Evaluating Standardized Momordica Charantia (Bitter Melon) Extracts as A Therapeutic Intervention for Obesity

Obesity is a chronic condition with a progressive nature that even rebounds at times and it has now hit global epidemic proportions [1]. It carries with it a wide range of complications, chronic diseases and a significant burden on health systems globally. Recent data showed 3.71 million estimated deaths and 129 million disability-adjusted life-years because of overweight and obesity alone in 2021 [2]. Moreover, these risks are some of the leading global risks and they are the fastest growing risks in terms of disease burden [2]. Obesity is increasingly treated within medical and public health frameworks as a disease entity, yet this classification raises important conceptual and practical concerns. Traditionally, diseases are understood as conditions that disrupt normal physiological function, producing identifiable changes in organs or tissues that lead to both objectively measurable abnormalities and subjectively experienced symptoms such as pain, fatigue, or dysfunction. In contrast, obesity does not always conform neatly to this definition. While it is associated with altered metabolic processes and increased risk of comorbidities, it does not invariably produce immediate or uniform pathological changes in all individuals. This creates an inherent tension in defining obesity strictly as a disease, particularly when compared with more classical disease models [3]. One of the most debated aspects of this issue is the reliance on the Body Mass Index (BMI) as a primary diagnostic criterion. BMI is a simple, population-level screening tool based on height and weight, but it does not directly measure body fat distribution, metabolic health, or functional impairment. As a result, individuals with similar BMI values may have vastly different health profiles. For instance, some individuals categorized as obese by BMI may be metabolically healthy, while others within the “normal” BMI range may exhibit significant metabolic dysfunction. This disconnect highlights a deviation from standard disease definitions, where diagnosis is typically based on direct evidence of pathological changes rather than indirect or surrogate markers [3]. The consequences of this definitional ambiguity are significant. Clinically, it may lead to overdiagnosis or misclassification, resulting in unnecessary medical interventions for some individuals while potentially overlooking others who are at genuine risk. Financially, it places a burden on healthcare systems by allocating resources toward generalized treatment approaches that may not be appropriate or effective for all patients. The broad labeling of obesity as a disease can also influence insurance policies, pharmaceutical development and treatment priorities, sometimes shifting focus away from individualized care toward standardized and occasionally oversimplified, management strategies. Beyond clinical and economic implications, the classification of obesity as a disease carries important political and psychological ramifications. Public health policies may become overly prescriptive, emphasizing weight reduction without consideration of social, cultural and behavioral contexts. This can inadvertently stigmatize individuals, reinforcing negative perceptions and contributing to psychological distress, including low self-esteem, anxiety and depression. Moreover, framing obesity strictly as a disease may reduce personal agency in some contexts while simultaneously placing undue responsibility on individuals in others, creating a paradox in how responsibility and blame are assigned. It is also crucial to recognize that body weight and composition are influenced by a complex interplay of genetic, environmental, behavioral and socio-economic factors. Everyday behaviors such as dietary habits, physical activity levels and lifestyle choices exist along a spectrum and are often shaped by cultural norms and environmental constraints. Therefore, there is a risk that normal variations in body weight or natural adaptive behaviors could be medicalized if diagnostic thresholds are applied too rigidly. This could lead to the unnecessary labeling of individuals as “overweight” or “diseased,” even when their condition does not result in functional impairment or reduced quality of life. In light of these considerations, a more nuanced approach to obesity is needed—one that balances the recognition of its potential health risks with an appreciation of individual variability and context. Rather than relying solely on simplified metrics like BMI, a comprehensive assessment incorporating metabolic health, functional capacity and psychosocial well-being would provide a more accurate and meaningful framework. Such an approach would help ensure that interventions are both clinically appropriate and ethically sound, avoiding the pitfalls of overmedicalization while still addressing genuine health concerns [3]. Obesity is a complex chronic disease rendering premature death and complications of health as well as an escalation of costs related to ill health. In 2015, estimates were about 603.7 million adults and 107.7 million children with obesity accounting for 50% of missed years of life owing to premature death, among other health problems. It was also found that the proportion of obese individuals had increased twofold in almost half the countries since 1980.[4].It has been projected that by the year 2030, obesity would affect one in every two adults in the United States. The health care sector alone in the United States bears the burden of an estimated $480 billion annually due to obesity [5],[6].

