What is the function of Dipeptidyl Peptidase-4 (DPP-4)?

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From the Guidelines

Dipeptidyl Peptidase-4 (DPP-4) is a cell-surface enzyme that deactivates several peptides, including glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1 (GLP-1).

Function of DPP-4

  • DPP-4 inhibitors increase the endogenous level of GLP-1 by reducing the deactivation of GLP-1 in vivo through inhibition of DPP-4 1
  • The enzyme plays a crucial role in glucose regulation by deactivating peptides that enhance insulin secretion and inhibit glucagon secretion in a glucose-dependent manner 1
  • DPP-4 is involved in the regulation of insulin and glucagon secretion, and its inhibition has a moderate glucose-lowering efficacy 1

Clinical Implications

  • DPP-4 inhibitors are well tolerated, have a neutral effect on weight, and have minimal risk of hypoglycemia when used as monotherapy 1
  • The use of DPP-4 inhibitors alone does not increase the risk of hypoglycaemia and includes a neutral or mild effect on weight gain 1
  • DPP-4 inhibitors have been shown to be effective in reducing HbA1c levels in patients with type 2 diabetes, with a reduction of 0.4% to 0.9% 1

From the Research

Function of Dipeptidyl Peptidase-4 (DPP-4)

  • DPP-4 is a multi-functional protein that exhibits catalytic activity, functions as a binding protein, and acts as a ligand for various extracellular molecules 2.
  • It is an integral membrane protein expressed on cells throughout the body and also circulates as a soluble protein in the plasma 2.
  • DPP-4 plays a crucial role in glucose homeostasis by cleaving the incretin hormone glucagon-like peptide-1 (GLP-1), which is essential for maintaining normal glucose levels 2, 3.
  • The enzyme also influences metabolic control by proteolytically affecting other regulatory peptides and potentially modulating insulin sensitivity through non-enzymatic interactions with membrane proteins 2.
  • DPP-4 has been implicated in the pathogenesis of type 2 diabetes, obesity, and non-alcoholic fatty liver disease, with its expression and activity altered in these conditions 3, 4.

Mechanism of Action

  • DPP-4 inhibitors work by preventing the degradation of incretins, such as GLP-1 and glucose-dependent insulinotropic peptide (GIP), thereby increasing their levels and enhancing insulin secretion 5, 6.
  • This mechanism of action is distinct from other anti-diabetic drugs and offers a physiological approach to controlling hyperglycemia 5.
  • DPP-4 inhibitors have been shown to stimulate insulin secretion from beta-cells, decrease glucagon secretion from pancreatic alpha-cells, and reduce glucose production by the liver 5.

Role in Disease Pathogenesis

  • Altered expression and activity of DPP-4 have been associated with increasing body mass index and hyperglycemia, suggesting a link between DPP-4 and the development of type 2 diabetes and obesity 2, 4.
  • DPP-4 may also play a role in modulating beta-cell function and influencing the progression of metabolic disease through its effects on inflammation and insulin resistance 2, 3.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Dipeptidyl Peptidase-4 at the Interface Between Inflammation and Metabolism.

Clinical medicine insights. Endocrinology and diabetes, 2020

Research

DPP4 in Diabetes.

Frontiers in immunology, 2015

Research

Mechanism of action of inhibitors of dipeptidyl-peptidase-4 (DPP-4).

Best practice & research. Clinical endocrinology & metabolism, 2009

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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