The way their body deals with bile acids changes. This helps their body use energy better and respond to insulin. Bariatric surgery also seems to help with some big health problems like obesity-related cancers and sleep apnea. It even helps slow down kidney disease. Bariatric surgery is really making a difference, in the lives of people with obesity.

Patient selection and long-term adherence remain critical determinants of success. Comprehensive preoperative evaluation, including nutritional, psychological, and medical assessment, is essential to identify suitable candidates and optimize outcomes. Postoperative success relies heavily on sustained lifestyle modification, regular clinical monitoring, and lifelong nutritional supplementation. As surgical techniques evolve and minimally invasive approaches advance, bariatric surgery continues to play an expanding role in the multidisciplinary management of severe and treatment-resistant obesity.

Integrated approach

An integrated model combining dietician-led nutrition therapy and bariatric surgery provides optimal outcomes for patients with obesity. While nutrition therapy remains foundational for all patients, bariatric surgery offers a powerful therapeutic option for those with severe disease. Long-term success depends on continuous dietician involvement, behavioral modification, and multidisciplinary care.

[25,26,27]

5.4 Monitoring and Patient Education

Compelling administration of steroid-induced weight gain depends intensely on normal observing and comprehensive understanding instruction. early recognizable proof of weight pick up and related metabolic changes permits convenient mediations that can anticipate long-term complications checking thought to start some time recently starting long-term corticosteroid treatment pattern appraisal of body weight body mass index (BMI) midsection circumference blood weight fasting blood glucose and lipid profile is basic amid treatment intermittent monitoring monthly in the introductory stages and at that point at standard intervalshelps track patterns in weight pick up and fat redistribution uncommon consideration ought to be paid to central corpulence a trademark of corticosteroid abundance research facility observing for hyperglycemia dyslipidemia and electrolyte awkwardness is too imperative as these conditions regularly coexist with steroid-induced weight pick up in patients getting tall dosages or delayed treatment screening for highlights of cushingoid appearance ought to be joined into schedule follow-up understanding instruction plays a significant part in minimizing corpulence hazard patients ought to be educated at the begin of treatment around the potential for weight pick up expanded craving and fat redistribution related with corticosteroids clear clarifications make strides adherence to preventive methodologies and decrease uneasiness when physical changes happen dietary counseling ought to center on calorie control decreased admissions of refined carbohydrates and immersed fats satisfactory protein and low-sodium diets to restrain liquid maintenance empowering customary physical movement custom-made to the patients age and comorbidities makes a difference check muscle squandering and abundance fat amassing patients must too be taught on the significance of pharmaceutical adherence and cautioned against unexpected cessation of steroids which can lead to adrenal inadequate self-monitoring of body weight blood glucose particularly in diabetics or high-risk people and way of life propensities ought to be energized including patients in shared decision-making and giving ceaseless support through follow-up visits altogether moves forward results in overseeing steroid-induced weight. [28,29,30]

6. Future direction and research gaps

Steroid induced weight demonstrated as clinically crucial. however beneath inquired about result of inveterate corticosteroid treatment, whereas the metabolic impacts of glucocorticoids are well built up critical gaps stay in understanding the pathophysiology chance stratification, anticipation and administration of steroid related weight pick up, tending to these gaps through focused on inquire about will progress persistent results and direct prove based clinical practice. robotic research although glucocorticoids are known to impact craving adipogenesis and affront affectability the point by point atomic pathways that interspecific differential fat dissemination stay not completely characterized future investigate thought to prioritize cell type specific and tissue level examinations to depict how corticosteroids associated with fat tissue central apprehensive framework craving centers and skeletal muscle the parts of novel components such as glucocorticoid receptor isoforms epigenetic controllers and intestine microbiome modifications in steroid actuated weight warrant encourage investigation understanding these instruments may distinguish restorative targets for moderating weight pick up without decreasing against fiery efficacy. accuracy hazard stratification current clinical hone needs dependable devices to anticipate which patients are most helpless to noteworthy weight pick up or metabolic complications amid corticosteroid treatment expansive imminent cohort considers are required to distinguish hereditary statistic and clinical indicators of steroid actuated corpulence integration of polygenic hazard scores pattern adiposity measures and biomarkers of metabolic push may permit clinicians to tailor checking and preventive procedures based on person chance profiles. comparative adequacy of steroid alternatives research is required to assess the long term metabolic impacts of steroid saving operators and elective against fiery treatments over assorted maladies in spite of the fact that immunomodulators and biologics are progressively utilized head to head comparisons with corticosteroids centering on weight body composition and cardiometabolic results are restricted randomized controlled trials ought to join corpulence related endpoints to educate risk benefit assessments and restorative choice making. mediation studies there is a striking shortage of interventional trials outlined to avoid or decrease steroid initiated weight way of life mediations eat less work out pharmacotherapy eg operators focusing on craving or affront affectability and behavioral procedures require thorough testing particularly in the setting of corticosteroid utilize ponders ought to decide ideal mediation timing escalated and supportability as well as impacts on quality of life and malady activity 65 pediatric and geriatric populations special populaces require centered investigate children and teenagers uncovered to delayed corticosteroids may encounter special development and metabolic directions however longitudinal information are inadequate so also more seasoned grown-ups frequently have concomitant sarcopenia and metabolic defenselessness that may be exacerbated by steroids age particular ponders are basic to illuminate custom fitted rules. [31,32,]

