State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Chaoyang District, Beijing, People's Republic of China.
J Comp Physiol B. 2011 Aug;181(6):829-39. doi: 10.1007/s00360-011-0560-8. Epub 2011 Mar 3.
Maternal serum leptin concentrations have been suggested as a key factor in programming growth patterns and protecting against adult metabolic disease in human offspring. However, the role of maternal leptin in the development of wild rodent offspring is not clear. We tested the hypothesis that maternal hyperleptinemia in lactating Brandt's voles (Lasiopodomys brandtii) can protect their offspring from the risks of high-fat-diet-induced-obesity and insulin resistance. Lactating voles were supplemented with murine leptin (0.64 μg g(-1 ) day(-1)) or phosphate-buffered saline (control) on days 10-17 of lactation (peak lactation). At 12 weeks of age, the female and male offspring of the two maternal groups were randomly assigned to two groups each and fed either a high-fat diet (41% of gross energy as fat) or a control diet (14% of gross energy as fat) until the age of 23 weeks. Body mass, food intake, glucose tolerance and resting metabolic rate were determined in the four offspring groups. After animals were sacrificed, organ masses and adipose tissue distribution, and serum leptin and insulin concentrations were measured. Offspring of leptin-treated mothers showed no significant differences in body mass, energy intake or energy expenditure, body composition, glucose tolerance or serum leptin and insulin concentrations from offspring of control mothers. The high-fat diet induced increases in body mass (by 23% in female and 17% in male offspring) and reduced glucose tolerance in both female and male offspring, indicative of the emergence of insulin resistance, even though digestible energy intake of the male offspring decreased on the high-fat diet. These results indicate that maternal hyperleptinemia during peak lactation in Brandt's voles did not protect against diet-induced obesity or glucose intolerance in their offspring.
母体血清瘦素浓度被认为是人类后代生长模式编程和预防成年代谢性疾病的关键因素。然而，母体瘦素在野生啮齿动物后代发育中的作用尚不清楚。我们检验了这样一个假设，即在哺乳期布氏田鼠（Lasiopodomys brandtii）中，母体高瘦素血症可以保护其后代免受高脂肪饮食诱导肥胖和胰岛素抵抗的风险。在哺乳期的第 10-17 天，给哺乳期的田鼠补充鼠源瘦素（0.64 μg g(-1) day(-1))或磷酸盐缓冲盐水（对照）。在 12 周龄时，两个母体组的雌性和雄性后代被随机分为两组，每组分别喂食高脂肪饮食（总能量的 41%为脂肪）或对照饮食（总能量的 14%为脂肪），直到 23 周龄。在四个后代组中测定体重、食物摄入量、葡萄糖耐量和静息代谢率。动物被处死后，测量器官质量和脂肪组织分布，以及血清瘦素和胰岛素浓度。与对照组母亲的后代相比，瘦素处理组母亲的后代的体重、能量摄入或能量消耗、身体成分、葡萄糖耐量或血清瘦素和胰岛素浓度没有显著差异。高脂肪饮食诱导雌性后代体重增加（增加 23%）和雄性后代体重减轻（减少 17%），并且降低了雌性和雄性后代的葡萄糖耐量，表明出现了胰岛素抵抗，尽管雄性后代的高脂肪饮食中可消化能量摄入减少。这些结果表明，布氏田鼠哺乳期高峰期的母体高瘦素血症并不能预防饮食诱导的肥胖或后代的葡萄糖不耐受。
