ArticleThe Journal of biological chemistry2009
DGAT1 expression increases heart triglyceride content but ameliorates lipotoxicity.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.
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Who cites it
143 citing papers in PubMed.
- Alterations in plasma triglycerides and ceramides: links with cardiac function in humans with type 2 diabetes.Journal of lipid research · 2020Trial
- Withaferin A-Loaded CS/β-GP Thermosensitive Hydrogel Attenuates Diabetes-Associated Renal Injury in a Diabetic Rat Model.Applied biochemistry and biotechnology · 2026Article
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- Lipid droplet-associated proteins: Roles in cardiovascular diseases.Journal of lipid research · 2026Review
- Pyruvate metabolism enzyme Dlat induces mitochondria protein hyperacetylation to limit fatty acid oxidation in the HFpEF heart.Nature communications · 2026Article
- Decoding the Lipid Droplet Proteome: New Frontiers in Cardiovascular Disease Research.International journal of molecular sciences · 2025Review
- Intrauterine Growth-Restricted Female Yucatan Miniature Pig Neonates Fed Parenteral Nutrition Exhibit Early Catch-Up Growth Leading to Obesity and Ectopic Fat Deposition in Adulthood.The Journal of nutrition · 2025Article
- Essential Biology of Lipid Droplets.Annual review of biochemistry · 2025Review
- Plin5: A potential therapeutic target for type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- The role of Perilipin 5 in pathological myocardial remodeling.Frontiers in pharmacology · 2025Review
- CD36 knockdown attenuates pressure overload-induced cardiac injury by preventing lipotoxicity and improving myocardial energy metabolism.International journal of medical sciences · 2025Article
- Diurnal expression of Dgat2 induced by time-restricted feeding maintains cardiac health in the Drosophila model of circadian disruption.Aging cell · 2024Article
- Hypertensive Heart Disease: Mechanisms, Diagnosis and Treatment.Reviews in cardiovascular medicine · 2024Review
- Cardiac Metabolism, Reprogramming, and Diseases.Journal of cardiovascular translational research · 2024Review
- Lipotoxicity as a therapeutic target in obesity and diabetic cardiomyopathy.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024Review
- FGF21 ameliorates diabetic nephropathy through CDK1-dependently regulating the cell cycle.Frontiers in pharmacology · 2024Article
- Role ofJournal of microbiology and biotechnology · 2023Article
- The roles of DGAT1 and DGAT2 in human myotubes are dependent on donor patho-physiological background.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Differential intracellular management of fatty acids impacts on metabolic stress-stimulated glucose uptake in cardiomyocytes.Scientific reports · 2023Article
- Metabolic flux in the driver's seat during cardiac health and disease.Journal of molecular and cellular cardiology · 2023Review
83 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
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Abstract
Intracellular lipid accumulation in the heart is associated with cardiomyopathy, yet the precise role of triglyceride (TG) remains unclear. With exercise, wild type hearts develop physiologic hypertrophy. This was associated with greater TG stores and a marked induction of the TG-synthesizing enzyme diacylglycerol (DAG) acyltransferase 1 (DGAT1). Transgenic overexpression of DGAT1 in the heart using the cardiomyocyte- specific alpha-myosin heavy chain (MHC) promoter led to approximately a doubling of DGAT activity and TG content and reductions of approximately 35% in cardiac ceramide, 26% in DAG, and 20% in free fatty acid levels. Cardiac function assessed by echocardiography and cardiac catheterization was unaffected. These mice were then crossed with animals expressing long-chain acyl-CoA synthetase via the MHC promoter (MHC-ACS), which develop lipotoxic cardiomyopathy. MHC-DGAT1XMHC-ACS double transgenic male mice had improved heart function; fractional shortening increased by 74%, and diastolic function improved compared with MHC-ACS mice. The improvement of heart function correlated with a reduction in cardiac DAG and ceramide and reduced cardiomyocyte apoptosis but increased fatty acid oxidation. In addition, the survival of the mice was improved. Our study indicates that TG is not likely to be a toxic lipid species directly, but rather it is a feature of physiologic hypertrophy and may serve a cytoprotective role in lipid overload states. Moreover, induction of DGAT1 could be beneficial in the setting of excess heart accumulation of toxic lipids.
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