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The Alberta Heart Failure Etiology and Analysis Research Team (HEART) study.
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Role of PI3Kα and sarcolemmal ATP-sensitive potassium channels in epoxyeicosatrienoic acid mediated cardioprotection.
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Pharmacogenomic analysis of ATP-sensitive potassium channels coexpressing the common type 2 diabetes risk variants E23K and S1369A.
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The ATP-sensitive K(+) channel ABCC8 S1369A type 2 diabetes risk variant increases MgATPase activity.
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Myocardial ATGL overexpression decreases the reliance on fatty acid oxidation and protects against pressure overload-induced cardiac dysfunction.
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Alterations in skeletal muscle fatty acid handling predisposes middle-aged mice to diet-induced insulin resistance.
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The molecular mechanisms and pharmacotherapy of ATP-sensitive potassium channel gene mutations underlying neonatal diabetes.
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Distinct early signaling events resulting from the expression of the PRKAG2 R302Q mutant of AMPK contribute to increased myocardial glycogen.
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Coexpression of the type 2 diabetes susceptibility gene variants KCNJ11 E23K and ABCC8 S1369A alter the ATP and sulfonylurea sensitivities of the ATP-sensitive K(+) channel.
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Reactive oxygen species directly modify sodium-calcium exchanger activity in a splice variant-dependent manner.
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Diastolic calcium is elevated in metabolic recovery of cardiomyocytes expressing elevated levels of the Na+/H+ exchanger.
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The third intracellular loop stabilizes the inactive state of the neuropeptide Y1 receptor.
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Resveratrol inhibits cardiac hypertrophy via AMP-activated protein kinase and Akt.
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Hypothalamic protein kinase C regulates glucose production.
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Upper intestinal lipids trigger a gut-brain-liver axis to regulate glucose production.
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Inhibition of matrix metalloproteinases prevents peroxynitrite-induced contractile dysfunction in the isolated cardiac myocyte.
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