ArticleJournal of molecular and cellular cardiology2010
SGLT1, a novel cardiac glucose transporter, mediates increased glucose uptake in PRKAG2 cardiomyopathy.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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Who cites it
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.
- Effect of pharmacological selectivity of SGLT2 inhibitors on cardiovascular outcomes in patients with type 2 diabetes: a meta-analysis.Scientific reports · 2024Pooled it
- Comparative outcomes of heart failure among existent classes of anti-diabetic agents: a network meta-analysis of 171,253 participants from 91 randomized controlled trials.Cardiovascular diabetology · 2019Pooled it
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- Canagliflozin restores electrical properties and suppresses structural damage in isoproterenol-induced myocardial injury models.Scientific reports · 2025Article
- Cardiac sodium-glucose co-transporter 1 (SGLT1) contributes to heart failure in a mouse model of diabetic cardiomyopathy.Basic research in cardiology · 2025Article
- Management of ROS and Regulatory Cell Death in Myocardial Ischemia-Reperfusion Injury.Molecular biotechnology · 2025Review
- Targeting Lactic Acid Modification in Ischemic Heart Diseases: Novel Therapeutics and Mechanism.Journal of cardiovascular translational research · 2025Review
- Protective Mechanisms of SGLTi in Ischemic Heart Disease.Journal of cardiovascular translational research · 2024Review
- The Off-Target Cardioprotective Mechanisms of Sodium-Glucose Cotransporter 2 Inhibitors: An Overview.International journal of molecular sciences · 2024Review
- Sodium-glucose cotransporter 1 promotes the biofunctions of perivascular preadipocytes mediated by Akt/mTOR/p70S6K signaling pathway.American journal of physiology. Cell physiology · 2024Article
- Article
- Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.Redox biology · 2023Review
- Sotagliflozin attenuates cardiac dysfunction and remodeling in myocardial infarction rats.Heliyon · 2023Article
- Expression of SGLT1 in the Mouse Endometrial Epithelium and its Role in Early Embryonic Development and Implantation.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Effects of SGLT2 Inhibitors beyond Glycemic Control-Focus on Myocardial SGLT1.International journal of molecular sciences · 2021Review
- Left Ventricular SGLT1 Protein Expression Correlates with the Extent of Myocardial Nitro-Oxidative Stress in Rats with Pressure and Volume Overload-Induced Heart Failure.Antioxidants (Basel, Switzerland) · 2021Article
- Molecular characterization and nutritional regulation of sodium-dependent glucose cotransporter 1 (Sglt1) in blunt snout bream (Megalobrama amblycephala).Scientific reports · 2021Article
- New insight in understanding the contribution of SGLT1 in cardiac glucose uptake: evidence for a truncated form in mice and humans.American journal of physiology. Heart and circulatory physiology · 2021Article
- Sotagliflozin, a Dual SGLT1/2 Inhibitor, Improves Cardiac Outcomes in a Normoglycemic Mouse Model of Cardiac Pressure Overload.Frontiers in physiology · 2021Article
- Estrogen Regulates Glucose Metabolism in Cattle Neutrophils Through Autophagy.Frontiers in veterinary science · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Human mutations in the gene PRKAG2 encoding the gamma2 subunit of AMP-activated protein kinase (AMPK) cause a glycogen storage cardiomyopathy. Transgenic mice (TG(T400N)) with the human T400N mutation exhibit inappropriate activation of AMPK and consequent glycogen storage in the heart. Although increased glucose uptake and activation of glycogen synthesis have been documented in PRKAG2 cardiomyopathy, the mechanism of increased glucose uptake has been uncertain. Wildtype (WT), TG(T400N), and TG(alpha2DN) (carrying a dominant negative, kinase dead alpha2 catalytic subunit of AMPK) mice were studied at ages 2-8 weeks. Cardiac mRNA expression of sodium-dependent glucose transporter 1 (SGLT1), but not facilitated-diffusion glucose transporter 1 (GLUT1) or GLUT4, was increased approximately 5- to 7-fold in TG(T400N) mice relative to WT. SGLT1 protein was similarly increased at the cardiac myocyte sarcolemma in TG(T400N) mice. Phlorizin, a specific SGLT1 inhibitor, attenuated cardiac glucose uptake in TG(T400N) mice by approximately 40%, but not in WT mice. Chronic phlorizin treatment reduced cardiac glycogen content by approximately 25% in TG(T400N) mice. AICAR, an AMPK activator, increased cardiac SGLT1 mRNA expression approximately 3-fold in WT mice. Relative to TG(T400N) mice, double transgenic (TG(T400N)/TG(alpha2DN)) mice had decreased ( approximately 50%) cardiac glucose uptake and decreased (approximately 70%) cardiac SGLT1 expression. TG(T400N) hearts had increased binding activity of the transcription factors HNF-1 and Sp1 to the promoter of the gene encoding SGLT1. Our data suggest that upregulation of cardiac SGLT1 is responsible for increased cardiac glucose uptake in the TG(T400N) mouse. Increased AMPK activity leads to upregulation of SGLT1, which in turn mediates increased cardiac glucose uptake.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.