Dietary lipids inhibit mitochondria transfer to macrophages to divert adipocyte-derived mitochondria into the blood.
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
Journal
Cell metabolism
ISSN: 1932-7420
Titre abrégé: Cell Metab
Pays: United States
ID NLM: 101233170
Informations de publication
Date de publication:
04 10 2022
04 10 2022
Historique:
received:
24
08
2021
revised:
06
06
2022
accepted:
15
08
2022
pubmed:
8
9
2022
medline:
12
10
2022
entrez:
7
9
2022
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 36070756
pii: S1550-4131(22)00353-9
doi: 10.1016/j.cmet.2022.08.010
pmc: PMC9547954
mid: NIHMS1834840
pii:
doi:
Substances chimiques
Antioxidants
0
Fatty Acids
0
Starch
9005-25-8
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1499-1513.e8Subventions
Organisme : NIAID NIH HHS
ID : R01 AI168044
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK060022
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL045095
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI139540
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK056341
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007081
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL152245
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK131188
Pays : United States
Organisme : NHLBI NIH HHS
ID : K08 HL159359
Pays : United States
Organisme : NIDDK NIH HHS
ID : R00 DK122019
Pays : United States
Organisme : NIH HHS
ID : DP5 OD028125
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL161185
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests J.R.B. has a pending patent application related to intercellular mitochondria transfer for the treatment of mitochondrial disorders, is a consultant for DeciBio and Flagship Pioneering, and is a scientific advisor to LUCA Science, Inc.
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