IGF-1 attenuates high fat diet-elicited cardiomyopathy via arachidylcarnitine-dependent suppression of ferroptosis and mitochondrial dysfunction - PubMed
5 hours ago
- #cardiomyopathy
- #ferroptosis
- #metabolomics
- IGF-1 protects against high-fat diet-induced cardiomyopathy by reducing ferroptosis and mitochondrial damage.
- Obesity in mice and humans shifts metabolism towards glycolysis, impairs fatty acid homeostasis, and activates ferroptosis in the heart.
- High-fat diet in mice caused hypertriglyceridemia, cardiac hypertrophy, fibrosis, and reduced contractile function.
- Cardiac-specific IGF-1 overexpression prevented heart remodeling, dysfunction, mitochondrial injury, and ferroptosis without affecting systemic glucose.
- Arachidylcarnitine (C20:0) was identified as a key discriminative metabolite in obese individuals, linked to lipid metabolism disruption.
- L-carnitine supplementation in mice restored heart geometry and function, suggesting a role in mitigating diet-induced cardiac damage.