CONCLUSION

Corticosteroid-induced obesity is a significant and often underestimated complication of long-term glucocorticoid therapy it results from complex metabolic effects including increased appetite fat redistribution insulin resistance and reduced energy expenditure this condition not only affects physical appearance but also increases the risk of comorbidities such as diabetes hypertension and cardiovascular disease thereby impacting overall quality of life early recognition regular monitoring and patient education are essential to minimize its burden a multidisciplinary approach involving dose optimization lifestyle modification and alternative therapies where possible can help prevent or mitigate corticosteroid-induced obesity and improve long-term patient outcomes

REFERENCES

  1. Fardet L, Petersen I, Nazareth I. Prevalence of long-term oral glucocorticoid prescriptions in the UK. BMJ Open. 2019;9(5):e024783.
  2. Schäcke H, Döcke WD, Asadullah K. Mechanisms involved in the side effects of glucocorticoids. Pharmacol Ther. 2002;96(1):23–43.
  3. van Staa TP, Leufkens HG, Abenhaim L, et al. Use of oral corticosteroids and risk of fractures. J Bone Miner Res. 2000;15(6):993–1000.
  4. Arterburn DE, Sofer T, Boudreau DM, et al. Obesity as a chronic disease. JAMA. 2020;324(8):794–795.
  5. Rizzoli R, Adachi JD, Cooper C, et al. Management of glucocorticoid-induced osteoporosis. Osteoporos Int. 2012;23(9):2257–2276.
  6. Tomlinson JW, Stewart PM. Cortisol metabolism and the role of 11β-HSD1. Endocr Rev. 2001;22(6):714–737.
  7. Tamez-Pérez HE, Quintanilla-Flores DL, Rodríguez-Gutiérrez R, et al. Steroid hyperglycemia. J Diabetes. 2015;7(1):9–20.
  8. Youssef J, Novosad SA, Winthrop KL. Infection risk with corticosteroids. Rheum Dis Clin North Am. 2016;42(1):157–176.
  9. Lee JM, Kim MK, Ko SH, et al. Pathophysiology of obesity. J Obes Metab Syndr. 2021;30(1):1–10.
  10. Peckett AJ, Wright DC, Riddell MC. Glucocorticoids and energy balance. Am J Physiol Endocrinol Metab. 2011;300(2):E201–E214.
  11. Walker BR. Cortisol and obesity. Int J Obes (Lond). 2001;25(Suppl 5):S47–S52.
  12. Pivonello R, Isidori AM, De Martino MC, et al. Complications of Cushing’s syndrome. Endocr Rev. 2016;37(1):12–45.
  13. McKay LI, Cidlowski JA. Molecular control of immune responses by glucocorticoids. Physiol Rev. 1999;79(2):387–432.
  14. Dallman MF, Pecoraro NC, la Fleur SE. Chronic stress and obesity. Physiol Behav. 2005;86(5):717–727.
  15. Fadul CE, Wood DK, Thaler HT, et al. Morbidity and mortality of corticosteroids. Neurology. 1988;38(11):1726–1729.
  16. Liu D, Ahmet A, Ward L, et al. Glucocorticoid-induced diabetes and adrenal suppression. CMAJ. 2013;185(11):E486–E490.
  17. Stanbury RM, Graham EM. Systemic corticosteroid therapy—side effects. Arch Dis Child. 1998;79(1):73–77.
  18. Clore JN, Thurby-Hay L. Glucocorticoid-induced hyperglycemia. Endocr Pract. 2009;15(5):469–474.
  19. Tirosh A, Shai I, Tekes-Manova D, et al. Changes in fat distribution with weight gain. Diabetes Care. 2011;34(4):960–965.
  20. Krishnan S, Rosenberg L, Djoussé L, et al. Body fat distribution and metabolic risk. JAMA. 2004;292(20):2571–2577.
  21. Rother KI. Diabetes treatment—bridging the gap. N Engl J Med. 2007;356(15):1499–1501.
  22. Laferrère B. Bariatric surgery and metabolic effects. J Clin Endocrinol Metab. 2011;96(8):2354–2362.
  23. Greenberg AS, Obin MS. Obesity and inflammation. J Clin Invest. 2006;116(7):1793–1801.
  24. Winer DA, Winer S, Shen L, et al. Adipose tissue immune responses. Nat Med. 2009;15(8):921–929.
  25. Fardet L, Kassar A, Cabane J, et al. Corticosteroid-induced adverse events. Drug Saf. 2007;30(10):861–881.
  26. Schäcke H, Döcke WD, Asadullah K. Glucocorticoid pharmacology. Pharmacol Ther. 2002;96(1):23–43.
  27. Bray GA, Kim KK, Wilding JPH. Obesity: a chronic relapsing disease. Lancet. 2017;390(10101):1947–1956.
  28. Garvey WT, Mechanick JI, Brett EM, et al. AACE obesity guidelines. Endocr Pract. 2016;22(Suppl 3):1–203.
  29. Jensen MD, Ryan DH, Apovian CM, et al. 2013 AHA/ACC/TOS obesity guidelines. Circulation. 2014;129(25 Suppl 2):S102–S138.
  30. Leung DY, Bloom JW. Update on glucocorticoid pharmacology. J Allergy Clin Immunol. 2003;111(1):3–22.
  31. Epel ES, Lapidus R, McEwen B, et al. Stress and body fat distribution. Psychoneuroendocrinology. 2001;26(1):37–49.
  32. Rosmond R. Role of cortisol in metabolic syndrome. Endocrinol Metab Clin North Am. 2005;34(1):1–20.

