Protective Effects of Adiponectin Against Diabetic Renal Injury in a Mouse Model of Diabetes.

BACKGROUND/AIMS: Adiponectin (Apn) has shown anti-diabetic and anti-inflammatory potential. In the study, we studied and tested the protective effects of Apn against diabetic renal injury and the possible mechanism of these effects.

METHODS: After 1 week of adaptive feeding, 30 mice were randomly divided into 5 groups: the control group, the model group, the Apn (L) group, the Apn (M) group and the Apn (H) group. All mice were marked and weighed. Following 4 weeks of a pro-diabetic high-fat diet, the model group and Apn groups were injected intraperitoneally with a high dose of STZ (85 mg/kg), while the normal control group was injected with sodium citrate. Fasting blood glucose was measured daily, starting 3 days after STZ injection. After confirming the success of the diabetic model by measuring blood glucose of more than 16.7 nM for 3 successive days, we observed the animal models for an additional 4 weeks. After body weights were measured, urinary albumin, urinary protein, SOD activity and malondialdehyde (MDA) were measured by ELISA, BCA and biochemical assay respectively . Moreover, plasma insulin was assayed by radioimmunoassay, insulin expression in pancreatic β cells was assayed by immunohistochemistry and receptor for advanced glycation end products (RAGE) and corresponding PKC and PKA signaling in the kidney cortex were also assayed by Western blot and Real-time PCR.

RESULTS: The results showed that Apn can significantly reduce MDA and enhance SOD activity. Moreover, Apn promoted the synthesis and secretion of insulin by islet β-cells and reduced RAGE accumulation in the kidney, which was associated with down-regulated PKC expression and upregulated PKA expression.

CONCLUSION: Apn has protective effects against hyperglycemia and can effectively enhance antioxidation, promote the secretion of insulin and reduce the accumulation of glycosylated products in T2DM mice; these effects were associated with inhibition of PKC and promotion of PKA signaling.