Liver Metaflammation in Diabetes is Mediated by JNK Signaling; Protective Effects of Combined Training

Rezumat

Objectives: Glucotoxicity-induced diabetes which aggravates chronic and progressive hyperglycemia of systemic glucose metabolism, leads to the activation of stress kinase -c-Jun N-terminal kinases (JNK) - for subsequent down regulatory catabolic responses and deterioration of β-cell function called liver metaflammation. Regarding the non-invasive property and anti-inflammatory effects of exercise training, we aimed to investigate the effects of 8 weeks of combined training (endurance and resistance), on the Gene expression levels of JNK, TNFα, Catalase, GPX, SOD as well as protein levels of pJNK and JNK in the liver tissue of type 2 diabetic male rats.

Methods: In this experimental study, 24 male Wistar rats (aged 8 weeks, 260±20 g) were randomly divided into 3 groups (n = 8/group), Normal Control (NC), Diabetic Control (DC), and Diabetes + Combined Training (DT). After the induction of diabetes, the training group implemented the combined training for 8 weeks. About 48 hours after the final training session, serum levels of glucose, insulin, and HOMA-IR along with gene expression and protein levels of pJNK, JNK, TNFα, Catalase, GPX, SOD were assessed through Elisa, RT-PCR, and Western blot techniques.

Results: Findings showed that 8 weeks of combined training significantly down regulated the serum levels of Insulin Resistance (IR) indexes (glucose, insulin, and HOMA-IR) and tissue levels of inflammatory indexes (pJNK, and TNFα); In contrast, combined training significantly increased tissue Enzymatic antioxidant activity (Catalase, GPX, SOD) compared to the diabetic group (P< 0.05).

Conclusions: Modality of Combined training (endurance + resistance) can reduce the risk factors associated with liver metaflammation of type 2 diabetic rats.