Journal
SCIENCE
Volume 373, Issue 6550, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.abe9383
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Funding
- NIH/NCI [P30CA008748, F32CA225036]
- NIH/NIAID [1R01AI130345]
- NIH/NHLBI [R01HL138090]
- Ludwig Institute for Cancer Research basic immunology grant
- Cycle for Survival grants
- Leducq Transatlantic Network of Excellence program
- Alan and Sandra Gerry Metastasis and Tumor Ecosystems Center fellowship
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This study identified a macrophage-dependent mechanism involving the PDGFcc ortholog that controls lipid storage in adipose tissues of mice. Production of PDGFcc is regulated by diet and blocking PDGFcc leads to redirection of excess lipids toward thermogenesis in brown fat.
The mechanisms by which macrophages regulate energy storage remain poorly understood. We identify in a genetic screen a platelet-derived growth factor (PDGF)/vascular endothelial growth factor (VEGF)-family ortholog, Pvf3, that is produced by macrophages and is required for lipid storage in fat-body cells of Drosophila larvae. Genetic and pharmacological experiments indicate that the mouse Pvf3 ortholog PDGFcc, produced by adipose tissue-resident macrophages, controls lipid storage in adipocytes in a leptin receptor- and C-C chemokine receptor type 2-independent manner. PDGFcc production is regulated by diet and acts in a paracrine manner to control lipid storage in adipose tissues of newborn and adult mice. At the organismal level upon PDGFcc blockade, excess lipids are redirected toward thermogenesis in brown fat. These data identify a macrophage-dependent mechanism, conducive to the design of pharmacological interventions, that controls energy storage in metazoans.
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