Obesity is actually described by the World Health Organization as excessive adiposity, which brings additional health implications. Commonly classified as a BMI over 30 kg/m².it poses a risk to many metabolic complications. Its grandeurs are not limited to ischemic heart disease but include toxic endocrine specific-disease connections, muscular dystrophy and chronic illness [7]. Obesity is formally described by the World Health Organization as a condition characterized by excessive or abnormal accumulation of adipose tissue that presents a risk to health. This definition emphasizes not merely an increase in body weight, but specifically an increase in body fat that has the potential to disrupt normal physiological processes. In clinical and epidemiological practice, obesity is most commonly identified using the Body Mass Index (BMI), with a value of 30 kg/m² or higher serving as the standard threshold for classification. Although BMI is a convenient and widely used screening tool, it is important to recognize that it provides only an indirect estimate of body fat and does not account for variations in fat distribution, muscle mass, or individual metabolic differences. Despite these limitations, the classification of obesity as a BMI greater than 30 kg/m² has been instrumental in identifying populations at risk and guiding public health strategies. Individuals within this category are known to have an increased likelihood of developing a wide range of metabolic complications. These include insulin resistance, dyslipidemia, hypertension and ultimately metabolic syndrome, which collectively contribute to a higher risk of morbidity and mortality. The metabolic disturbances associated with obesity arise from complex interactions between adipose tissue, inflammatory mediators and hormonal imbalances, leading to systemic effects that extend far beyond simple weight gain. The health consequences of obesity are extensive and multifaceted. While it is widely recognized as a major risk factor for cardiovascular diseases such as ischemic heart disease, its impact is not confined to the cardiovascular system alone. Obesity is strongly associated with a variety of endocrine-related disorders, including type 2 diabetes mellitus, thyroid dysfunction and abnormalities in reproductive hormones. Excess adipose tissue acts as an active endocrine organ, secreting adipokines and cytokines that influence insulin sensitivity, appetite regulation and inflammatory pathways. These endocrine disruptions can lead to chronic metabolic imbalance and contribute to disease progression over time. In addition to metabolic and endocrine complications, obesity also affects the musculoskeletal system. The increased mechanical load placed on joints, particularly weight-bearing joints such as the knees and hips, can lead to degenerative conditions like osteoarthritis. Over time, this can result in reduced mobility, chronic pain and decreased quality of life. In more severe or prolonged cases, obesity-related physical inactivity may contribute to muscle wasting or conditions resembling muscular dysfunction, further compounding physical limitations. Furthermore, obesity is closely linked with a range of chronic illnesses that span multiple organ systems. These include non-alcoholic fatty liver disease (NAFLD), certain types of cancer, respiratory disorders such as obstructive sleep apnea and even neurodegenerative conditions. The chronic low-grade inflammation associated with excess adiposity plays a central role in the pathogenesis of many of these conditions. This persistent inflammatory state can impair normal cellular function and promote disease development over time. Ultimately, obesity represents a complex and systemic health condition with far-reaching consequences. Its characterization as excessive adiposity underscores the importance of understanding not just body weight, but the biological and metabolic implications of fat accumulation. While BMI remains a practical tool for classification, a broader perspective that includes metabolic health, hormonal balance and functional outcomes is essential for accurately assessing its impact. Recognizing the diverse complications associated with obesity highlights the need for comprehensive management strategies that address both its underlying causes and its wide-ranging effects on human health [7]. Obesity also lowers the life expectancy directly. Also, it is the worst risk factor for hospitalization and death related to corona virus disease 2019 (COVID-19). [8] Thus, smoking remains the leading risk factor for disease burden associated globally in many countries while high BMI has become the culprit in many regions, including Australasia and southwestern Latin America[9].