Reference

  1. Fardet L, Petersen I, Nazareth I. Prevalence of long-term oral glucocorticoid prescriptions in the UK. BMJ Open. 2019;9(5):e024783.
  2. Schäcke H, Döcke WD, Asadullah K. Mechanisms involved in the side effects of glucocorticoids. Pharmacol Ther. 2002;96(1):23–43.
  3. van Staa TP, Leufkens HG, Abenhaim L, et al. Use of oral corticosteroids and risk of fractures. J Bone Miner Res. 2000;15(6):993–1000.
  4. Arterburn DE, Sofer T, Boudreau DM, et al. Obesity as a chronic disease. JAMA. 2020;324(8):794–795.
  5. Rizzoli R, Adachi JD, Cooper C, et al. Management of glucocorticoid-induced osteoporosis. Osteoporos Int. 2012;23(9):2257–2276.
  6. Tomlinson JW, Stewart PM. Cortisol metabolism and the role of 11β-HSD1. Endocr Rev. 2001;22(6):714–737.
  7. Tamez-Pérez HE, Quintanilla-Flores DL, Rodríguez-Gutiérrez R, et al. Steroid hyperglycemia. J Diabetes. 2015;7(1):9–20.
  8. Youssef J, Novosad SA, Winthrop KL. Infection risk with corticosteroids. Rheum Dis Clin North Am. 2016;42(1):157–176.
  9. Lee JM, Kim MK, Ko SH, et al. Pathophysiology of obesity. J Obes Metab Syndr. 2021;30(1):1–10.
  10. Peckett AJ, Wright DC, Riddell MC. Glucocorticoids and energy balance. Am J Physiol Endocrinol Metab. 2011;300(2):E201–E214.
  11. Walker BR. Cortisol and obesity. Int J Obes (Lond). 2001;25(Suppl 5):S47–S52.
  12. Pivonello R, Isidori AM, De Martino MC, et al. Complications of Cushing’s syndrome. Endocr Rev. 2016;37(1):12–45.
  13. McKay LI, Cidlowski JA. Molecular control of immune responses by glucocorticoids. Physiol Rev. 1999;79(2):387–432.
  14. Dallman MF, Pecoraro NC, la Fleur SE. Chronic stress and obesity. Physiol Behav. 2005;86(5):717–727.
  15. Fadul CE, Wood DK, Thaler HT, et al. Morbidity and mortality of corticosteroids. Neurology. 1988;38(11):1726–1729.
  16. Liu D, Ahmet A, Ward L, et al. Glucocorticoid-induced diabetes and adrenal suppression. CMAJ. 2013;185(11):E486–E490.
  17. Stanbury RM, Graham EM. Systemic corticosteroid therapy—side effects. Arch Dis Child. 1998;79(1):73–77.
  18. Clore JN, Thurby-Hay L. Glucocorticoid-induced hyperglycemia. Endocr Pract. 2009;15(5):469–474.
  19. Tirosh A, Shai I, Tekes-Manova D, et al. Changes in fat distribution with weight gain. Diabetes Care. 2011;34(4):960–965.
