Magnus F Grøndahl1, Damien J Keating2,3, Tina Vilsbøll1,4,5, Filip K Knop6,7,8. 1. Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark. 2. Discipline of Human Physiology and Centre for Neuroscience, Flinders University of South Australia, Adelaide, Australia. 3. Nutrition and Metabolism, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia. 4. Department of Clinical Medicine, Faculty of Health and Medical sciences, University of Copenhagen, Copenhagen, Denmark. 5. Steno Diabetes Center Copenhagen, University of Copenhagen, Gentofte, Denmark. 6. Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark. filipknop@dadlnet.dk. 7. Department of Clinical Medicine, Faculty of Health and Medical sciences, University of Copenhagen, Copenhagen, Denmark. filipknop@dadlnet.dk. 8. Novo Nordisk Foundation Center for Metabolic Research, Faculty of Health and Medical sciences, University of Copenhagen, Copenhagen, Denmark. filipknop@dadlnet.dk.
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. 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.
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. 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.
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