Dietary Bitter Melon Seed Increases Peroxisome Proliferator-Activated Receptor-γ Gene Expression in Adipose Tissue, Down-Regulates the Nuclear Factor-κB Expression, and Alleviates the Symptoms Associated with Metabolic Syndrome

Abstract

The objective of this study was to examine the extent to which bitter melon seed (BMS) alleviates the symptoms associated with metabolic syndrome and elucidate the mechanism by which BMS exerts beneficial effects. Three-month-old female Zucker rats were assigned to following groups: lean control (L-Ctrl), obese control (O-Ctrl), and obese + BMS (O-BMS). The control groups were fed AIN-93M purified rodent diet, and the O-BMS group was fed AIN-93M diet modified to contain 3.0% (wt/wt) ground BMS for 100 days. After 100 days of treatment, BMS supplementation in the obese rats lowered the total serum cholesterol by 38% and low-density lipoprotein-cholesterol levels by about 52% and increased the ratio of serum high-density lipoprotein-cholesterol to total cholesterol compared to the O-Ctrl group. The percentage of total liver lipids was about 32% lower and serum triglyceride levels were 71% higher in the O-BMS group compared to the O-Ctrl group. Serum glucose levels were significantly lowered partly because of the increase in the serum insulin levels in the BMS-based diet groups. BMS supplementation increased the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) in the white adipose tissue of the obese rats significantly (P < .05) and down-regulated the expression of PPAR-γ, nuclear factor-κB (NF-κB), and interferon-γ mRNA in heart tissue of the obese rats. The findings of this study suggest that BMS improves the serum and liver lipid profiles and serum glucose levels by modulating PPAR-γ gene expression. To our knowledge, this study for the first time shows that BMS exerts cardioprotective effects by down-regulating the NF-κB inflammatory pathway.

Antidiabetic effects of Momordica charantia (bitter melon) and its medicinal potency

“…The findings suggest that M. charantia protects pancreatic β-cells through downregulation of MAPKs and NF-κB in MIN6N8 cells. A similar study suggest that M. charantia improves the serum and liver lipid profiles and serum glucose levels by modulating PPAR-γ gene expression [66] . According to Ragasa et al, clerosterol and 5α-stigmasta-7-en-3β-ol were isolated as sterols from M. charantia having significant hypoglycemic effects [67] .…”

“…charantia and its various extracts and components are believed to exert their hypoglycemic effects via different physiological, pharmacological and biochemical modes [62][63][64] . The possible modes of the hypoglycemic actions of M. charantia and its various extracts and compounds are its hypoglycemic effect [67,70] , stimulation of peripheral and skeletal muscle glucose utilisation [71,72] , inhibition of intestinal glucose uptake [73][74][75] , inhibition of adipocyte differentiation [76] , suppression of key gluconeogenic enzymes [77,78] , stimulation of key enzyme of HMP pathway [77] , and preservation of islet β cells and their functions [66] . Today, over 140 different studies worldwide have investigated anti-hyperglycemic and hypoglycemic effects of the different extracts and ingredients of M. charantia in both human and animal models [32,33,62] .…”

Wild bitter gourd improves metabolic syndrome: A preliminary dietary supplementation trial

“…Among these, the anti-diabetic activity and possible mechanisms of BG have been demonstrated in molecular, cellular and animal models as well as in human studies and extensively reviewed [3-5]. In addition, BG has been shown to ameliorate metabolic syndrome (MetS) in animal studies [6-8]. Nevertheless, it remains unclear if BG has beneficial effects on MetS in human.…”

“…BG extract activated PPARα [14] and PPARγ [15,16], and thus were recognized as a PPARα/γ dual agonist [17]. In animal models, BG up-regulated PPARγ and PPARα-mediated pathways which is associated with improved MetS [6,18]. Together with other evidences that BG improved insulin signaling [8], BG is considered a potential "traditional Chinese medicines" in treating MetS [19].…”

Treating Hyperinsulinemia with Momordica charantia

“…Its mechanisms of action include increased phosphorylation of acetylCoA carboxylase and AMP-activated protein kinase (AMPK) [5], reduction of lipogenesis, enhanced thermogenesis and lipolysis [6]. The extract down-regulates the expression of peroxisome proliferatoractivated receptor (PPAR)-gamma, nuclear factor kappaB (NF-kB), and interferon-gamma in heart tissue, with cardio-protective effect thanks to reduction of inflammation [7]. In addition, Momordica exerts an interesting endocrine effect where it inhibits the enzyme 11β-hydroxysteroid dehydrogenase type 1, that metabolises the mineralocorticoid cortisone to the glucocorticoid cortisol [8].…”