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Deletion of Androgen Receptor in LepRb Cells Improves Estrous Cycles in
Prenatally Androgenized Mice.
Authors Cara AL, Burger LL, Beekly BG, Allen SJ, Henson EL, Auchus RJ, Myers MG, Moenter
SM, Elias CF
Submitted By Submitted Externally on 3/10/2023
Status Published
Journal Endocrinology
Year 2023
Date Published 1/1/2023
Volume : Pages 164 : Not Specified
PubMed Reference 36683455
Abstract Androgens are steroid hormones crucial for sexual differentiation of the brain
and reproductive function. In excess, however, androgens may decrease fertility
as observed in polycystic ovary syndrome, a common endocrine disorder
characterized by oligo/anovulation and/or polycystic ovaries. Hyperandrogenism
may also disrupt energy homeostasis, inducing higher central adiposity, insulin
resistance, and glucose intolerance, which may exacerbate reproductive
dysfunction. Androgens bind to androgen receptors (ARs), which are expressed in
many reproductive and metabolic tissues, including brain sites that regulate the
hypothalamo-pituitary-gonadal axis and energy homeostasis. The neuronal
populations affected by androgen excess, however, have not been defined. We and
others have shown that, in mice, AR is highly expressed in leptin receptor
(LepRb) neurons, particularly in the arcuate (ARH) and the ventral premammillary
nuclei (PMv). Here, we assessed if LepRb neurons, which are critical in the
central regulation of energy homeostasis and exert permissive actions on puberty
and fertility, have a role in the pathogenesis of female hyperandrogenism.
Prenatally androgenized (PNA) mice lacking AR in LepRb cells (LepRb?AR) show no
changes in body mass, body composition, glucose homeostasis, or sexual
maturation. They do show, however, a remarkable improvement of estrous cycles
combined with normalization of ovary morphology compared to PNA controls. Our
findings indicate that the prenatal androgenization effects on adult
reproductive physiology (ie, anestrus and anovulation) are mediated by a
subpopulation of LepRb neurons directly sensitive to androgens. They also
suggest that the effects of hyperandrogenism on sexual maturation and
reproductive function in adult females are controlled by distinct neural


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