哺乳是哺乳動(dòng)物非常耗能的一個(gè)生理時(shí)期,。雌性小型哺乳動(dòng)物在哺乳期經(jīng)常是能量攝入增加，并將其身體的脂肪儲(chǔ)存降到很低的水平,，身體脂肪含量降低的生理功能尚不清楚,。身體脂肪含量降低曾被認(rèn)為是母體的高能量需求導(dǎo)致的。但通過計(jì)算,，動(dòng)物從消耗的脂肪中獲取的能量份額對(duì)整個(gè)能量平衡來講是微不足道的,。一個(gè)假說認(rèn)為，動(dòng)物身體脂肪含量降低會(huì)導(dǎo)致一些脂肪激素的降低（如瘦素）,，瘦素在哺乳期具有刺激攝食的作用,。
中科院動(dòng)物研究所動(dòng)物生理生態(tài)學(xué)研究組科研人員利用微滲透泵技術(shù)，在野生嚙齒動(dòng)物布氏田鼠哺乳期的最后7天,，通過施加外源瘦素以確定瘦素在哺乳高峰期的生理功能,。布氏田鼠是分布在內(nèi)蒙古典型草原的小型嚙齒動(dòng)物，不冬眠,，植食性,。研究組對(duì)于布氏田鼠的生理生態(tài)學(xué)特征和適應(yīng)環(huán)境的生理機(jī)理已有多年的研究，包括哺乳期的能量消耗。
研究結(jié)果發(fā)現(xiàn),，施加外源瘦素可以降低哺乳田鼠的體重和攝食量,，這種效應(yīng)具有劑量效應(yīng)。與非繁殖田鼠個(gè)體比較,，由脂肪含量降低導(dǎo)致的循環(huán)瘦素水平降低，可以解釋哺乳母體16%的能量過度攝入是瘦素水平降低導(dǎo)致的,。哺乳期瘦素水平降低,，可以通過（部分）刺激下丘腦的增食類神經(jīng)肽（如NPY和AgRP）和厭食類神經(jīng)肽（如POMC）的變化，從而調(diào)節(jié)哺乳期田鼠母體的高攝食量,。瘦素的這種生理效應(yīng)可以通過施加外源瘦素而反轉(zhuǎn),。結(jié)果還發(fā)現(xiàn)，外源瘦素處理并沒有影響動(dòng)物的每日能量消耗,、泌乳量或幼崽生長,，但卻導(dǎo)致非顫抖性產(chǎn)熱組織（褐色脂肪組織, BAT）中線粒體內(nèi)膜上解偶聯(lián)蛋白UCP1表達(dá)的增加（一般在哺乳期動(dòng)物BAT中UCP1的含量降低），這表明在哺乳高峰期動(dòng)物身體脂肪含量降低和瘦素水平降低可能還具有其他的生理功能,。（生物谷Bioon.com）
生物谷推薦原文：
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 The function of this reduction is unclear, as calculations suggest that the contribution of the withdrawn energy from fat to the total energy balance of lactation is trivial.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.
