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During pregnancy, hPL stimulates DNA synthesis in mammary epithelial cells and growth of ductal epithelium, helping prepare for lactation [51]. During pregnancy, the high levels of prolactin stimulate growth of glandular epithelial cells and alveolar cells of the breast, as well as production of components of breast milk. Prolactin levels fall markedly after delivery, while breastfeeding induces pulsatile bursts of prolactin. Adiponectin, which falls throughout pregnancy, falls further during lactation, a change that may be mediated by prolactin [55]. Serum leptin falls postpartum but is not different between lactating and nonlactating women [56]. Lactating women manifested a greater postpartum increase in HDL cholesterol 6 weeks after delivery than did nonlactating women [57]. The primary source of milk lactose is circulating glucose. Lactating women, compared to nonlactating women, demonstrate approximately one-third greater glucose production during fasting, mediated by increased glycogenolysis [58]. Lactating women with previous gestational diabetes who were breastfeeding during an oral glucose tolerance test (OGTT) demonstrated lower postchallenge glucose values and greater insulin sensitivity than those who did not breastfeed during their OGTT, despite similar fasting glucose and insulin levels [59].