Oxyresveratrol has been proven effective in inhibiting adipogenesis in a 3T3-L1 cell model. We investigated the preventive effect of oxyresveratrol supplementation on obesity development in high-fat diet-fed mice. Male C57bl/6 mice were randomly subjected to control (5% fat by weight, LF), high-fat (30% fat by weight, HF), and high-fat supplemented with 0.25% and 0.5% oxyresveratrol (OXY1 and OXY2, respectively) diet groups for eight weeks. Oxyresveratrol supplementation effectively alleviated obesity-associated symptoms such as insulin resistance, hyperglycemia, and hepatic steatosis in high-fat diet-fed mice. Compared to the high-fat diet group, oxyresveratrol supplementation suppressed expression of glucose-6-phosphatase, sterol regulatory element-binding proteins 1, fatty acid synthase and CCAAT/Enhancer-binding proteins α, and elevated AMP-activated protein kinase (α2-catalytic subunit) level in liver, upregulated insulin-dependent glucose transporter type 4 level in adipose tissue, and increased expression of insulin receptor substrate 1, insulin-dependent glucose transporter type 4, AMP-activated protein kinase α, peroxisome proliferator-activated receptor γ coactivator-1α, and sirtuin 1 in muscle to regulate lipid and glucose homeostasis in these tissues. This study demonstrated that oxyresveratrol supplementation effectively ameliorated obesity-associated symptoms in high-fat diet-fed mice, presumably attributed to mediating critical regulators involved in lipid and glucose homeostasis in liver, visceral fat, and muscle.

Bitter melon (BM; Momordica charantia) supplementation slows weight gain and tissue fat accumulation in fat diet‐induced obese rat. Liver and muscle carnitine palmitoyl transferase‐I expression was enhanced in BM rats, suggesting increased lipid oxidation. This study was designed to determine if extracts from BM juice can suppress triglyceride (TG) content in the 3T3‐L1 cell line. 3T3‐L1 pre‐adipocytes were induced to differentiate in the presence or absence of an ethanol‐water extract of BM juice. The latter was obtained by stepwise gradient elution of an organic extract of BM juice. Two fractions (eluted by 10% & 30% ethanol respectively and then freeze‐dried; F2 at 350μg/mL & F3 at 50μg/mL) were found to reduce TG content on day 10 (p<0.01, F3) & day 12 (p<0.01, both); and GPDH activity on day 10 & 12 (p<0.01, both) of a 12‐day study. Two‐way ANOVA indicated reduced mRNA expression of fatty acid synthase (p<0.001), acetyl CoA carboxylase 1 (p<0.01) and Glut‐4 (p<0.01) in BM‐treated adipocytes. With F3, these effects primarily occurred between days 8–10. Downregulation of PPARγ (p<0.001) and SREBP‐1c (p<0.001) mRNA expression was observed in F3‐treated cells on day 12. The data suggest that bioactive ingredient(s) in BM may suppress TG synthesis in 3T3‐L1 cells through suppressing the expression of certain lipogenic genes and transcription factors. (Supported by the Faculty Development Fund, HKU)