RT Journal Article
SR Electronic
T1 Adaptive thermogenesis in mice requires adipocyte light-sensing via Opsin 3
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 721381
DO 10.1101/721381
A1 Gowri Nayak
A1 Shruti Vemaraju
A1 Kevin X. Zhang
A1 Yoshinobu Odaka
A1 Ethan D. Buhr
A1 Amanda Holt-Jones
A1 April N. Smith
A1 Brian A. Upton
A1 Jesse J. Zhan
A1 Nicolás Diaz
A1 Kazutoshi Murakami
A1 Shane D’Souza
A1 Minh-Thanh Nguyen
A1 Shannon A. Gordon
A1 Gang Wu
A1 Robert Schmidt
A1 Xue Mei
A1 Nathan T. Petts
A1 Matthew Batie
A1 Sujata Rao
A1 Takahisa Nakamura
A1 Alison M. Sweeney
A1 John B. Hogenesch
A1 Russell N. Van Gelder
A1 Joan Sanchez-Gurmaches
A1 Richard A. Lang
YR 2019
UL http://biorxiv.org/content/early/2019/08/01/721381.abstract
AB Almost 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.