Rosiglitazone improved insulin resistance mechanism of high-fat feeding study in rats.doc
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Rosiglitazone improved insulin resistance mechanism of high-fat feeding study in rats
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Rosiglitazone improved insulin resistance mechanism of high-fat feeding study in rats
[Abstract] Objective To investigate the rosiglitazone improved insulin sensitivity in rats with high-fat diet mechanisms. Methods SD rats were randomly divided into normal control group, high-fat diet control group, high-fat diet rosiglitazone-treated group, treatment group was fed with rosiglitazone. Use of glucose - insulin tolerance insulin sensitivity in rats with experimental K values, and to observe the different parts of the weight of adipose tissue and its relationship with insulin sensitivity in the relationship between the K values. RT-PCR assay using rat peritoneal adipose tissue TNF-α , leptin, PPAR-γ expression changes; application TUNNEL apoptosis was observed by the changes in intra-abdominal fat cells. Results 7 weeks later, high-fat diet rosiglitazone treated rats with high-fat control group, significant improvement in insulin resistance, K value is increased; intra-abdominal fat mass reduction relative increase in the weight of subcutaneous fat; intra-abdominal adipose tissue TNF - α , leptin expression was significantly decreased, PPAR-γ expression of no change; rat intra-abdominal fat cell apoptosis. However, when compared with the normal control group, no significant difference. Conclusions Insulin resistance and abdominal fat tissue close; rosiglitazone improved insulin sensitivity in rats with high-fat diet may be through the mechanism of regulation of fat cell apoptosis and affect the distribution of fat cells and reduce insulin resistance caused by the expression of cytokines, thereby improving insulin resistance.
[Keywords:] rosiglitazone; insulin resistance; fat cells; apoptosis; leptin; PPAR-γ ; tumor necrosis factor
In recent years, studies have shown that [1,2], such as rosiglitazone can significantly improve the high-fat diet-induced insulin resistance (IR) state, but the exact mechanism has yet to be explored. Thi
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