哺乳是哺乳动物非常耗能的一个生理时期。雌性小型哺乳动物在哺乳期经常是能量摄入增加，并将其身体的脂肪储存降到很低的水平，身体脂肪含量降低的生理功能尚不清楚。身体脂肪含量降低曾被认为是母体的高能量需求导致的。但通过计算，动物从消耗的脂肪中获取的能量份额对整个能量平衡来讲是微不足道的。一个假说认为，动物身体脂肪含量降低会导致一些脂肪激素的降低（如瘦素），瘦素在哺乳期具有刺激摄食的作用。

中科院动物研究所动物生理生态学研究组科研人员利用微渗透泵技术，在野生啮齿动物布氏田鼠哺乳期的最后7天，通过施加外源瘦素以确定瘦素在哺乳高峰期的生理功能。布氏田鼠是分布在内蒙古典型草原的小型啮齿动物，不冬眠，植食性。研究组对于布氏田鼠的生理生态学特征和适应环境的生理机理已有多年的研究，包括哺乳期的能量消耗。

研究结果发现，施加外源瘦素可以降低哺乳田鼠的体重和摄食量，这种效应具有剂量效应。与非繁殖田鼠个体比较，由脂肪含量降低导致的循环瘦素水平降低，可以解释哺乳母体16%的能量过度摄入是瘦素水平降低导致的。哺乳期瘦素水平降低，可以通过（部分）刺激下丘脑的增食类神经肽（如NPY和AgRP）和厌食类神经肽（如POMC）的变化，从而调节哺乳期田鼠母体的高摄食量。瘦素的这种生理效应可以通过施加外源瘦素而反转。结果还发现，外源瘦素处理并没有影响动物的每日能量消耗、泌乳量或幼崽生长，但却导致非颤抖性产热组织（褐色脂肪组织, BAT）中线粒体内膜上解偶联蛋白UCP1表达的增加（一般在哺乳期动物BAT中UCP1的含量降低），这表明在哺乳高峰期动物身体脂肪含量降低和瘦素水平降低可能还具有其他的生理功能。

推荐原文：

American Journal of Physiology     DOI: 10.?1152/?ajpregu.?00121.?2010

Effects of leptin infusion during peak lactation on food intake, body composition, litter growth, and maternal neuroendocrine status in female Brandt's voles (Lasiopodomys brandtii)

Jian-Guo Cui, Gang-Bin Tang, De-Hua Wang, and John R. Speakman

During lactation, female small mammals frequently reduce their fat reserves to very low levels. The function of this reduction is unclear, as calculations suggest that the contribution of the withdrawn energy from fat to the total energy balance of lactation is trivial. An alternative hypothesis is that reducing fat leads to a reduction in circulating adipokines, such as leptin, that play a role in stimulating the hyperphagia of lactation. We investigated the role of circulating leptin in lactation by repleting leptin levels using miniosmotic pumps during the last 7 days of lactation in Brandt's voles (Lasiopodomys brandtii), a model small wild mammal we have extensively studied in the context of lactation energy demands. Repletion of leptin resulted in a dose-dependent reduction of body mass and food intake in lactating voles. Comparisons to nonreproducing individuals suggests that the reduced leptin in lactation, due to reduced fat stores, may account for ～16% of the lactational hyperphagia. Reduced leptin in lactation may, in part, cause lactational hyperphagia via stimulatory effects on hypothalamic orexigenic neuropeptides (neuropeptide Y and agouti-related peptide) and inhibition of the anorexigenic neuropeptide (proopiomelanocortin). These effects were reversed by the experimental repletion of leptin. There was no significant effect of leptin treatment on daily energy expenditure, milk production or pup growth, but leptin repletion did result in a reversal of the suppression of uncoupling protein-1 levels in brown adipose tissue, indicating an additional role for reducing body fat and leptin during peak lacation.