ArticleCardiovascular diabetology2024
SGLT2 inhibition improves coronary flow velocity reserve and contractility: role of glucagon signaling.
Article in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Type 2 Diabetes Mellitus in the Northern Tree Shrew (Tupaia belangeri).Journal of the American Association for Laboratory Animal Science : JAALAS · 2026Article
- Role and mechanisms of vascular smooth muscle cell phenotypic transition in diabetic macrovascular complications.Biological research · 2026Review
- Adverse event reporting signals for SGLT-2 inhibitor-metformin combination therapy: a disproportionality analysis of the FAERS database.Frontiers in endocrinology · 2026Article
- SGLT2 inhibitors in cardiac amyloidosis: mechanistic insights and clinical perspectives-a narrative review.Cardiovascular diabetology. Endocrinology reports · 2025Review
- Beyond Glycemic Control: Vascular Biologic Effects of Antidiabetic Drugs and Their Cardiovascular Promise.Reviews in cardiovascular medicine · 2025Article
- Epicardial adipose tissue volume is associated with impaired left ventricular strain in patients with metabolic syndrome: the mediating role of myocardial energetic efficiency.Cardiovascular diabetology · 2025Article
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Authors and funding
12 authors.
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Abstract
backgroundSGLT2 inhibitors, a T2DM medication to lower blood glucose, markedly improve cardiovascular outcomes but the underlying mechanism(s) are not fully understood. SGLT2i's produce a unique metabolic pattern by lowering blood glucose without increasing insulin while increasing ketone body and glucagon levels and reducing body weight. We tested if glucagon signaling contributes to SGLT2i induced improvement in CV function.
methodsCardiac contractility and coronary flow velocity reserve (CFVR) were monitored in ob/ob mice and rhesus monkeys with metabolic syndrome using echocardiography. Metabolic status was characterized by measuring blood ketone levels, glucose tolerance during glucose challenge and Arg and ADMA levels were measured. Baysian models were developed to analyse the data.
resultsDapagliflozin improved CFVR and contractility, co-application of a glucagon receptor inhibitor (GcgRi) blunted the effect on CFVR but not contractility. Dapagliflozin increased the Arg/ADMA ratio and ketone levels and co-treatment with GcgRi blunted only the Dapagliflozin induced increase in Arg/ADMA ratio but not ketone levels.
conclusionsSince GcgRi co-treatment only reduced the Arg/ADMA increase we hypothesize that dapagliflozin via a glucagon-signaling dependent pathway improves vascular function through the NO-signaling pathway leading to improved vascular function. Increase in ketone levels might be a contributing factor in SGLT2i induced contractility increase and does not require glucagon signaling.
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