Myricitrin Ameliorates Hyperglycemia, Glucose Intolerance, Hepatic Steatosis, and Inflammation in High-Fat Diet/Streptozotocin-Induced Diabetic Mice

• Published in: International journal of molecular sciences Vol. 21; no. 5; p. 1870
• Main Authors: Kim, Do Yeon, Kim, Sang Ryong, Jung, Un Ju
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 09.03.2020; MDPI
• Subjects: Animals; Beta cells; Blood Glucose - drug effects; Blood Glucose - metabolism; Body weight; Diabetes; Diabetes mellitus (non-insulin dependent); Diabetes Mellitus, Experimental - chemically induced; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - metabolism; Diabetes Mellitus, Type 2 - chemically induced; Diabetes Mellitus, Type 2 - drug therapy; Diet, High-Fat - adverse effects; Enzymes; Fasting; Fatty liver; Fatty Liver - drug therapy; Fatty Liver - metabolism; Fatty-acid synthase; Flavonoids - pharmacology; Food; Food intake; Gene expression; Glucokinase; Glucokinase - metabolism; Glucose; glucose intolerance; Glucose Intolerance - drug therapy; Glucose Intolerance - metabolism; Glucose tolerance; Glucose-6-phosphatase; hepatic steatosis; High fat diet; Homeostasis; Hyperglycemia; Hyperglycemia - drug therapy; Hyperglycemia - metabolism; Inflammation; Inflammation - chemically induced; Inflammation - drug therapy; Inflammation - metabolism; Insulin Resistance; Intolerance; Lipid Metabolism - drug effects; Lipids; Liver; Liver - drug effects; Liver - metabolism; Male; Metabolism; Mice; Mice, Inbred C57BL; Monocyte chemoattractant protein 1; myricitrin; Oral administration; Oxidative stress; Pancreas; Phosphohydrolase; Plasma; Steatosis; Streptozocin; Streptozocin - pharmacology; Triglycerides; Triglycerides - metabolism; Tumor necrosis factor-TNF; Tumor necrosis factor-α; glucose intolerance; hyperglycemia; myricitrin; inflammation; diabetes; hepatic steatosis
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21051870

To test the hypothesis that myricitrin (MYR) improves type 2 diabetes, we examined the effect of MYR on hyperglycemia, glucose intolerance, hepatic steatosis, and inflammation in high-fat diet (HFD) and streptozotocin (STZ)-induced type 2 diabetic mice. Male C57BL/6J mice were randomly divided into three groups: non-diabetic, diabetic control, and MYR (0.005%, / )-supplemented diabetic groups. Diabetes was induced by HFD and STZ, and MYR was administered orally for 5 weeks. Myricitrin exerted no significant effects on food intake, body weight, fat weight, or plasma lipids levels. However, MYR significantly decreased fasting blood glucose levels, improved glucose intolerance, and increased pancreatic β-cell mass compared to the diabetic control group. Myricitrin administration also markedly increased glucokinase mRNA expression and activity as well as lowered glucose-6-phosphatase and phosphoenolpyruvate carboxykinase mRNA expression and activity in the liver. In addition, liver weight, hepatic triglyceride content, and lipid droplet accumulation were markedly decreased following MYR administration. These changes were seemingly attributable to the suppression of the hepatic lipogenic enzymes-fatty acid synthase and phosphatidate phosphohydrolase. Myricitrin also significantly lowered plasma MCP-1 and TNF-α levels and the mRNA expression of hepatic pro-inflammatory genes. These results suggest that MYR has anti-diabetic potential.