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SUMMARY
The serum concentration of gonadotrophin during several stages of pregnancy was determined in seven mares bred to a stallion and in four mares bred to a jack. To eliminate individual differences, two mares were bred successively to a stallion and to a jack. When the mare is carrying a mule foetus the hormone concentration is approximately one-tenth that associated with a horse foetus. One mare carrying a mule foetus was killed on the 69th day of pregnancy. Though the endometrial cups appeared normal histologically, the endometrial cup secretion was scanty and low in potency. The amount of hormone in the cups themselves was also low.
The genotype of the foetus, we conclude, influences the secretory activity of the endometrial cups.
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Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, USA
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Loss of ovarian hormones leads to increased adiposity and insulin resistance (IR), increasing the risk for cardiovascular and metabolic diseases. The purpose of this study was to investigate whether the molecular mechanism behind the adverse systemic and adipose tissue-specific metabolic effects of ovariectomy requires loss of signaling through estrogen receptor alpha (ERα) or estrogen receptor β (ERβ). We examined ovariectomized (OVX) and ovary-intactwild-type (WT), ERα-null (αKO), and ERβ-null (βKO) female mice (age ~49 weeks; n = 7–12/group). All mice were fed a phytoestrogen-free diet (<15 mg/kg) and either remained ovary-intact (INT) or were OVX and followed for 12 weeks. Body composition, energy expenditure, glucose tolerance, and adipose tissue gene and protein expression were analyzed. INT αKO were ~25% fatter with reduced energy expenditure compared to age-matched INT WT controls and βKO mice (all P < 0.001). Following OVX, αKO mice did not increase adiposity or experience a further increase in IR, unlike WT and βKO, suggesting that loss of signaling through ERα mediates OVX-induced metabolic dysfunction. In fact, OVX in αKO mice (i.e., signaling through ERβ in the absence of ERα) resulted in reduced adiposity, adipocyte size, and IR (P < 0.05 for all). βKO mice responded adversely to OVX in terms of increased adiposity and development of IR. Together, these findings challenge the paradigm that ERα mediates metabolic protection over ERβ in all settings. These findings lead us to suggest that, following ovarian hormone loss, ERβ may mediate protective metabolic benefits.
