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J Lipid Res. 2018 Feb;59(2):224-236. doi: 10.1194/jlr.M078469. Epub 2017 Dec 3.

UCP1 deficiency increases adipose tissue monounsaturated fatty acid synthesis and trafficking to the liver.

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Departments of Biochemistry University of Wisconsin-Madison, Madison, WI 53706.
Departments of Biochemistry University of Wisconsin-Madison, Madison, WI 53706
Nutritional Sciences, University of Wisconsin-Madison, Madison, WI 53706.


Uncoupling protein-1 (UCP1) facilitates thermogenesis in brown and beige adipocytes and can promote energy expenditure by decreasing mitochondrial respiratory efficiency. Defects in UCP1 and brown adipose tissue thermogenesis subject animals to chronic cold stress and elicit compensatory responses to generate heat. How UCP1 regulates white adipose tissue (WAT) lipid biology and tissue crosstalk is not completely understood. Here, we probed the effect of UCP1 deficiency on FA metabolism in inguinal and epididymal WAT and investigated how these metabolic perturbations influence hepatic lipid homeostasis. We report that at standard housing temperature (21°C), loss of UCP1 induces inguinal WAT de novo lipogenesis through transcriptional activation of the lipogenic gene program and elevated GLUT4. Inguinal adipocyte hyperplasia and depot expansion accompany the increase in lipid synthesis. We also found that UCP1 deficiency elevates adipose stearoyl-CoA desaturase gene expression, and increased inguinal WAT lipolysis supports the transport of adipose-derived palmitoleate (16:1n7) to the liver and hepatic triglyceride accumulation. The observed WAT and liver phenotypes were resolved by housing animals at thermoneutral housing (30°C). These data illustrate depot-specific responses to impaired BAT thermogenesis and communication between WAT and liver in UCP1-/- mice.


fatty acid/desaturases; fatty acid/metabolism; hepatic; lipid; thermogenesis; β-oxidation

[Available on 2019-02-01]

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