Key points are not available for this paper at this time.
Design
Editorial
This editorial discusses the organ-specific fate of endogenous or ingested lipids in humans, particularly in the context of impaired glucose tolerance and cardiovascular risk.
ardiovascular disease and heart failure are leading complications in patients with type 2 diabetes, prediabetes, and obesity in whom circulating fatty acid (FA) levels are commonly elevated. Abnormalities in FA handling in skeletal muscle, liver, and adipose tissue may initiate or perpetuate a cycle of insulin resistance, impaired glucose utilization, and dyslipidemia, thereby leading to substrate overflow to the heart. From animal studies, we learn that once an excess of FA is forced to enter myocardial cells, lipotoxicity and functional loss occur (1-4). However, less is known about the organspecific fate of endogenous or ingested lipids in humans. This is because systemic fluxes of nonesterified fatty acids (NEFAs) and triglycerides (TGs) cannot be extrapolated to individual organs because local mechanisms such as perfusion, lipolysis, oxygen availability, and inward transport may intervene in the response of individual tissues to the oversupply of FAs. In this issue of Diabetes, Labb et al. (
No takes yet. Share an insight, caveat, or question.
Patricia Iozzo (2012) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: