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G. T. Waites, P. L. Wood, R. A. Walker and S. C. Bell

Summary. The distribution of α2-PEG, a human analogue of β-lactoglobulin, in endometrium at different phases of the cycle was determined using immunohistochemistry with monoclonal and polyclonal antibodies. In the epithelial cells of glands in the functional zone of the endometrium, α2-PEG was first detectable from Days 19 to 21 during the mid-luteal phase and maximal immunostaining was observed during the end of the late luteal phase. Intense staining in the glandular secretions and weaker staining in surface luminal epithelial cells during this period were observed. A minor population of basal glands contained α2-PEG during the follicular phase. These results suggest that α2-PEG synthesis by the glandular epithelium of the regenerated endometrium is hormonally regulated. Maximal staining occurring during the late luteal phase suggests that regulation may be related to the hormonal requirement for pre-decidualization rather than that required for histologically defined glandular epithelial secretion.

Keywords: endometrium; human; menstrual cycle; pregnancy-associated endometrial α2-globulin; pregnancy proteins

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S. C. Bell, S. Patel, M. W. Hales, P. H. Kirwan and J. O. Drife

Summary. Antisera raised against the soluble antigens of the endometrium of early pregnancy detected two antigenic proteins of α1 and α2 mobility in extracts of this tissue and were termed antigens A and B. Neither antigen was detected in pregnancy sera or extracts of proliferative endometrium, but antigen B was detected in extracts of secretory endometrium and both were present in amniotic fluid and medium from in-vitro incubations of pregnancy endometrium. Fractionation of radiolabelled medium on ion-exchange chromatography demonstrated that antigens A and B co-eluted with the proteins from which EP14 and EP15 were derived and which were the major secretory polypeptides of pregnancy endometrium in vitro. Further biochemical purification revealed that EP14 (M r 32 000) was derived from a protein of native molecular weight 36 000 which existed in two forms, whereas EP15 (M r 28 000) was derived from a dimeric glycoprotein of native molecular weight 56 000. Immunochemical studies demonstrated that antigens A and B are identical to these two secretory proteins and have been termed pregnancy-associated endometrial α1- and α2-globulins (α1- and α2-PEG).

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S P Sébert, M A Hyatt, L L Y Chan, M Yiallourides, H P Fainberg, N Patel, D Sharkey, T Stephenson, S M Rhind, R C Bell, H Budge, D S Gardner and M E Symonds

The recent discovery of an association between body composition, energy intake and the fat mass and obesity-associated (FTO) gene represents a promising new therapeutic target in obesity prevention. In a well, pre-established large animal model, we investigated the regulation of FTO gene expression under conditions either leading to obesity or increased risk of obesity related disorders: i) a sedentary ‘Western’ lifestyle and ii) prenatal exposure to nutrient restriction. Pregnant sheep were either fed to fully meet their nutritional requirements throughout gestation or 50% of this amount from early-to-mid gestation. Following weaning, offspring were either made obese through exposure to a sedentary obesogenic environment or remained lean. A significant positive relationship between placental FTO gene expression and fetal weight was found at 110 days gestation. In both the newborn and adult offspring, the hypothalamus was the major site of FTO gene expression. Hypothalamic FTO gene expression was upregulated by obesity and was further increased by prenatal nutrient restriction. Importantly, we found a strong negative relationship between the hypothalamic FTO gene expression and food intake in lean animals only that may imply FTO as a novel controller of energy intake. In contrast, FTO gene expression in the heart was downregulated in obese offspring born to nutrient restricted mothers. In addition, FTO gene expression was unaffected by obesity or prenatal diet in insulin-dependent tissues, where it changed with age possibly reflecting adaptations in cellular energetic activity. These findings extend information gained from human epidemiology and provide new insights into the regulation of in vivo energy metabolism to prevent obesity.