期刊
SCIENCE IMMUNOLOGY
卷 3, 期 21, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.aan4626
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资金
- Natural Sciences and Engineering Research Council of Canada (NSERC) [PDF-471745-2015]
- Canadian Institutes of Health Research (CIHR) [324573, 221478]
- Heart and Stroke Foundation [G-16-00014658]
- Foundation Fighting Blindness (FFB) Canada
- Canadian Diabetes Association [OG-3-11-3329-PS]
- NSERC [418637]
- Burroughs Wellcome Fund Career Award for Medical Scientists
- FFB
- Fonds de recherche du Quebec-Sante (FRQS)
- CIHR
- NSERC
- Le Fonds de recherche du Quebec
- Consortium quebecois sur la decouverte du medicament
Obesity gives rise to metabolic complications by mechanisms that are poorly understood. Although chronic inflammatory signaling in adipose tissue is typically associated with metabolic deficiencies linked to excessive weight gain, we identified a subset of neuropilin-1 (NRP1)-expressing myeloid cells that accumulate in adipose tissue and protect against obesity and metabolic syndrome. Ablation of NRP1 in macrophages compromised lipid uptake in these cells, which reduced substrates for fatty acid beta-oxidation and shifted energy metabolism of these macrophages toward a more inflammatory glycolytic metabolism. Conditional deletion of NRP1 in LysM Cre-expressing cells leads to inadequate adipose vascularization, accelerated weight gain, and reduced insulin sensitivity even independent of weight gain. Transfer of NRP1(+) hematopoietic cells improved glucose homeostasis, resulting in the reversal of a prediabetic phenotype. Our findings suggest a pivotal role for adipose tissue-resident NRP1(+)-expressing macrophages in driving healthy weight gain and maintaining glucose tolerance.
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