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Current Diabetes Reports

, 17:128 | Cite as

Current Therapies That Modify Glucagon Secretion: What Is the Therapeutic Effect of Such Modifications?

  • Magnus F. Grøndahl
  • Damien J. Keating
  • Tina Vilsbøll
  • Filip K. KnopEmail author
Pharmacologic Treatment of Type 2 Diabetes (HE Lebovitz and G Bahtiyar, Section Editors)
Part of the following topical collections:
  1. Topical Collection on Pharmacologic Treatment of Type 2 Diabetes

Abstract

Purpose of Review

Hyperglucagonemia contributes significantly to hyperglycemia in type 2 diabetes and suppressed glucagon levels may increase the risk of hypoglycemia. Here, we give a brief overview of glucagon physiology and the role of glucagon in the pathophysiology of type 2 diabetes and provide insights into how antidiabetic drugs influence glucagon secretion as well as a perspective on the future of glucagon-targeting drugs.

Recent Findings

Several older as well as recent investigations have evaluated the effect of antidiabetic agents on glucagon secretion to understand how glucagon may be involved in the drugs’ efficacy and safety profiles. Based on these findings, modulation of glucagon secretion seems to play a hitherto underestimated role in the efficacy and safety of several glucose-lowering drugs.

Summary

Numerous drugs currently available to diabetologists are capable of altering glucagon secretion: metformin, sulfonylurea compounds, insulin, glucagon-like peptide-1 receptor agonists, dipeptidyl peptidase-4 inhibitors, sodium-glucose cotransporter 2 inhibitors and amylin mimetics. Their diverse effects on glucagon secretion are of importance for their individual efficacy and safety profiles. Understanding how these drugs interact with glucagon secretion may help to optimize treatment.

Keywords

Glucagon secretion Incretin therapy Alpha cell regulation Glucagon-like peptide 1 Diabetes Hyperglucagonemia 

Notes

Compliance With Ethical Standards

Conflict of Interest

Magnus F. Grøndahl is a minority shareholder in the Danish biotech company Zealand Pharma; Damien J. Keating has no conflict of interest. Tina Vilsbøll has received lecture fees from, participated in advisory boards of, consulted for and/or received research grants from Amgen, AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly, MSD/Merck, Novo Nordisk, and Sanofi. Filip K. Knop has received lecture fees from, participated in advisory boards of, consulted for and/or received research grants from Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, MSD/Merck, Novo Nordisk, Sanofi, and Zealand Pharma.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

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Copyright information

© Springer Science+Business Media, LLC 2017

Authors and Affiliations

  • Magnus F. Grøndahl
    • 1
  • Damien J. Keating
    • 2
    • 3
  • Tina Vilsbøll
    • 1
    • 4
    • 5
  • Filip K. Knop
    • 1
    • 4
    • 6
    Email author
  1. 1.Center for Diabetes Research, Gentofte HospitalUniversity of CopenhagenHellerupDenmark
  2. 2.Discipline of Human Physiology and Centre for NeuroscienceFlinders University of South AustraliaAdelaideAustralia
  3. 3.Nutrition and MetabolismSouth Australian Health and Medical Research Institute (SAHMRI)AdelaideAustralia
  4. 4.Department of Clinical Medicine, Faculty of Health and Medical sciencesUniversity of CopenhagenCopenhagenDenmark
  5. 5.Steno Diabetes Center CopenhagenUniversity of CopenhagenGentofteDenmark
  6. 6.Novo Nordisk Foundation Center for Metabolic Research, Faculty of Health and Medical sciencesUniversity of CopenhagenCopenhagenDenmark

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