Intra-pituitary follicle-stimulating hormone signaling regulates hepatic lipid metabolism in mice

Author:

Qiao SenORCID,Alasmi Samer,Wyatt AmandaORCID,Wartenberg Philipp,Wang Hongmei,Candlish Michael,Das Debajyoti,Aoki Mari,Grünewald Ramona,Zhou Ziyue,Tian Qinghai,Yu Qiang,Götz Viktoria,Belkacemi Anouar,Raza Ahsan,Ectors FabienORCID,Kattler KathrinORCID,Gasparoni GillesORCID,Walter JörnORCID,Lipp PeterORCID,Mollard PatriceORCID,Bernard Daniel J.ORCID,Karatayli Ersin,Karatayli Senem Ceren,Lammert Frank,Boehm UlrichORCID

Abstract

AbstractInter-organ communication is a major hallmark of health and is often orchestrated by hormones released by the anterior pituitary gland. Pituitary gonadotropes secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH) to regulate gonadal function and control fertility. Whether FSH and LH also act on organs other than the gonads is debated. Here, we find that gonadotrope depletion in adult female mice triggers profound hypogonadism, obesity, glucose intolerance, fatty liver, and bone loss. The absence of sex steroids precipitates these phenotypes, with the notable exception of fatty liver, which results from ovary-independent actions of FSH. We uncover paracrine FSH action on pituitary corticotropes as a mechanism to restrain the production of corticosterone and prevent hepatic steatosis. Our data demonstrate that functional communication of two distinct hormone-secreting cell populations in the pituitary regulates hepatic lipid metabolism.

Funder

Deutsche Forschungsgemeinschaft

Publisher

Springer Science and Business Media LLC

Subject

General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry,Multidisciplinary

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