Research
Mixed
In states of fatty acid overload (obesity, diabetes), intramyocardial triglyceride accumulation acts as a cytoprotective buffer that prevents lipotoxicity and cardiac damage; however, once this storage capacity is exhausted, toxic lipid intermediates accumulate, leading to dysfunction.
If you have metabolic issues, your heart stores fat to protect itself from toxic fatty acids. Simply trying to reduce heart fat without fixing the underlying metabolic overload (via diet/exercise) might remove this protective buffer and worsen heart health. Focus on reducing fatty acid overload rather than just fat mass.
GoodQualifiesHIGH confidence
progressive exhaustion of storage capacity provokes the build-up of acyl-CoA and ceramide in the cytoplasm (top right), contributing to lipotoxicity. Amplification of storage capacity by enzymatic overexpression of diacylglycerol acyltransferase 1 (DGAT1) slows the progression of cardiac damage (bottom right), suggesting a defensive role of triglyceride accumulation in fatty acid overload states.
Why this rating
Supported by multiple human imaging studies, transgenic mouse models, and cell culture data, though causality in humans is described as 'elusive'.
Source
Myocardial, Perivascular, and Epicardial Fat
Patricia Iozzo · Diabetes Care · 2011
DOI 10.2337/dc11-s250
narrative_reviewCited 269×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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