2007Zhonghua neifenmi daixie zazhiRequires access

Increased expression of protein tyrosine phosphatase 1B in pancreas of high fat diet-induced obese rats

Zhen Zhang

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Abstract

Objective To investigate the expression of protein tyrosine phosphatase(PTP)1B in pancreas of obese rats induced by high fat diet.Methods Twenty male SD rats were randomly divided into control group on regular diet(n=10),and obesity model group on high fat diet(n=10).After twelve weeks,fasting serum insulin,blood glucose,triglyceride,total cholesterol,epididymal fat weight were measured and the histomorphological change in liver were observed;glucose tolerance test and insulin releasing test were performed; The protein expression of PTP-1B in pancreas of rats was determined with Western blotting and immunohistochemistry.The phosphorylation of insulin receptor substrate-1(IRS-1)and insulin receptor(IR)were detected by immuno-precipitation.Results(1)The insulin sensitive index was significantly decreased in the high-fat-diet rats compared with the normal rats(0.36±0.18 vs 0.91±0.28,P0.05).(2)In obese rats, glucose tolerance and the acute first-phase insulin secretory response to glucose were impaired.(3)The protein levels of PTP-1 B in pancreas of obesity rats was significantly increased by 86% compared with the control group(P0.01).Insulin-stimulated IR and IRS-I phosphorylation in the pancreas were reduced in the obese rats. Conclusion The increased PTP-I B level and the reduced insulin-stimulated IR and IRS-I phosphorylations in pancreas seem to play an important role in the pathogenesis of islet insulin resistance induced by high fat diet.

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Objective To investigate the expression of protein tyrosine phosphatase(PTP)1B in pancreas of obese rats induced by high fat diet.Methods Twenty male SD rats were randomly divided into control group on regular diet(n=10),and obesity model group on high fat diet(n=10).After twelve weeks,fasting serum insulin,blood glucose,triglyceride,total cholesterol,epididymal fat weight were measured and the histomorphological change in liver were observed;glucose tolerance test and insulin releasing test were performed; The protein expression of PTP-1B in pancreas of rats was determined with Western blotting and immunohistochemistry.The phosphorylation of insulin receptor substrate-1(IRS-1)and insulin receptor(IR)were detected by immuno-precipitation.Results(1)The insulin sensitive index was significantly decreased in the high-fat-diet rats compared with the normal rats(0.36±0.18 vs 0.91±0.28,P0.05).(2)In obese rats, glucose tolerance and the acute first-phase insulin secretory response to glucose were impaired.(3)The protein levels of PTP-1 B in pancreas of obesity rats was significantly increased by 86% compared with the control group(P0.01).Insulin-stimulated IR and IRS-I phosphorylation in the pancreas were reduced in the obese rats. Conclusion The increased PTP-I B level and the reduced insulin-stimulated IR and IRS-I phosphorylations in pancreas seem to play an important role in the pathogenesis of islet insulin resistance induced by high fat diet.

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Available abstract

Objective To investigate the expression of protein tyrosine phosphatase(PTP)1B in pancreas of obese rats induced by high fat diet.Methods Twenty male SD rats were randomly divided into control group on regular diet(n=10),and obesity model group on high fat diet(n=10).After twelve weeks,fasting serum insulin,blood glucose,triglyceride,total cholesterol,epididymal fat weight were measured and the histomorphological change in liver were observed;glucose tolerance test and insulin releasing test were performed; The protein expression of PTP-1B in pancreas of rats was determined with Western blotting and immunohistochemistry.The phosphorylation of insulin receptor substrate-1(IRS-1)and insulin receptor(IR)were detected by immuno-precipitation.Results(1)The insulin sensitive index was significantly decreased in the high-fat-diet rats compared with the normal rats(0.36±0.18 vs 0.91±0.28,P0.05).(2)In obese rats, glucose tolerance and the acute first-phase insulin secretory response to glucose were impaired.(3)The protein levels of PTP-1 B in pancreas of obesity rats was significantly increased by 86% compared with the control group(P0.01).Insulin-stimulated IR and IRS-I phosphorylation in the pancreas were reduced in the obese rats. Conclusion The increased PTP-I B level and the reduced insulin-stimulated IR and IRS-I phosphorylations in pancreas seem to play an important role in the pathogenesis of islet insulin resistance induced by high fat diet.

Key concepts: Internal medicine, Endocrinology, Insulin, Insulin receptor, Insulin resistance, IRS1, Triglyceride, Pancreas

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