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Targeting cardiometabolic risk in type 1 diabetes through incretin physiology
Ruth Frampton1, Samantha Hocking2, Jennifer R Snaith3
1Clinical Diabetes and Metabolism, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia; St Vincent's Healthcare Clinical Campus, School of Clinical Medicine, University of New South Wales Medicine and Health, University of New South Wales, Sydney, New South Wales, Australia; Department of Diabetes and Endocrinology, St Vincent's Hospital Sydney, Darlinghurst, New South Wales, Australia; Department of Diabetes and Endocrinology, The Canberra Hospital, Garran, Australian Capital Territory, Australia.
Abstract:
People living with type 1 diabetes have significantly increased cardiovascular risk compared with the general population. Traditional risk factors include hypertension, dyslipidaemia, and obesity. However, those with type 1 diabetes contend with treatment-induced insulin resistance and pancreatic and incretin hormone dysfunction, leading to dysglycaemia, which also impacts cardiovascular risk. Here, we highlight the underlying metabolic environment in type 1 diabetes with a focus on glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and glucagon physiology. With the emergence of incretin-based therapies such as semaglutide (a GLP-1 receptor agonist) and tirzepatide (a combined GLP-1/GIP receptor agonist) targeting these receptor pathways, there is now potential to directly target metabolic deficits to address cardiometabolic risk in a type 1 diabetes population.
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