High body fat increases the risk of several dysfunctions such as diabetes, Hyperlipidaemia and hypertension that may lead to arteriosclerotic disease and metabolic syndrome [10]. Thus, there is a growing alarm concerning obesity, thereby increasing numbers of complications associated with cardiovascular, in both developed and developing countries can also cause adipocyte dysfunction and inflammation. Recently, an endocrine organ is a concept of adipose tissues as secretors of many hormones that regulate fat and glucose - adipokines as well as cytokines--adiponectin, leptin and tumor necrosis factor-α (TNF-α) [11],[12]. Consequently, an elevated concentration of TNF-α, followed by interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), promotes adipocyte dysfunction and insulin resistance [13]. In addition, inflammatory cells infiltration into adipose tissues also increases [14]. Proinflammatory cytokines and oxidative stress play a central and interconnected role in the development of metabolic disturbances, particularly in the context of obesity and related disorders. Cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and other inflammatory mediators are released in increased amounts from enlarged adipocytes and infiltrating immune cells, especially macrophages, within adipose tissue. This chronic low-grade inflammation is now recognized as a key driver of metabolic dysfunction, rather than merely a consequence of excess fat accumulation. These proinflammatory signals disrupt normal cellular communication and interfere with insulin signaling pathways, ultimately contributing to insulin resistance [15]. Insulin resistance is a hallmark of metabolic disorders such as type 2 diabetes mellitus. Under normal physiological conditions, insulin facilitates glucose uptake into cells, particularly in muscle and adipose tissue and suppresses glucose production in the liver. However, in an inflammatory environment, cytokines activate intracellular signaling pathways such as the nuclear factor-kappa B (NF-κB) pathway and c-Jun N-terminal kinase (JNK), which impair insulin receptor signaling. This leads to reduced glucose uptake by peripheral tissues and increased hepatic glucose output, resulting in elevated blood glucose levels. Over time, the pancreas compensates by producing more insulin, but this compensatory mechanism may eventually fail, leading to overt hyperglycemia. Oxidative stress further exacerbates these disturbances by generating an excess of reactive oxygen species (ROS) that overwhelm the body’s antioxidant defense systems. ROS are produced during normal cellular metabolism, but their levels increase significantly in conditions such as obesity, overnutrition and mitochondrial dysfunction. Elevated ROS can directly damage cellular components, including lipids, proteins and DNA and also act as signaling molecules that amplify inflammatory responses. This creates a vicious cycle in which oxidative stress promotes inflammation and inflammation in turn increases oxidative stress. The liver, adipose tissue and skeletal muscle are particularly affected by these processes, as they are central to metabolic regulation. In the liver, pro-inflammatory cytokines and oxidative stress contribute to hepatic insulin resistance and promote the accumulation of fat, leading to conditions such as non-alcoholic fatty liver disease (NAFLD). In adipose tissue, chronic inflammation alters adipokine secretion, reducing beneficial factors like adiponectin while increasing harmful ones, thereby impairing lipid and glucose metabolism. In skeletal muscle, which is a major site of glucose disposal, inflammation and oxidative damage reduce insulin sensitivity and mitochondrial function, limiting the tissue’s ability to utilize glucose efficiently. Moreover, these metabolic disturbances are closely linked to activation of the immune response. The infiltration of immune cells into metabolic tissues further amplifies the production of cytokines and perpetuates the inflammatory state. This crosstalk between metabolic and immune systems has led to the concept of “metaflammation,” a chronic, low-grade inflammatory condition driven by metabolic excess. Ultimately, the combined effects of pro-inflammatory cytokines and oxidative stress disrupt metabolic homeostasis across multiple organs, contributing to the progression of insulin resistance and associated chronic diseases [15, 16]. If there is an acute activation of inflammation pathways in hepatocytes, it results in local and systemic insulin resistance additionally [17, 18].

Bitter Melon is a climbing shrub that is mostly cultivated in Bangladesh, India, China and Korea, majorly in various Asian countries. The plant is also naturally spread in the tropical regions of Amazon, East Africa and the Caribbean. Bitter Melon is an inhabitant of the family Cucurbitaceae with the scientific name Momordica charantia  L. Normally, two varieties of the plant are found in Bangladesh, with the small type being referred to locally as "Ucche" and the larger-size one as "Karela" (Figure 1). However, some other wild-type African species are also found in the country: M. balsamina L., M. foetida Schum and M. rostrata  A. Zimm. Throughout Bangladesh and the Indian subcontinent, the bitter melon fruits are consumed as a culinary vegetable, although this plant is used as a traditional medicinal plant for the treatment of different diseases in such developing countries as Brazil, China, Colombia, Cuba, Ghana, Haiti, India, Mexico, Malaya, Nicaragua, Panama and Peru [19]. The most commonly known traditional use amongst many countries for this plant is the treatment of diabetes. It is also used for alleviating various other pathological conditions like dysmenorrhea, eczema, emmenagogue, galactagogue, gout, jaundice, kidney (stone), leprosy, leucorrhea, piles, pneumonia, psoriasis, rheumatism and scabies [20]. Momordica charantia has been used for abortifacient, anthelmintics, contraceptives, antimalarials and laxatives [20].