  20. Krishnan S, Rosenberg L, Djoussé L, et al. Body fat distribution and metabolic risk. JAMA. 2004;292(20):2571–2577.
  21. Rother KI. Diabetes treatment—bridging the gap. N Engl J Med. 2007;356(15):1499–1501.
  22. Laferrère B. Bariatric surgery and metabolic effects. J Clin Endocrinol Metab. 2011;96(8):2354–2362.
  23. Greenberg AS, Obin MS. Obesity and inflammation. J Clin Invest. 2006;116(7):1793–1801.
  24. Winer DA, Winer S, Shen L, et al. Adipose tissue immune responses. Nat Med. 2009;15(8):921–929.
  25. Fardet L, Kassar A, Cabane J, et al. Corticosteroid-induced adverse events. Drug Saf. 2007;30(10):861–881.
  26. Schäcke H, Döcke WD, Asadullah K. Glucocorticoid pharmacology. Pharmacol Ther. 2002;96(1):23–43.
  27. Bray GA, Kim KK, Wilding JPH. Obesity: a chronic relapsing disease. Lancet. 2017;390(10101):1947–1956.
  28. Garvey WT, Mechanick JI, Brett EM, et al. AACE obesity guidelines. Endocr Pract. 2016;22(Suppl 3):1–203.
  29. Jensen MD, Ryan DH, Apovian CM, et al. 2013 AHA/ACC/TOS obesity guidelines. Circulation. 2014;129(25 Suppl 2):S102–S138.
  30. Leung DY, Bloom JW. Update on glucocorticoid pharmacology. J Allergy Clin Immunol. 2003;111(1):3–22.
  31. Epel ES, Lapidus R, McEwen B, et al. Stress and body fat distribution. Psychoneuroendocrinology. 2001;26(1):37–49.
  32. Rosmond R. Role of cortisol in metabolic syndrome. Endocrinol Metab Clin North Am. 2005;34(1):1–20.

Photo
Chokkakula Sridevi
Corresponding author

Associate Professor, Malla Reddy Pharmacy College.

Photo
Roshini Kannavena
Co-author

Department of Pharmacy Practice, Malla Reddy Pharmacy College, Telangana, India

Photo
Manisha Panyala
Co-author

Department of Pharmacy Practice, Malla Reddy Pharmacy College, Telangana, India

Photo
Tulja Rani Gampa
Co-author

Department of Pharmacy Practice, Malla Reddy Pharmacy College, Telangana, India

Chokkakula Sridevi, Roshini Kannavena, Manisha Panyala, Tulja Rani Gampa, Obesity as a Complication of Chronic Corticosteroid Use: Clinical Evidence and Management Strategies, Int. J. of Pharm. Sci., 2026, Vol 4, Issue 5, 1078-1095, https://doi.org/10.5281/zenodo.20051444

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