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Parikh, S.* ; Parikh, R.* ; Michael, K.* ; Bikovski, L.* ; Barnabas, G.* ; Mardamshina, M.* ; Hemi, R.* ; Manich, P.* ; Goldstein, N.* ; Malcov-Brog, H.* ; Ben-Dov, T.* ; Glaich, O.* ; Liber, D.* ; Bornstein, Y.* ; Goltseker, K.* ; Ben-Bezalel, R.* ; Pavlovsky, M.* ; Golan, T.* ; Spitzer, L.* ; Matz, H.* ; Gonen, P.* ; Percik, R.* ; Leibou, L.* ; Perluk, T.* ; Ast, G.* ; Frand, J.* ; Brenner, R.* ; Ziv, T.* ; Khaled, M.* ; Ben-Eliyahu, S.* ; Barak, S.* ; Karnieli-Miller, O.* ; Levin, E.* ; Gepner, Y.* ; Weiss, R.* ; Pfluger, P.T. ; Weller, A.* ; Levy, C.*

Food-seeking behavior is triggered by skin ultraviolet exposure in males.

Nat. Metab. 4, 883-900 (2022)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Sexual dimorphisms are responsible for profound metabolic differences in health and behavior. Whether males and females react differently to environmental cues, such as solar ultraviolet (UV) exposure, is unknown. Here we show that solar exposure induces food-seeking behavior, food intake, and food-seeking behavior and food intake in men, but not in women, through epidemiological evidence of approximately 3,000 individuals throughout the year. In mice, UVB exposure leads to increased food-seeking behavior, food intake and weight gain, with a sexual dimorphism towards males. In both mice and human males, increased appetite is correlated with elevated levels of circulating ghrelin. Specifically, UVB irradiation leads to p53 transcriptional activation of ghrelin in skin adipocytes, while a conditional p53-knockout in mice abolishes UVB-induced ghrelin expression and food-seeking behavior. In females, estrogen interferes with the p53-chromatin interaction on the ghrelin promoter, thus blocking ghrelin and food-seeking behavior in response to UVB exposure. These results identify the skin as a major mediator of energy homeostasis and may lead to therapeutic opportunities for sex-based treatments of endocrine-related diseases.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
ISSN (print) / ISBN 2522-5812
e-ISSN 2522-5812
Zeitschrift Nature metabolism
Quellenangaben Band: 4, Heft: 7, Seiten: 883-900 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)