Impact JPQHR Nonalcoholic Fatty Liver And On The Role Of Leptin And Insulin Resistance

Backgro und and purpose： Non-alcoholic fatty liver disease(nonalcoholicfatty liver disease, NAFLD) is a non-excessive drinking history,from a variety of causes to the accumulation of fat in the liver cells as themain feature of the clinical and pathological syndrome. With the improvementof living standards and changing lifestyles, NAFLD with high morbidity andthe growing trend of younger people’s attention. Has become the world’ssocial and medical issues of common concern. Although the exactpathogenesis of NAFLD is unclear, but the "two-hit theory" point of view ismore popular. Recent studies show that fatty liver and leptin (leptin), insulinresistance (IR) is closely related to [1-2]. On the basis of previous researchgroup studies, theexperimental rat models of fatty liver by using the modelJPQHF intervene, and by observing rats leptin, insulin and insulin resistanceindex changes,understanding the spleen Thanh Hoa fatty liver side effects of treatment andeffective mechanism. Is widely used in clinical laboratories JPQHF providethe foundation and theoretical basis.Methods: Male SD rats50, weighing140±10g. Eight randomly selected asnormal control group fed the basal diet, the remaining group of high-fat,high-fat diet for10weeks. To test the first10weeks were randomly selectedfrom the manufacturing module2, the normal group2, chloral hydrateanesthesia, were sacrificed liver biopsy done, verify successful model. Thehigh-fat group was randomly divided into model group, JPQHF low, mediumand high dose groups. All rats were sacrificed at18weeks measured serumleptin (leptin), fasting glucose (fasting blood glucose, FBG) and fasting insulin (fasting insulin, FINS) levels, insulin resistance by homeostasis modelassessment (homeostasis model assessment, HOMA) insulin resistance indexsaid. The rats were fed with normal diet for comparison.Results: The model group compared with the control group, the bodyweight, liver pathological inflammatory activity, the degree of hepaticsteatosis cells were significantly increased, increased (P<0.05). JPQHFlow-dose treatment group compared with the model group, serum leptin,insulin was no significant difference (P>0.05). ISED prescription dose groupand high-dose group compared with the model group, serum leptin and insulinwere significantly lower (P<0.05).Conclusions:(1) leptin and insulin resistance may play an important role inthe pathogenesis of nonalcoholic fatty liver.(2) JPQHF be significantly reduced non-alcoholic fatty liver fattydegeneration in rats, regulate lipid metabolism disorders.