期刊
CELL METABOLISM
卷 30, 期 4, 页码 768-+出版社
CELL PRESS
DOI: 10.1016/j.cmet.2019.07.001
关键词
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资金
- US National Institutes of Health (NIH) [R01DK077097, R01DK102898, R01HL106173, P01GM095467, R01DK099511, P30DK036836]
- National Institute of Diabetes and Digestive and Kidney Diseases
- US Army Medical Research [W81XWH-17-1-0428]
- American Diabetes Association [1-16-PDF-063]
- Sao Paulo Research Foundation (FAPESP) [2017/02684]
- NIH [T32DK007260, F32DK102320, K01DK111714, R21NS087165]
- Deutsche Forschungsgemeinschaft research fellowship [BA 4925/1-1]
- Deutsches Zentrum fur Herz-Kreislauf-Forschung
- NRSA from the NIH [HL136044]
Distinct oxygenases and their oxylipin products have been shown to participate in thermogenesis by mediating physiological adaptations required to sustain body temperature. Since the role of the lipoxygenase (LOX) family in cold adaptation remains elusive, we aimed to investigate whether, and how, LOX activity is required for cold adaptation and to identify LOX-derived lipid mediators that could serve as putative cold mimetics with therapeutic potential to combat diabetes. By utilizing mass-spectrometry-based lipidomics in mice and humans, we demonstrated that cold and beta 3-adrenergic stimulation could promote the biosynthesis and release of 12-LOX metabolites from brown adipose tissue (BAT). Moreover, 12-LOX ablation in mouse brown adipocytes impaired glucose uptake and metabolism, resulting in blunted adaptation to the cold in vivo. The cold-induced 12-LOX product 12-HEPE was found to be a batokine that improves glucose metabolism by promoting glucose uptake into adipocytes and skeletal muscle through activation of an insulin-like intracellular signaling pathway.
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