3 Scopus citations

Abstract

Adipocytes transfer mitochondria to macrophages in white and brown adipose tissues to maintain metabolic homeostasis. In obesity, adipocyte-to-macrophage mitochondria transfer is impaired, and instead, adipocytes release mitochondria into the blood to induce a protective antioxidant response in the heart. We found that adipocyte-to-macrophage mitochondria transfer in white adipose tissue is inhibited in murine obesity elicited by a lard-based high-fat diet, but not a hydrogenated-coconut-oil-based high-fat diet, aging, or a corn-starch diet. The long-chain fatty acids enriched in lard suppress mitochondria capture by macrophages, diverting adipocyte-derived mitochondria into the blood for delivery to other organs, such as the heart. The depletion of macrophages rapidly increased the number of adipocyte-derived mitochondria in the blood. These findings suggest that dietary lipids regulate mitochondria uptake by macrophages locally in white adipose tissue to determine whether adipocyte-derived mitochondria are released into systemic circulation to support the metabolic adaptation of distant organs in response to nutrient stress.

Original languageEnglish
Pages (from-to)1499-1513.e8
JournalCell metabolism
Volume34
Issue number10
DOIs
StatePublished - Oct 4 2022

Keywords

  • CD36
  • EXT1
  • aging
  • beige fat
  • brown adipose tissue
  • cell-free mitochondria
  • fatty acids
  • heparan sulfate
  • horizontal mitochondria transfer
  • intercellular mitochondria transfer
  • lipids
  • macrophage
  • mitochondria
  • obesity
  • palmitate
  • white adipose tissue

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