期刊论文详细信息
Endocrine Journal
Hypoadiponectinemia in Lean Lactating Women: Prolactin Inhibits Adiponectin Secretion from Human Adipocytes
Hiroshi YOSHIDA1  Masaya ENDO1  Tsuneo TAKAHASHI1  Machi OKAMOTO1  Hideya SAKAKIBARA1  Mariko MURASE1  Fumiki HIRAHARA1  Mikiko ASAI-SATO1  Mario IKEDA1 
[1] Department of Obstetrics, Gynecology and Molecular Reproductive Science, Yokohama City University Graduate School of Medicine
关键词: Adiponectin;    Prolactin;    Pregnancy;    Lactation;   
DOI  :  10.1507/endocrj.K06-026
学科分类:内分泌与代谢学
来源: Japan Endocrine Society
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【 摘 要 】

References(31)Cited-By(29)Adiponectin is an adipocyte-derived hormone involved in glucose, lipid and energy metabolism. A low plasma adiponectin concentration is associated with insulin resistance, obesity and atherosclerosis. In women, energy homeostasis is remarkably changed during gestation and lactation in order to supply sufficient nutrition for a fetus or newborn. In this study we aimed to elucidate the physiological impact of gestation and lactation on the plasma adiponectin levels and the influence of reproduction-related hormones on adiponectin secretion. We studied the longitudinal changes in plasma adiponectin concentration during pregnancy (1st, 2nd and 3rd trimester) and lactation (3 days and 1 month after the delivery) in lean healthy women (n = 22). The plasma adiponectin level declined slightly as the pregnancy advanced and reached its lowest level during lactation (12.25 ± 0.182 μg/ml at early pregnancy vs. 6.88 ± 0.375 μg/ml at 3 days postpartum, p<0.001). In order to investigate the role of the lactogenic hormone prolactin in the decrease of plasma adiponectin levels during lactation, we further performed in vitro experiments using human primary cultured adipocytes. Western blotting of the adipocyte lysate and ELISA of the culture medium revealed that exogenous prolactin inhibited both production and secretion of adiponectin in a dose-dependent manner. Our results thus suggests that prolactin affects the regulation of maternal metabolism through suppression of adiponectin.

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