Prenatal influences on leptin sensitivity and susceptibility to diet-induced obesity
Prenatal influences on leptin sensitivity and susceptibility to diet-induced obesity
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DOI：
10.1677/joe.1.06679
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发表时间：
2006-05-01
影响因子：
4
通讯作者：
Breier, Bernhard H.
中科院分区：
文献类型：
--
作者：
Krechowec, Stefan O.;Vickers, Mark;Breier, Bernhard H.
肥胖和2型糖尿病是世界性的健康问题，其发病率正在迅速增加。目前，对肥胖症发展的生物学因素仅部分了解。最近的研究表明，孕妇怀孕期间的营养可能会对后代产生长期的代谢影响。在本研究中，我们调查了产前和产后营养对瘦素敏感性和肥胖发展的相互作用。将Wistar大鼠定时交配，并在整个妊娠期间随机分配至自由采食（AD）或30%自由采食（UN）。断奶后，雌性后代喂食标准食物、高脂肪饮食或热量限制饮食。联合国母鼠的雌性后代在出生时生长迟缓，并表现出对高脂饮食引起的肥胖的易感性增加。在142 +/-15日龄时，测量瘦素敏感性作为对14天瘦素治疗（2.5 μ g/g/天，s.c.）的响应。在喂食食物的联合国后代中，瘦素治疗未能减少食物摄入量，体重减轻也有所减少。在UN后代中观察到的瘦素抵抗与饮食诱导的肥胖无关，与空腹高胰岛素血症和高胆固醇血症相关。我们的研究表明，产前营养可以通过改变瘦素敏感性和成年后能量代谢的变化来塑造未来对肥胖的易感性。
Obesity and type 2 diabetes are world wide health issues and their incidence is rapidly increasing. Currently the biological factors responsible for the development of obesity are only partially understood. Recent research has shown that maternal nutrition during pregnancy may have long-term metabolic consequences in offspring. In the present study we investigated interactions between prenatal and postnatal nutrition on leptin sensitivity and obesity development. Wistar rats were time-mated and randomly assigned to either ad-libitum (AD) or to 30% of ad-libitum (UN) food intake throughout pregnancy. After weaning, female offspring were fed standard chow, a high-fat diet or a calorie restricted diet. Female offspring of UN dams were growth retarded at birth and showed increased susceptibility to diet-induced obesity on a high-fat diet. At 142 +/- 15 days of age, leptin sensitivity was measured as a response to 14 days of leptin treatment (2.5 mu g/g/day, s.c.). In UN offspring fed chow, leptin treatment failed to reduce food intake and weight loss was diminished. This leptin resistance observed in UN offspring was independent of diet-induced obesity and was associated with fasting hyperinsulinemia and hypertriglyceridemia. Our study suggests that prenatal nutrition can shape future susceptibility to obesity through alterations in leptin sensitivity and changes in energy metabolism during adult life.