The Effect of Quinoa (Chenopodium Quinoa) on Apoptotic, Autophagic, Antioxidant and Inflammation Markers in Glucocorticoid-Induced Insulin Resistance in Rats

Abstract

Background Insulin resistance plays an important role in predicting type 2 diabetes that may develops. This study was planned in order to investigate the beneficial effects of quinoa (Chenopodium quinoa) use in glucocorticoid induced-insulin resistance. Methods and results Forty-two rats were used as the material (experimental) groups: the control group (C), the quinoa-administered group (Q), the insulin resistance-created group (IR), the IR + metformin group (IM), the IR + quinoa for treatment group (IQ) and the quinoa + IR for prophylaxis group (QI). Blood glucose, insulin levels and HOMA-IR were found to be highest (p < 0.05) in the IR group (p < 0.05). Glucose levels decreased significantly with the administration of quinoa and approached the levels of the control, but the insulin levels and the HOMA-IR did not significantly change. It was also observed that other biochemical parameters (ALT, AST, ALP, total cholesterol, total protein, urea and creatinine) changed significantly in the IR group and approached the levels of the control group with the administration of quinoa. Apoptotic (BCL2 5, BAX 9, CAS 3), autophagic (SQSTM1 7, ATG5) and inflammation (IL-1 beta, TNF-alpha) genes were upregulated by 5-11-fold in the IR group. In the groups in which quinoa was administered for treatment and protection, all these genes were found to be upregulated to a lower extent than the IR group. Antioxidant genes (GPX1, SOD1) increased by nine to tenfold in the quinoa groups. Conclusion As a result, after administration of quinoa, it was determined that the glucose level increased due to experimental insulin resistance and the liver and kidney damage indicators decreased. It was determined that quinoa (Chenopodium quinoa) had significant beneficial effects on biochemical parameters and apoptotic, autophagic, antioxidant and inflammatory markers in experimental glucocorticoid-induced insulin resistance.