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

Jing Qiao1, Lei Li1, Yanchun Ma2

  • 1Department of VIP, Gaomi People's Hospital, Shandong, China.

Abstract

Insights

Dipeptidyl peptidase-4 (DPP4) levels are elevated in type 2 diabetes (TD2) patients and diabetic mice, suggesting DPP4 plays a role in TD2 development. Inhibiting DPP4 reduced its expression in diabetic mice.

Area of Science:

  • Biochemistry
  • Endocrinology
  • Metabolic Disorders

Background:

  • Type 2 diabetes (TD2) is a metabolic disorder characterized by hyperglycemia and insulin resistance (IR).
  • Dipeptidyl peptidase-4 (DPP4) is implicated in hyperglycemia, oxidative stress, and inflammation-associated IR.
  • The association between DPP4 and TD2 requires further investigation.

Purpose of the Study:

  • To investigate the association between Dipeptidyl peptidase-4 (DPP4) and Type 2 Diabetes (TD2).
  • To explore the role of DPP4 in the pathogenesis of TD2.
  • To assess the effect of DPP4 inhibition on TD2 markers.

Main Methods:

  • Collected blood samples from clinically diagnosed TD2 patients for biochemical analysis.
  • Utilized a mouse model of TD2 induced by high-fat diet (HFD) and streptozotocin (STZ).
  • Assessed DPP4 biological characteristics using biochemical tests, ELISA, immunofluorescence staining, and western blot assays; included DPP4 inhibitor treatment in mice.

Main Results:

  • TD2 patients exhibited increased fasting blood glucose (FBG), HbA1c, HOMA-IR, lipids, and IL6 compared to controls.
  • Blood DPP4 levels were significantly higher in TD2 patients and diabetic mice.
  • Hepatocellular DPP4 expression was upregulated in diabetic mice; DPP4 inhibition reduced serum DPP4 and liver DPP4 expression/content.

Conclusions:

  • DPP4 biomolecule is positively associated with TD2 development.
  • The underlying mechanism may involve the activation of DPP4 expression in liver cells.
  • DPP4 inhibition demonstrates potential therapeutic effects in a TD2 mouse model.

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