Glutamine Ameliorates Liver Steatosis via Regulation of Glycolipid Metabolism and Gut Microbiota in High-Fat Diet-Induced Obese Mice.
Xinbo ZhouJunjie ZhangYutong SunJian ShenBo SunQingquan MaPublished in: Journal of agricultural and food chemistry (2023)
Obesity and its associated conditions, such as nonalcoholic fatty liver disease (NAFLD), are risk factors for health. The aim of this study was to explore the effects of glutamine (Gln) on liver steatosis induced by a high-fat diet (HFD) and HEPG2 cells induced by oleic acid. Gln demonstrated a positive influence on hepatic homeostasis by suppressing acetyl CoA carboxylase (ACC) and fatty acid synthase (FAS) and promoting sirtuin 1 (SIRT1) expression while improving glucose metabolism by regulating serine/threonine protein kinase (AKT)/factor forkhead box O1 (FOXO1) signals in vivo and in vitro. Obese Gln-fed mice had higher colonic short-chain fatty acid (SCFA) contents and lower inflammation factor protein levels in the liver, HEPG2 cells, and jejunum. Gln-treated obese mice had an effective decrease in Firmicutes abundance. These findings indicate that Gln serves as a nutritional tool in managing obesity and related disorders.
Keyphrases
- high fat diet induced
- insulin resistance
- high fat diet
- fatty acid
- adipose tissue
- protein kinase
- metabolic syndrome
- type diabetes
- transcription factor
- skeletal muscle
- oxidative stress
- binding protein
- public health
- signaling pathway
- healthcare
- weight loss
- poor prognosis
- mental health
- risk assessment
- mouse model
- health information
- ischemia reperfusion injury
- liver fibrosis
- weight gain