Neuronal Modulation of Brown Adipose Activity Through Perturbation of White Adipocyte Lipogenesis [preprint]
AuthorsGuilherme, Adilson L.
Pedersen, David J.
Bedard, Alexander H.
Morgan, Donald A.
Czech, Michael P.
UMass Chan AffiliationsProgram in Molecular Medicine
KeywordsBrown Adipose Activity
White Adipocyte Lipogenesis
White adipose tissue
fatty acid synthase
Biochemical Phenomena, Metabolism, and Nutrition
Cellular and Molecular Physiology
MetadataShow full item record
AbstractWhite adipose tissue (WAT) secretes factors to communicate with other metabolic organs to maintain energy homeostasis. We previously reported that perturbation of adipocyte de novo lipogenesis (DNL) by deletion of fatty acid synthase (FASN) causes expansion of sympathetic neurons within white adipose tissue (WAT) and the appearance of beige adipocytes. Here we report evidence that white adipocyte DNL activity is also coupled to neuronal regulation and thermogenesis in brown adipose tissue (BAT). Induced deletion of FASN in all adipocytes in mature mice (iAdFASNKO) enhanced sympathetic innervation and neuronal activity as well as UCP1 expression in both WAT and BAT. In contrast, selective ablation of FASN in brown adipocytes of mice (iUCP1FASNKO) failed to modulate sympathetic innervation and the thermogenic program in BAT. Surprisingly, DNL in brown adipocytes was also dispensable in maintaining euthermia when UCP1FASNKO mice were cold-exposed. These results indicate that DNL in white adipocytes influences long distance signaling to BAT, which can modify BAT sympathetic innervation and expression of genes involved in thermogenesis.
bioRxiv 324160; doi: https://doi.org/10.1101/324160. Link to preprint on bioRxiv service
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/29265
RightsThe copyright holder for this preprint (which was not peer-reviewed) is the author/funder. It is made available under a CC-BY-NC-ND 4.0 International license.
Except where otherwise noted, this item's license is described as The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. It is made available under a CC-BY-NC-ND 4.0 International license.