{"title":"Physiopathology of prolactin secretion in obesity.","authors":"P G Kopelman","doi":"10.1038/sj.ijo.0801291","DOIUrl":null,"url":null,"abstract":"<p><p>In many species prolactin is of biological importance and has a major role in determining the deposition and mobilization of fat. In human physiology, outside pregnancy, prolactin secretion is altered by increasing body weight in both children and adults. Prolactin in this circumstance appears to be marker of hypothalamic-pituitary function: the prolactin response to insulin-hypoglycaemia, thyrotrophin releasing hormone stimulation and other stimulatory factors may be diminished. In addition, obesity alters the 24h spontaneous release of prolactin with a generalised dampening of release. A number of explanations have been given as possible causes for these alterations, but it seems likely that they reflect obesity per se and are associated with hyperinsulinaemia. Weight reduction, with accompanying decrease in plasma insulin levels, leads to a normalization of prolactin responses in most, but not all, circumstances. To date, no molecular basis has been identified which links prolactin with increasing body fatness, weight and appetite: new data suggests a possible link in obese men between fasting plasma prolactin and leptin concentrations.</p>","PeriodicalId":14227,"journal":{"name":"International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity","volume":"24 Suppl 2 ","pages":"S104-8"},"PeriodicalIF":0.0000,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/sj.ijo.0801291","citationCount":"64","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1038/sj.ijo.0801291","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 64

Abstract

In many species prolactin is of biological importance and has a major role in determining the deposition and mobilization of fat. In human physiology, outside pregnancy, prolactin secretion is altered by increasing body weight in both children and adults. Prolactin in this circumstance appears to be marker of hypothalamic-pituitary function: the prolactin response to insulin-hypoglycaemia, thyrotrophin releasing hormone stimulation and other stimulatory factors may be diminished. In addition, obesity alters the 24h spontaneous release of prolactin with a generalised dampening of release. A number of explanations have been given as possible causes for these alterations, but it seems likely that they reflect obesity per se and are associated with hyperinsulinaemia. Weight reduction, with accompanying decrease in plasma insulin levels, leads to a normalization of prolactin responses in most, but not all, circumstances. To date, no molecular basis has been identified which links prolactin with increasing body fatness, weight and appetite: new data suggests a possible link in obese men between fasting plasma prolactin and leptin concentrations.

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肥胖中催乳素分泌的生理病理。
在许多物种中,催乳素具有重要的生物学意义,在决定脂肪的沉积和动员方面起着重要作用。在人体生理学中,在怀孕之外,催乳素的分泌会随着儿童和成人体重的增加而改变。在这种情况下,催乳素似乎是下丘脑-垂体功能的标志:催乳素对胰岛素-低血糖、促甲状腺激素释放激素刺激和其他刺激因素的反应可能减弱。此外,肥胖改变了催乳素的24小时自发释放,并普遍抑制释放。关于这些变化的可能原因,人们给出了许多解释,但似乎它们反映了肥胖本身,并与高胰岛素血症有关。体重减轻,伴随着血浆胰岛素水平的降低,在大多数情况下(但不是全部)导致催乳素反应正常化。迄今为止,还没有发现催乳素与肥胖、体重和食欲增加之间的分子基础:新的数据表明,肥胖男性空腹血浆催乳素和瘦素浓度之间可能存在联系。
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Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis. Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores. Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance. Fat storage in pancreas and in insulin-sensitive tissues in pathogenesis of type 2 diabetes. Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases.
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