Research On Effects Of Emodin On Reducing Lipid Accumulation In Lipid Induced Insulin Resistance And Key Protein Expression Of Lipid Oxidation

Dyslipidemia and lipid ectopic deposition, especially skeletal muscle lip id accumulation, play an important role in the occurrence and development of insulin resistance. Emodin, an anthraquinone extracts from rhubarb, is associated with reduced body weight of obesity patients and improved insulin resistance. However, the effects of emodin on lipid metabolism in insulin resistance patients and its mechanisms have not been understood clearly. We infer whether emodin can improve insulin resistance by influencing fatty acid metabolism to alleviate lipid accumulation in skeletal muscle. In our research, we set up high-fat diet induced insulin resistance rats model, palmitate-incubation induced isolate soleus and L6 myotubes insulin resistance models. After treatment with emodin, we observe the effects of emodin on lipid accumulation and expression of fatty acid metabolism proteins in skeletal muscle. Lastly, we found that:(1) in insulin resistance rats, emodin reduces blood glucose, improves insulin resistance, alleviates soleus lipid accumulation, enhances soleus AMPK phosphorylation and further increases expression of CPT1, UCP2, UCP3 and PGC-1α; (2) in palmitate induced isolated soleus and L6 myotubes insulin resistance models, emodin reduces fatty acid content and significantly improves lip id accumulation; (3) in palmitate induced L6 myotubes insulin resistance model, emodin inhibits Complex IV activity, promotes AMPK phosphorylation, further enhances expression of CPT1, UCP2 and UCP3, increases expression of PGC-1α and number of mitochondria, keeps morphology of mitochondria. In conclusion, these data suggest that emodin could decrease lipid accumulation in insulin resistance muscles by enhancing key protein expression of fatty acid metabolism and improving mitochondria biologic function.