Adaptive thermogenesis in mice requires adipocyte light-sensing via Opsin 3

Author:

Nayak GowriORCID,Vemaraju Shruti,Zhang Kevin X.,Odaka YoshinobuORCID,Buhr Ethan D.ORCID,Holt-Jones Amanda,Smith April N.,Upton Brian A.,Zhan Jesse J.,Diaz Nicolás,Murakami KazutoshiORCID,D’Souza ShaneORCID,Nguyen Minh-Thanh,Gordon Shannon A.,Wu Gang,Schmidt Robert,Mei Xue,Petts Nathan T.,Batie Matthew,Rao SujataORCID,Nakamura TakahisaORCID,Sweeney Alison M.ORCID,Hogenesch John B.ORCID,Van Gelder Russell N.ORCID,Sanchez-Gurmaches JoanORCID,Lang Richard A.

Abstract

SummaryAlmost all life forms can decode light information for adaptive advantage. Examples include the visual system, where photoreceptor signals are interpreted as images, and the circadian system, where light entrains a physiological clock. Here we describe a local, non-visual light response in mice that employs encephalopsin (OPN3, a 480 nm, blue light responsive opsin) to regulate the function of adipocytes. Germ line null and adipocyte-specific conditional null mice show a deficit in thermogenesis that is phenocopied in mice under blue-light deficient conditions. We show that blue light stimulation of adipocytes activates hormone sensitive lipase, the rate limiting enzyme in the lipolysis pathway, and that this is OPN3-dependent. Opn3 adipocyte conditional null mice also use reduced levels of fat mass when fasted and cold exposed further suggesting a lipolysis deficit. These data suggest the hypothesis that in mice, a local, OPN3-dependent light response in adipocytes is a mechanism for regulation of energy homeostasis.

Publisher

Cold Spring Harbor Laboratory

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