| First Author | Son NH | Year | 2018 |
| Journal | J Clin Invest | PubMed ID | 30047927 |
| Mgi Jnum | J:264105 | Mgi Id | MGI:6194666 |
| Doi | 10.1172/JCI99315 | Citation | Son NH, et al. (2018) Endothelial cell CD36 optimizes tissue fatty acid uptake. J Clin Invest |
| abstractText | Movement of circulating fatty acids (FAs) to parenchymal cells requires their transfer across the endothelial cell (EC) barrier. The multi-ligand receptor cluster of differentiation 36 (CD36) facilitates tissue FA uptake and is expressed in ECs and parenchymal cells such as myocytes and adipocytes. Whether tissue uptake of FAs is dependent on EC or parenchymal cell CD36, or both, is unknown. Using a cell-specific deletion approach, we show that EC, but not parenchymal cell CD36 deletion increased fasting plasma FAs and postprandial triglycerides. EC-Cd36 knockout mice had reduced uptake of radiolabeled long chain FAs into heart, skeletal muscle, and brown adipose tissue; these uptake studies were replicated using [11C]palmitate PET scans. High fat diet-fed EC-CD36 deficient mice had improved glucose tolerance and insulin sensitivity. Both EC and cardiomyocyte (CM) deletion of CD36 reduced heart lipid droplet accumulation after fasting, but CM deletion did not affect heart glucose or FA uptake. Heart expression of several genes modulating glucose metabolism and insulin action increased with EC-CD36 deletion, but decreased with CM deletion. In conclusion, EC CD36 acts as a gatekeeper for parenchymal cell FA uptake, with important downstream effects on glucose utilization and insulin action. |
