The Effects of Wild Bitter Gourd on Mitochondrial Biogenesis in Skeletal Muscle of Diet-induced Obese Mice
Date Issued
2014
Date
2014
Author(s)
Chiang, Wen-Lung
Abstract
Obesity is a risk factor for various chronic diseases, and it has become a worldwide health issue due to the increasing global prevalence. Bitter gourd (Momordica charantia L.) is a common tropical vegetable, which has been shown to prevent metabolic disorder and obesity. Previous studies in our laboratory demonstrated that supplementation of 5% lyophilized wild bitter gourd powder (BGP) to a high sucrose diet up-regulated PGC-1α and TFAM mRNA expression in the muscle. This study thus tested the hypothesis that BGP might increase mitochondrial biogenesis in skeletal muscle, increase energy expenditure and ameliorate insulin resistance.
In the first experiment, 4 groups of C57BL/6J male mice were respectively fed high sucrose (HS) or high fat diets supplemented without or with 5% BGP based on a 2X2 factorial design. After 8 weeks of feeding, BGP significantly reduced serum glucose and triglyceride level, adipose mass, and body weight change and increased serum triiodothyronine (T3). But BGP did not affect mitochondria-related gene expression or mitochondria content in skeletal muscle. Through the metabolomic studies, we found supporting evidence that triterpenoid compounds of bitter gourd accumulated in liver of mice fed BGP. In addition, bile acid metabolism, prostaglandin metabolism and tryptophan metabolism might be affected by BGP.
In the second experiment, mice were daily injected with triiodothyronin (T3) (50 μg/kg/day) for 5 weeks to establish and validate the methods for evaluate mitochondria biogenesis in skeletal muscle. T3 significantly increased O2 consumption and CO2 production of animals, and stimulated TFAM, COX7a1 and UCP2 gene expression mainly in slow-twitch oxidative skeletal muscle. However, PGC-1α level, mitochondrial DNA (mtDNA) copy number and citrate synthase (CS) activity were not altered.
In the third experiment, 3 groups of mice were respectively fed the HS, HS+5% BGP or chow diets for 25 weeks. Similar to results in the first experiment, BGP inhibited diet-induced obesity and reduced serum glucose to a level that was even lower than that of the chow diet-fed mice. In spite of unchanged serum T3 level, BGP up-regulated DIO2 gene expression in both glycolytic and oxidative muscle and UCP2 level in oxidative muscle. High sucrose diet down-regulated mitochondria- related gene expression in glycolytic muscle, but BGP restored it to the normal level. The expression levels of these genes in the oxidative muscle of the BG group were higher than those of the other 2 groups. BG did not significantly change mtDNA copy number, CS activity, tissue oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), but increase the OCR/ECAR ratio.
In summary, BGP reduced serum glucose and triglyceride level, improved insulin sensitivity, increase metabolic rate, up-regulated mRNA expressions of DIO2, UCP2 and mitochondria-related gene expression in glycolytic and oxidative muscle.
Subjects
苦瓜
骨骼肌
粒線體
甲狀腺素
SDGs
Type
thesis
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