In beta cells of rats with TYPE 2 diabetes; explanation relationship of expressions of PPARγ and TGF(β1) and membranous lipid changes with the formation of diabetes

Diabetes is a disease that we have had to struggle with for thousands of years, but as stated by the WHO, it has not been able to get out of the disease class with no cure, and its prevalence is increasing. Therefore, in our study, we aimed to address the problem fundamentally and to find out what disrupts insulin secretion in beta cells in the pancreas. 21 Winstar albino, male, adult 350 g rats were divided into 7 as control group and 14 as diabetic group. We compared the expression results in diabetic rats and healthy rats, thinking that TGFβ molecule, which acts as a cell transformant, differentiator and apoptosis, will be an indicator of the destruction of beta cells. Due to the incidence of obesity in diabetes and the effect of beta cell membrane permeability in insulin secretion, we measured the process of lipids being taken into the body and metabolized in beta cells. We measured FPG, insulin and C-peptide values in plasma of diabetic rats and compared them with healthy rats. We also determined the membrane lipid composition of Beta cells and erythrocytes by GC-FID/TLC and compared them with plasma lipids and fatty acids. We analyzed the expression of PPARγ, which is an important marker of lipid oxidation disorders, in diabetic beta cells and examined its relationship with healthy cells. We found that TGFβ expression was decreased by 15% and PPARγ expression by 18% in beta cells of diabetic rats compared to healthy rats, and there was a significant correlation between them. We also determined that PC phospholipid decreased by 15% and PI phospholipid by 8% in the cell membranes of diabetic beta cells. We showed that while beta cells, erythrocytes and plasma of diabetic rats had similar fatty acid amounts, SFA fatty acids such as 16:0 and 18:0 C were significantly increased and unsaturated omega fatty acids such as DHA, EPA, OA, LA and AA were significantly decreased in diabetic rats. . As a result, we have obtained important evidence for our hypothesis that beta cell destruction and insulin dysfunction are caused by disturbances in lipid metabolism in diabetes. We are of the opinion that diabetes is not a diabetes but a lipid disease.