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Baicalin against obesity and insulin resistance through activation of AKT/AS160/GLUT4 pathway
Penghua Fang1, Mei Yu2, Lei Zhang3
1Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Medical College, Yangzhou University, Yangzhou 225001, China; Department of Physiology, Nanjing University of Chinese Medicine Hanlin College, Taizhou, Jiangsu, 225300, China.
Abstract:
Obesity may cause several metabolic complications, including insulin resistance and type 2 diabetes mellitus. Despite great advances in medicine, people still keep exploring novel and effective drugs for treatment of obesity and insulin resistance. The aim of this study was to survey if baicalin might ameliorate obesity-induced insulin resistance and to explore its signal mechanisms in skeletal muscles of mice. Diet-induced obese (DIO) mice were given 50 mg/kg baicalin intraperitoneally (i.p.) once a day for 21 days, and C2C12 myotubes were treated with 100, 200, 400 μM baicalin for 12 h in this study. Then insulin resistance indexes and insulin signal protein levels in skeletal muscles were examined. We discovered that administration of baicalin decreased food intake, body weight, HOMA-IR and NT-PGC-1α levels, but enhanced GLUT4, PGC-1α, pP38MAPK, pAKT and pAS160 contents, as well as GLUT4 mRNA, PGC-1α mRNA, PPARγ mRNA, GLUT1 mRNA expression in skeletal muscles of obese mice and myotubes of C2C12 cells, and reversed high fat diet-induced glucose and insulin intolerance, hyperglycemia and insulin resistance in the mice. These results suggest that baicalin is a powerful and promising agent for treatment of obesity and insulin resistance via Akt/AS160/GLUT4 and P38MAPK/PGC1α/GLUT4 pathway.
Insights
Baicalin, a natural compound, effectively combats obesity and insulin resistance in mice by improving glucose metabolism and enhancing key signaling pathways in skeletal muscles.
Area of Science:
- Metabolic disorders
- Pharmacology
- Molecular biology
Background:
- Obesity is a major risk factor for metabolic complications like insulin resistance and type 2 diabetes.
- Novel therapeutic agents for obesity and insulin resistance are continuously sought.
- Baicalin is being investigated for its potential therapeutic benefits.
Purpose of the Study:
- To evaluate the efficacy of baicalin in ameliorating obesity-induced insulin resistance.
- To elucidate the underlying molecular mechanisms of baicalin's action in skeletal muscle.
Main Methods:
- Diet-induced obese (DIO) mice were treated with baicalin (50 mg/kg/day) for 21 days.
- C2C12 myotubes were exposed to varying concentrations of baicalin (100–400 μM) for 12 hours.
- Insulin resistance indices and key signaling protein/mRNA levels in skeletal muscle were assessed.
Main Results:
- Baicalin administration reduced food intake, body weight, and HOMA-IR in DIO mice.
- Baicalin treatment increased the expression of GLUT4, PGC-1α, pP38MAPK, pAKT, and pAS160 in skeletal muscle.
- Baicalin reversed high-fat diet-induced glucose and insulin intolerance, hyperglycemia, and insulin resistance.
Conclusions:
- Baicalin demonstrates significant potential as a therapeutic agent for obesity and insulin resistance.
- Baicalin acts through the Akt/AS160/GLUT4 and P38MAPK/PGC1α/GLUT4 signaling pathways.
- Further research into baicalin's application in metabolic disease treatment is warranted.