Investigation of the effects of ketogenic diet on adipokine levels, oxidant-antioxidant status and some biochemical parameters in rats for which an experimental diabetes model was created

In this study, it was aimed to investigate the effects of ketogenic diet (KD) on glycemic control, lipid profile, adipokines, antioxidant and oxidative stress markers in rats with Type 2 Diabetes Mellitus (DM) model created with streptozocin (STZ). 32 wistar albino male rats were divided into 4 groups as standard feed, KD, diabetes +standard feed and diabetes+KD. Each group of rats was fed with the specified diet type for four weeks. At the end of the experiment, glycemic control and lipid profile, serum adipokines (chemerin, omentin-1, nesfatin-1 and ZAG), oxidative stress markers (MDA and NO) and antioxidant enzyme activities (SOD, KAT) were analyzed in blood and tissue samples obtained from rats. The lowest body weight was observed in the diabetes+standard diet group, and the highest weight gain was observed in the KD group. While KD provided blood glucose control in diabetic rats, it prevented the increase of HbA1c level. HOMA-IR values, which are an indicator of insulin resistance, increased significantly in the diabetes+standard feed group, while KD was able to prevent the formation of insulin resistance in diabetic rats. Feeding with KD also caused an increase in lipid parameters in rats compared to groups fed with standard feed. ZAG was significantly increased in the KD groups compared to the standard feed group. Chemerin increased only in other groups compared to the standard feed group. Omentin-1 levels increased in KD groups. The levels of nesfatin-1 were increased in the diabetes+KD group compared to the diabetes+standard feed group. It was observed that oxidative stress due to diabetes was significantly reduced with KD and antioxidant capacity increased. In conclusion, the biochemical and histological data presented in this study show that KD has a significant beneficial effect in improving the diabetic condition and helping to stabilize hyperglycemia, but KD can lead to disruptions in lipid metabolism and hepatic steatosis. Detailed clinical studies are needed to support the findings obtained.