 

 

Figure 1: Fruits of different variety of Momordica charantia available in India (a) commonly known as Karela and (b) as Ucche

 

 

Figure 1: Standard calibration curve of (A) Gallic acid for total phenolic content and (B) Quercetin for total flavonoid content.

 

 

Figure 2: Inhibitory concentration curve of extract of Momordica charantia and Ascorbic acid in DPPH scavenging assay.

 

 

Figure 3: Antioxidant efficacy of extract of Momordica charantia by DPPH scavenging assay.

 

 

Figure 4: Inhibitory concentration curve of extract of Momordica charantia and Ascorbic acid in ABTS radical cation decolorization assay.

 

 

Figure 5: Antioxidant efficacy of extract of Momordica charantia by ABTS radical cation decolorization assay.

 

 

Figure 6: Inhibitory concentration curve of extract of Momordica charantia and Ascorbic acid in FRAP assay.

 

 

Figure 7: Antioxidant efficacy of extract of Momordica charantia by FRAP assay.

 

 

Figure 8: Inhibitory concentration curve of extract of Momordica charantia and orlistat in pancreatic lipase inhibition assay.

 

 

Figure 9: Anti-lipase activity of extract of Momordica charantia by pancreatic lipase inhibition assay.

Table 8: Anti-adipogenic activity of extracts of Momordica charantia using 3T3-L1 cell.

Sample	Lipid Accumulation (%)
Control	100
Ethanolic extract	68.51 ± 2.43
Hydroalcoholic extract	45.62 ± 1.81
Ethyl acetate extract	61.54 ± 1.98
Standard (Drug)	30.16 ± 1.45

Note: Results are represented as mean ± standard deviation (n=3).

 

 

 

Figure 10: Anti-adipogenic property of extracts of Momordica charantia using 3T3-L1 cell model.

The results clearly indicate that the hydroalcoholic extract exhibits the strongest anti-adipogenic activity among the plant extracts. The reduction in lipid accumulation suggests that the extract may interfere with adipocyte differentiation and lipid storage processes. This effect may be attributed to the presence of bioactive compounds that regulate key transcription factors involved in adipogenesis, such as PPAR-γ and C/EBP-α, thereby inhibiting fat cell formation.

DISCUSSION

The present investigation was undertaken to systematically evaluate the antioxidant and anti-obesity potential of standardized extracts of Momordica charantia using a combination of phytochemical analysis, in vitro antioxidant assays, pancreatic lipase inhibition and anti-adipogenic studies. The integrated approach adopted in this study provides a comprehensive understanding of the relationship between phytochemical composition and biological activity, thereby addressing the existing research gap concerning standardization and mechanistic validation of this traditionally important medicinal plant.

The extraction yield data (Table 1) demonstrated that the hydroalcoholic extract yielded the highest percentage (15.2% w/w), followed by ethanolic (12.4% w/w) and ethyl acetate extract s (10.6% w/w). This finding highlights the critical role of solvent polarity in the extraction of phytoconstituents. Hydroalcoholic solvents, due to their intermediate polarity, are capable of dissolving a broader spectrum of compounds, including both hydrophilic and moderately lipophilic constituents. This observation is consistent with previous reports indicating that mixed solvent systems enhance extraction efficiency and yield a more diverse phytochemical profile [36].

The higher yield of the hydroalcoholic extract suggests that it may contain a richer reservoir of bioactive compounds, which subsequently contributes to its superior biological activity. This reinforces the importance of selecting appropriate extraction methods in phytopharmacological studies, particularly when the objective is to maximize therapeutic efficacy.

Qualitative phytochemical screening (Table 2) revealed the presence of alkaloids, flavonoids, tannins, saponins and steroids across different extracts. Notably, tannins and phenolic compounds were detected in all extracts, indicating their widespread distribution in M. charantia. However, the hydroalcoholic extract exhibited a more diverse phytochemical composition, including saponins and alkaloids, which are known to possess significant pharmacological activities.

