Decrease of chemerin by aerobic exercise improved glycolipid metabolism of diabetes through increasing key metabolism enzymes and protein mediated by PPARγ

Abstract

Background: Our previous work indicated that exercise-induced reduction of chemerin (an adipokine and chemokine) played an important role in the improvement of glycolipid metabolism of diabetic rats, and this manuscript are to: (1) clarify peroxisome proliferator-activated receptor (PPARγ) mediating the regulation of decreased chemerin on glycolipid metabolism key enzymes (including adipose triglyceride lipase (ATGL), lipoprotein lipase (LPL), glucose transporter 4 (GLUT4) and phosphoenolpyruvate carboxykinase (PEPCK)) in diabetic rats; (2) demonstrate the crucial role of decreased chemerin on exercise-induced improvement of glycolipid metabolism in diabetic mice by exogenous chemerin supplement (for only mice-resource chemerin available). Methods: After establishing type 2 diabetes models, diabetic SD rats were randomly divided into 4 groups: diabetes (DM), exercised diabetes (EDM), EDM plus PPARγ agonist pioglitazone (EDP), and EDM plus PPARγ antagonist GW9662 (EDG), while diabetic ICR mice divided into 3 groups: DM, EDM and EDM plus exogenous chemerin supplementation (EDC). The exercised rodents participated in 4-week (rats) or 6-week (mice) moderate-intensity aerobic exercise, and at 30 min before exercise pioglitazone (10 mg/kg) and GW9662 (1 mg/kg) were intragastrically administered to EDP and EDG rats respectively, while recombinant mouse chemerin (8 µg/kg) was intraperitoneally injected to C and EDC mice. Glycolipid metabolism indexes were determined. Serum chemerin and the protein levels of the above molecules in metabolic organs (liver, gastrocnemius and epididymal fat) were detected by ELISA and Western blot, respectively. Results: (1) In diabetes rats, aerobic exercise-induced increases of ATGL and LPL (livers and gastrocnemius) as well as decrease of PEPCK (livers) were reversed by GW9662, and further strengthened by pioglitazones. (2) In diabetes mice, aerobic exercise also significantly increased the levels of PPARγ, ATGL, LPL and GLUT4 as well as decreased the level of PEPCK; furthermore, the changes of the above molecules and improvements of glycolipid metabolism and fatty liver were partly reversed by exogenous chemerin. Conclusion: The decreased chemerin played important roles in aerobic exercise-induced improvements of glycolipid metabolism and fatty liver in diabetes, through increasing glycolipid metabolism key enzymes and protein (ATGL, LPL and GLUT4) mediated by PPARg.