Effects of fenofibrate and pioglitazone on expressions of intracellular signaling molecules in pancreatic islet of high-fat diet-fed rats
- VernacularTitle:吡格列酮和非诺贝特对高脂饮食大鼠胰岛细胞内信号分子的影响
- Author:
Ting FENG
;
Bo YANG
;
Haoming TIAN
- Publication Type:Journal Article
- Keywords:
Islets of Langerhans;
Fenofibrate;
Pioglitazone;
PPAR-α;
PPAR-γ;
Intraeellular signalingpeptides and proteins
- From:
Chinese Journal of Endocrinology and Metabolism
2008;24(4):416-419
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of fenofibrate and pioglitazone on the expressions of PPAR- α, PPAR-γ, and intracellular signaling molecules in pancreatic islets of obese rats induced by high-fat diets. Methods SD obese rat models were established with high-fat diet, and 40 male rats were assigned to 4 groups including high-fat diet (HF group), high-fat diet with fenofibrate (FF group), pioglitazone (FP group) treatment, and control rats with normal diet (NC group). After 8 weeks intervention, immunohistochemistry was performed to evaluate the expressions of various proteins in islets; At the same time, islets mass were scored in tissue slides. Results Islets mass enlarged in HF group. The compositions of islet cells were the same as the control. The expression of insulin was lower in HF group than the control, but after using pioglitazone, less islets mass and more insulin expression were found in FP group. Compared with the control group, expressions of PPAR-α, PPAR-γ protein were reduced in HF group, and the expression of PPAR-α protein increased in FF group, and the expression of PPAR-γ protein was increased in FP group. The levels of NF-кB, p38 mitogen-activated protein kinase (MAPK), ERK1 proteins increased significantly in HF group, the expressions of NF-кB, p38 MAPK decreased in FF and FP groups, and the level of ERK1 decreased only in FP group, the protein level of I-кB showed no difference among control, HF group, and FF groups. Conclusion Fenofibrate and pioglitazone may partially protect islet cells function and improve survival by correcting the disturbance of intracellular signaling molecules.