The quantitative estimation of TPC and TFC (Table 3; Figure 1) further substantiated these findings, with the hydroalcoholic extract exhibiting the highest phenolic (112.75 mg GAE/g) and flavonoid content (89.61 mg QE/g) . Phenolic compounds are widely recognized for their antioxidant properties, primarily due to their ability to donate hydrogen atoms and electrons, thereby neutralizing free radicals [17]. Flavonoids, on the other hand, contribute through multiple mechanisms, including radical scavenging, metal chelation and modulation of enzyme activity.

The higher concentration of these bioactive compounds in the hydroalcoholic extract provides a biochemical basis for its enhanced antioxidant and anti-obesity activities. Furthermore, the presence of saponins and triterpenoids, as reported in previous studies [23], may contribute to lipid metabolism regulation and enzyme inhibition, thereby supporting the observed anti-obesity effects.

The antioxidant potential of M. charantia extracts was evaluated using three complementary assays such as DPPH, ABTS and FRAP (Tables 4 to 6; Figures 2 to 7) . These assays collectively assess different aspects of antioxidant activity, including free radical scavenging and reducing power.

In the DPPH assay (Table 4; Figures 2 and 3), all extracts exhibited a concentration-dependent increase in radical scavenging activity. Although the ethyl acetate extract  showed higher percentage inhibition at certain concentrations, IC₅₀ values indicated that the hydroalcoholic extract was more potent (30.28 µg/mL). This suggests that while ethyl acetate extract s may provide immediate radical quenching, the hydroalcoholic extract is more efficient at lower concentrations.

A similar trend was observed in the ABTS assay (Table 5; Figures 4 and 5), where the hydroalcoholic extract again demonstrated the lowest IC₅₀ value. The ABTS assay is particularly useful for evaluating both hydrophilic and lipophilic antioxidant activity, further supporting the broad-spectrum efficacy of the hydroalcoholic extract.

The FRAP assay (Table 6; Figures 6 and 7) revealed that all extracts possess reducing power, with the hydroalcoholic extract showing superior electron-donating capacity. This assay reflects the ability of antioxidants to reduce Fe³⁺ to Fe²⁺, indicating their potential to act as reductants in biological systems.

Mechanistically, the antioxidant activity observed in this study can be attributed to both hydrogen atom transfer (HAT) and single electron transfer (SET) mechanisms. Phenolic compounds donate hydrogen atoms to neutralize free radicals (HAT), while flavonoids and other compounds participate in electron transfer reactions (SET). The ability of the hydroalcoholic extract to perform effectively in all three assays suggests its involvement in multiple antioxidant pathways.

The relevance of these findings extends beyond free radical scavenging, as oxidative stress plays a pivotal role in the pathogenesis of obesity and related metabolic disorders. Increased production of reactive oxygen species (ROS) leads to lipid peroxidation, inflammation and insulin resistance [15]. Therefore, the strong antioxidant activity of M. charantia may contribute to its anti-obesity effects by mitigating oxidative stress and improving metabolic homeostasis.

Pancreatic Lipase Inhibition and Its Therapeutic Significance

The pancreatic lipase inhibition assay (Table 7; Figures 8 and 9) demonstrated that all extracts exhibited significant inhibitory activity in a concentration-dependent manner . The hydroalcoholic extract showed the highest inhibition (70.94% at 200 µg/mL) and the lowest IC₅₀ value (111.63 µg/mL), indicating superior potency among the plant extracts.

Pancreatic lipase is a crucial enzyme responsible for the hydrolysis of dietary triglycerides into absorbable fatty acids. Inhibition of this enzyme reduces fat absorption, thereby contributing to weight management. The observed inhibitory activity may be attributed to phenolic compounds, flavonoids and saponins, which are known to interact with the enzyme’s active site and inhibit its function.

The standard drug orlistat exhibited higher inhibition, as expected, but the significant activity of the hydroalcoholic extract highlights its potential as a natural alternative with possibly fewer side effects. This is particularly important given the limitations associated with synthetic anti-obesity drugs, including gastrointestinal disturbances and long-term safety concerns.

The anti-adipogenic activity evaluated using the 3T3-L1 cell model (Table 8; Figure 10) revealed that the hydroalcoholic extract significantly reduced lipid accumulation (45.62%) compared to ethanolic and ethyl acetate extract s . This indicates its ability to inhibit adipocyte differentiation and lipid storage.

Adipogenesis is regulated by key transcription factors such as PPAR-γ and C/EBP-α, which control the differentiation of preadipocytes into mature adipocytes [41]. The reduction in lipid accumulation suggests that the hydroalcoholic extract may downregulate these transcription factors, thereby inhibiting adipogenesis.

