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泌乳中期催乳素抑制作用对成年大鼠脂肪量和甲状腺功能的影响。

Prolactin inhibition at mid-lactation influences adiposity and thyroid function in adult rats.

机构信息

Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil.

出版信息

Horm Metab Res. 2010 Jul;42(8):562-9. doi: 10.1055/s-0030-1253434. Epub 2010 May 6.

DOI:10.1055/s-0030-1253434
PMID:20449792
Abstract

Maternal hypoprolactinemia at the end of lactation (a precocious weaning model) increases milk leptin transfer and results in overweight, leptin resistance, and secondary hypothyroidism at adulthood. We studied the effects of prolactin (PRL) inhibition during mid-lactation (a partial malnutrition model) on milk leptin transfer, leptinemia, body composition, and thyroid function. Lactating rats were treated with bromocryptine (BRO, 1 mg/twice daily) or saline on days 7, 8, and 9 of lactation. Offspring were sacrificed 10, 21, and 90 days after birth. After treatment, BRO-treated dams showed hypoprolactinemia and hyperleptinemia, and produced less milk with lower levels of lactose and higher milk triglycerides. Milk leptin levels were lower at weaning. Offspring of BRO-treated dams had lower body weight and length as well as less visceral fat during lactation and adulthood. Total fat was also lower at weaning and adult life, whereas total protein was higher at 90 days-old. BRO offspring presented lower serum T4 and TSH at 10 days-old and weaning, respectively. When adults, these rats exhibited hypoleptinemia, lower levels of thyroid hormones, and higher TSH. Early inhibition of PRL therefore leads to offspring malnutrition and affects subsequent growth. Also, inhibition of PRL during lactation predisposes offspring to hypothyroidism; however, when the inhibition occurs during late lactation, the hypothyroidism is secondary, whereas when it is restricted to mid-lactation, the thyroid hypofunction is primary. The programming effect of milk suppression thus depends on the developmental stage of offspring.

摘要

哺乳期末(即早断奶模型)的母体催乳素不足会增加乳汁瘦素的转移,导致成年后超重、瘦素抵抗和继发性甲状腺功能减退。我们研究了哺乳期中期(部分营养不良模型)抑制催乳素(PRL)对乳汁瘦素转移、瘦素血症、身体成分和甲状腺功能的影响。哺乳期大鼠在第 7、8 和 9 天接受溴隐亭(BRO,1 mg/次,每日 2 次)或生理盐水处理。后代在出生后 10、21 和 90 天被处死。治疗后,BRO 处理的母鼠表现出催乳素不足和高瘦素血症,并产生较少的乳汁,乳糖水平较低,乳脂水平较高。断奶时的乳汁瘦素水平较低。BRO 处理的母鼠的后代在哺乳期和成年期的体重和体长较低,内脏脂肪较少。断奶时和成年时的总脂肪也较低,而总蛋白在 90 天时较高。BRO 后代在 10 天和断奶时的血清 T4 和 TSH 水平较低。成年后,这些大鼠表现出低瘦素血症、甲状腺激素水平较低和 TSH 较高。因此,PRL 的早期抑制会导致后代营养不良,并影响随后的生长。此外,哺乳期催乳素抑制会使后代易患甲状腺功能减退症;然而,当抑制发生在晚期哺乳期时,甲状腺功能减退是继发性的,而当抑制仅限于中期哺乳期时,甲状腺功能减退是原发性的。因此,乳汁抑制的编程效应取决于后代的发育阶段。

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