AI Article Synopsis
- Cold-induced thermogenesis helps warm-blooded animals maintain their body temperature in low temperatures by increasing energy expenditure.
- Researchers found that when exposed to cold, the liver produces acylcarnitines, which are necessary for brown fat to generate heat, and this process is activated by white fat releasing free fatty acids.
- Additionally, providing L-carnitine or palmitoylcarnitine can improve cold sensitivity in older mice, demonstrating how different fat tissues work together to help manage body temperature in colder environments.
Article Abstract
Cold-induced thermogenesis is an energy-demanding process that protects endotherms against a reduction in ambient temperature. Using non-targeted liquid chromatography-mass spectrometry-based lipidomics, we identified elevated levels of plasma acylcarnitines in response to the cold. We found that the liver undergoes a metabolic switch to provide fuel for brown fat thermogenesis by producing acylcarnitines. Cold stimulates white adipocytes to release free fatty acids that activate the nuclear receptor HNF4α, which is required for acylcarnitine production in the liver and adaptive thermogenesis. Once in circulation, acylcarnitines are transported to brown adipose tissue, while uptake into white adipose tissue and liver is blocked. Finally, a bolus of L-carnitine or palmitoylcarnitine rescues the cold sensitivity seen with aging. Our data highlight an elegant mechanism whereby white adipose tissue provides long-chain fatty acids for hepatic carnitilation to generate plasma acylcarnitines as a fuel source for peripheral tissues in mice.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5658052 | PMC |
| http://dx.doi.org/10.1016/j.cmet.2017.08.006 | DOI Listing |
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