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Quantification of Endothelial Fatty Acid Uptake using Fluorescent Fatty Acid Analogs
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Endothelial cell CD36 optimizes tissue fatty acid uptake.

Ni-Huiping Son1, Debapriya Basu1, Dmitri Samovski2

  • 1Division of Endocrinology, Diabetes and Metabolism, New York University School of Medicine, New York, New York, USA.

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Endothelial cell CD36 acts as a gatekeeper for fatty acid uptake into tissues. Deleting it increases plasma fatty acids but improves glucose tolerance and insulin sensitivity.

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Area of Science:

  • Metabolic research
  • Cell biology
  • Cardiovascular science

Background:

  • Circulating fatty acids (FAs) move to parenchymal cells by crossing the endothelial cell (EC) barrier.
  • Cluster of differentiation 36 (CD36), a multiligand receptor, aids FA uptake and is present in ECs and parenchymal cells like myocytes and adipocytes.

Purpose of the Study:

  • To investigate whether tissue FA uptake depends on CD36 in ECs, parenchymal cells, or both.

Main Methods:

  • Utilized cell-specific deletion of CD36 in mice.
  • Measured fasting plasma FAs and postprandial triglycerides.
  • Tracked radiolabeled long-chain FA uptake using in vivo studies and [11C]palmitate PET scans.
  • Assessed glucose tolerance and insulin sensitivity in mice on a high-fat diet.
  • Examined CD36 deletion effects on cardiac lipid accumulation and gene expression.

Main Results:

  • Deletion of CD36 in ECs, but not parenchymal cells, elevated fasting plasma FAs and postprandial triglycerides.
  • EC CD36 deficiency reduced FA uptake in the heart, skeletal muscle, and brown adipose tissue.
  • Mice lacking EC CD36 showed improved glucose tolerance and insulin sensitivity on a high-fat diet.
  • Both EC and cardiomyocyte CD36 deletion reduced cardiac lipid droplets post-fasting, but only EC deletion affected cardiac FA uptake and related gene expression.

Conclusions:

  • Endothelial cell CD36 functions as a critical gatekeeper for parenchymal cell FA uptake.
  • EC CD36 plays a significant role in regulating glucose utilization and insulin action.
  • Targeting EC CD36 may offer therapeutic strategies for metabolic disorders.