Wild bitter gourd ameliorates high-fat diet induced metabolic disorder, fatty liver and hepatic mRNA expressions of related genes in C57BL/6J mice.
Date Issued
2016
Date
2016
Author(s)
Tung, Yu-Tzu
Abstract
The prevalence of obesity and metabolic disorders over the world increases in recent decades, as a result of changes in the diet and life style. Obesity are linked to high risks of many chronic diseases, such as metabolic syndrome, non-alcoholic fatty liver disease, and type 2 diabetes, etc. It has thus become a key issue in public health. Previous studies demonstrated that wild bitter gourd extracts activate PPARα in a transactivation assay and active compounds have been identified. PPARα is known to regulate hepatic lipid metabolism by up-regulating genes of some metabolic pathway and leading to enhanced fatty acid oxidation, less fat accumulation, etc. In addition, wild bitter gourd can improve hyperglycemia through various mechanisms. Recent in vivo studies in our lab demonstrated that mice fed 5% wild bitter gourd powder (BGP) increased the energy expenditure by promoting hepatic fatty acid metabolism, browning of epididymal white adipose tissue and the function of mitochondria in skeletal muscle and white adipose tissue; thus, wild bitter gourd can ameliorate the obesity and the insulin resistance resulting from a high-sugar or high-fat diet. This study aims to examine effects of wild bitter gourd supplementation to high-fat diet induced obese mice on serum glucose and lipid, as well as the mRNA expressions of the hepatic lipid metabolism and hepatic mitochondrial function. Five groups of C57BL/6J male mice were fed an AIN-93G modified high-fat diet for 15 weeks and then followed by supplementing 0%, 3% BGP, 5% BGP, 3% hydrolyzed BGP (BGPa) or 5% BGPa in high-fat diet respectively. Our data suggests that the supplement of wild bitter gourd improve metabolic disorders induced by the high-fat diet, including obesity, hyperglycemia, hypercholesterolemia, and non-alcoholic fatty liver disease. BGP and BGPa can both decrease the hepatic lipid accumulation by increasing the mRNA expression levels of genes related to fatty acid oxidation through activating hepatic PPARα. Noticeably, only BGPa can up-regulate the mRNA expression level of the gene related to bile acid synthesis possibly by activating hepatic LXRα. These data suggested that BGPa might have additional benefit improving the hepatic cholesterol accumulation. In addition, the function of BGPa to ameliorate the down-regulated mRNA expression level of genes related to mitochondrial biogenesis, fusion and fission due to the high-fat diet is significantly better than BGP. In conclusion, wild bitter gourd may alleviate the metabolic disorder from the high-fat diet by facilitating the hepatic fatty acid catabolism and promoting mitochondrial activity. Also, wild bitter gourd hydrolyzed by its endogenous glucosidase enhances its ability to improve the hepatic cholesterol accumulation and increase the mRNA expression level of genes related to hepatic mitochondrial function. Based on this, BGPa ameliorates the obesity-induced non-alcoholic fatty liver more effectively than BGP.
Subjects
wild bitter gourd
liver
lipid metabolism
mitochondria
non-alcoholic fatty liver
Type
thesis
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