Additionally, M. charantia has been reported to activate AMPK, a central regulator of energy metabolism that promotes fatty acid oxidation and inhibits lipogenesis [13]. Activation of AMPK also improves insulin sensitivity and reduces lipid accumulation, further supporting the anti-obesity potential of the extract.

The combined results of antioxidant, lipase inhibition and anti-adipogenic assays suggest that M. charantia exerts its anti-obesity effects through a multi-target mechanism:

• Reduction of oxidative stress through antioxidant activity
• Inhibition of dietary fat absorption via pancreatic lipase inhibition
• Suppression of adipocyte differentiation and lipid accumulation
• Modulation of metabolic pathways such as AMPK signaling
• This multi-faceted mechanism is advantageous in addressing the complex pathophysiology of obesity, which involves multiple interconnected pathways.
• Correlation with Literature and Research Gap

The findings of this study are consistent with previous reports highlighting the antioxidant and metabolic benefits of M. charantia [13,23]. However, clinical studies have shown inconsistent results regarding its effect on body weight and BMI. This discrepancy may be attributed to the lack of standardization in extract preparation and variability in phytochemical composition.

The present study addresses this limitation by demonstrating that a standardized hydroalcoholic extract, characterized by higher phenolic and flavonoid content, exhibits superior biological activity. This underscores the importance of standardization in herbal research and supports the hypothesis that phytochemical composition directly influences therapeutic efficacy.

Limitations and Future Perspectives: Despite the promising findings, the study has certain limitations. The results are based on in vitro assays, which may not fully replicate in vivo conditions. Further studies involving animal models and clinical trials are necessary to validate these findings. Additionally, detailed molecular studies are required to elucidate the exact mechanisms of action, particularly the role of signaling pathways such as AMPK, PI3K/Akt and PPAR-γ.

CONCLUSION

The present study provides comprehensive evidence supporting the antioxidant and anti-obesity potential of Momordica charantia, with a particular emphasis on the influence of extraction methods on biological activity. Among the three extracts evaluated, the hydroalcoholic extract emerged as the most potent, demonstrating superior performance across phytochemical, antioxidant, anti-lipase and anti-adipogenic assays.

The extraction yield analysis confirmed that the hydroalcoholic solvent system is more efficient in extracting bioactive compounds, which was further supported by phytochemical screening and quantitative analysis. The higher total phenolic and flavonoid content observed in the hydroalcoholic extract provides a strong biochemical basis for its enhanced biological activity.

The antioxidant assays (DPPH, ABTS and FRAP) demonstrated that the extracts possess significant free radical scavenging and reducing capabilities. The hydroalcoholic extract consistently exhibited the lowest IC₅₀ values, indicating higher potency. These findings highlight its ability to act through multiple mechanisms, including hydrogen atom transfer and electron transfer, thereby providing broad-spectrum antioxidant protection.

The anti-obesity potential of the extracts was validated through pancreatic lipase inhibition and anti-adipogenic assays. The hydroalcoholic extract showed significant inhibition of pancreatic lipase, suggesting its role in reducing dietary fat absorption. Furthermore, its ability to reduce lipid accumulation in 3T3-L1 cells indicates inhibition of adipogenesis, a key process in obesity development.

The integrated results suggest that Momordica charantia exerts its anti-obesity effects through a dual mechanism, targeting both fat digestion and fat storage, while also reducing oxidative stress. This multi-target approach is particularly beneficial in managing complex metabolic disorders such as obesity.

Importantly, the study highlights the critical role of extract standardization, as variations in solvent systems significantly influence phytochemical composition and biological activity. The use of a hydroalcoholic solvent system resulted in a more potent extract, emphasizing the need for standardized protocols in future research and therapeutic applications.

Thus, Momordica charantia represents a promising natural therapeutic agent for obesity management, with the hydroalcoholic extract showing the highest potential. However, further studies, including in vivo and clinical investigations, are required to confirm these findings and facilitate its translation into clinical practice.

Financial Support

Nil.

Consent for Publication

Not Applicable

Conflicts of Interest

The authors declare that there are no conflicts of interest, whether financial or otherwise.

Acknowledgements

The authors wish to thank all researchers for providing an eminent literature source for devising this manuscript.

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