Energy balance
In severe diabetes, reduced cardiac lipoprotein lipase (LPL) activity forces cardiomyocytes to rely on non-esterified fatty acids (NEFA) from adipose tissue, causing mitochondrial overload, lipid metabolite accumulation, and cardiac lipotoxicity.
In severe diabetes, the heart's ability to process fat from blood lipids (via LPL) drops. This forces the heart to burn fat directly from the blood (NEFA), which it cannot handle efficiently, leading to damage. Treatments must focus on restoring this specific fat-processing pathway in the heart, not just lowering overall blood fat.
This excessive supply of NEFA overwhelmed the mitochondrial capacity, leading to a mismatch between FA delivery and utilization, lipid metabolite build-up and cell death (Figure 2) [30].
Why this rating
Based on animal models (STZ-induced diabetes) and in vitro studies; human clinical data is referenced but specific trial outcomes for this specific mechanism are not detailed.
Source
Lipoprotein lipase as a target for obesity/diabetes related cardiovascular disease
Rui Shang et al. · Journal of Pharmacy & Pharmaceutical Sciences · 2024
DOI 10.3389/jpps.2024.13199
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