Biological function of dipeptidyl peptidase-4 on type 2 diabetes patients and diabetic mice.

BACKGROUND:Type 2 diabetes (TD2) is a sustained metabolic disorder, characterized by high blood glucose, insulin resistance (IR). Dipeptidyl peptidase-4 (DPP4) functions as an antigenic enzyme involved in hyperglycaemia, oxidative stress, and inflammation-associated IR. Therefore, association between DPP4 and TD2 warrants to be investigated. METHODS:In this study, blood samples of clinically diagnosed TD2 patients were harvested for biochemical tests. In addition, diabetic mice induced by high-fat diet (HFD) and single dose of streptozotocin (STZ) were used to assess the biological characteristics of DPP4 through biochemical and enzyme-linked immunosorbent assay (ELISA) tests, immunofluorescence staining, and western blot assay. RESULTS:Compared to controls, the clinical data of patients with TD2 resulted in increased contents of fasting blood glucose (FBG), glycated hemoglobin (HbA1c), homeostatic model assessment (HOMA)-IR, blood lipids of triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL-C), and interleukin 6 (IL6) in plasma samples (p < 0.05). Notably, blood levels of DPP4 in TD2 patients were increased significantly in comparison to that in non-diabetic adults (p < 0.01). In animal study, diabetic mice showed increased levels of glucose, insulin, lipids, DPP4 activity in sera. Visibly, hepatocellular DPP4 expression was up-regulated in diabetic mice. Interestingly, DPP4 inhibitor-treated mice showed significantly reduced DPP4 expression in serum (p < 0.01), and lowered DPP4-positive cells and protein content in the liver were observed when compared to those in diabetic mice (p < 0.01). CONCLUSIONS:Collectively, these findings reveal that DPP4 biomolecule may be positively associated with TD2 development, and the underlying mechanism may be attributed to activation of DPP4 expression in liver cells.

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