The Effects of Wild Bitter Gourd on High-Fat Diet Induced Metabolic Disorder and the Expression of Browning-Related Genes in White Adipose Tissue of C57BL/6J Mice

Obesity is defined as abnormal or excessive body fat accumulation due to excessive energy intake and less energy expenditure. Abdominal obesity is a risk factor for metabolic disorder related to diabetes, hyperlipidemia and cardiovascular diseases. Metabolic syndrome is the clustering of various risk factors those predictive higher risks of type 2 diabetes and cardiovascular diseases. Numerous studies have demonstrated that bitter melon (Momordica charantisa) has potential for ameliorating obesity and metabolic syndrome. Previous studies showed that mice fed high sucrose diet supplemented with bitter gourd powder (BGP) for 25 weeks had higher mRNA expression of genes related to browning in white adipose tissue, which is considered an effective way to increase energy expenditure and combat obesity. Bitter melon is known to have a number of health benefits. For instance, the triterpenoids in bitter melon, especially aglycone forms, have been shown to activate AMPK and increase glucose uptake in adipocytes and myocytes. It has been demonstrated the hexane extracts of acid-hydrolyzed BGP has been shown to induce “browning” related mRNA expressions in the 3T3-L1-cell model. In this study, we aimed to examine the effects of BGP and its hydrolysis product on ameliorating metabolic disorders and stimulating adipose tissue browning of high fat diet induced obese mice. C57BL/6J mice were fed the high fat diet for 15 weeks and then assigned into 5 groups, including: HF group (fed the high fat diet), 3%BGP group (fed the high fat diet supplemented with 3%BGP), 3%BGPa group (fed the high fat diet supplemented with 3% hydrolyzed BGP), 5%BGP group (fed the high fat diet supplemented with 5%BGP), and 5%BGPa group (fed the high fat diet supplemented with 5% hydrolyzed BGP). They were fed the respective test diets for 20 week. Another group of mice fed a chow diet throughout the 35 weeks periods served as the normal control. Compared to the HF group, mice in the 3%BGPa, 5%BGP and 5%BGPa groups had significantly lower serum glucose at 11 weeks, and significantly lower body weight gain after 20 weeks. Serum cholesterol level of 3%BGP, 3%BGPa, 5%BGP and 5%BGPa groups were significantly lower than those of the HF group at 11 and 20 week. The mRNA expressions of thermogenic and mitochondrial biogenic genes in BAT and RWAT of the 5%BGP were significantly higher than the HF group. In addition, mice fed the 5%BGPa diet showed significantly higher mRNA expression of beige markers and mitochondrial biogenic genes in EWAT. In conclusion, BGP and hydrolyzed BGP up-regulated the expression of thermogenic genes in BAT and brown-related genes in visceral white adipose tissue, reduced serum cholesterol and increased insulin sensitivity. Results of this study support the effects of BGP and its hydrolysis product on ameliorating the diet-induced obesity and metabolic disorder, and presumably can promote browning in mice.