胰岛素诱导的低血糖大鼠下丘脑增食欲素-A的表达

目的：探讨急性低血糖应激对大鼠下丘脑增食欲素-A（orexin—A）的表达影响。方法：胰岛素皮下注射建立急性低血糖大鼠模型,检测外周血中葡萄糖和胰岛素水平的变化。采用免疫组织化学染色观察下丘脑orexin-A表达的改变和灰度值测量,观察其染色强度。结果：低血糖禁食组大鼠下丘脑orexin-A的表达明显增加（P〈0．05）,而低血糖进食组orexin-A表达无明显改变。灰度分析显示低血糖禁食组染色强度最高,与对照组比较有明显统计学差异（P〈0．05）。结论：急性血糖的降低可以增强大鼠下丘脑orexin-A的表达,而摄食行为可抑制此效应。     

急性低血糖应激对大鼠下丘脑orexin-A表达的影响

目的研究胰岛素诱导的急性低血糖应激对大鼠下丘脑增食欲素-A(orexin-A)的表达影响。方法通过皮下注射胰岛素建立急性低血糖大鼠模型。采用免疫组织化学染色方法观察大鼠下丘脑orexin-A和Fos双标情况,并采用ELISA方法对脑脊液中的orexin-A含量进行检测。结果禁食组、低血糖进食组和低血糖禁食组阳性神经元计数明显高于对照组(P0.05),但三组之间计数比较差异无统计学意义(P0.05);Orexin-A/Fos双标细胞率(双标细胞占orexin-A阳性细胞的百分率)在低血糖禁食组最高,与禁食组和低血糖进食组比较差异有统计学意义(P0.05)。ELISA检测结果显示,低血糖禁食组脑脊液中的orexin-A含量显著高于其它三组,差异有统计学意义(P0.05)。结论急性血糖的降低可以增强大鼠下丘脑中orexin-A的表达,而摄食行为可以抑制此调控效应。     

马桑内酯激活的星形胶质细胞条件培养液对正常大鼠脑内及培养的神经元内PLCβ1的影响

目的揭示星形胶质细胞对大鼠脑内及培养的神经元磷脂酶Cβ1(PLCβ1)的影响及其在癫痫发病中的作用。方法将马桑内酯激活的星形胶质细胞条件培养液(astrocyte-conditioned medium,ACM)注射入正常SD大鼠侧脑室,观察大鼠的行为变化;运用免疫组织化学方法,观察大鼠大脑皮质、海马内PLCβ1免疫反应的变化;将培养的神经元随机分为2组:1.对照组(无血清培养基组),2.ACM组。各组细胞分别培养4、8、12h后,免疫细胞化学方法观察培养神经元内PLCβ1表达的变化,Western blot法检测各组培养神经元PLCβ1含量的变化。结果ACM组大鼠在注射ACM后30 min出现癫痫行为,2 h恢复正常;免疫组织化学显示:ACM作用后4h,大鼠大脑皮质、海马PLCβ1免疫反应阳性神经元数和平均光密度值显著增高(P<0.05);培养神经元的免疫细胞化学染色证明ACM组在作用4h时PLCβ1免疫阳性反应产物明显增加,与对照组比较有明显差异(P<0.05);Western blot结果表明PLCβ1含量在ACM作用4h较对照组明显增多(P<0.05)。结论马桑内酯激活的星形胶质细胞条件培养液可上调大鼠脑内及培养的神经元内PLCβ1的表达,并导致动物痫性发作。     

甘珀酸对内脏痛大鼠延髓星形胶质细胞和神经元反应的影响

目的:研究侧脑室注射甘珀酸后对福尔马林灌胃致内脏疼痛大鼠的延髓迷走孤束复合体内星形胶质细胞和神经元反应的影响.方法:经侧脑室注射缝隙连接阻断剂甘珀酸(carbenoxolone,CBX)后向大鼠胃内灌入2.5%福尔马林2ml诱发内脏疼痛,用免疫组织化学方法观察延髓迷走孤束复合体(VSC)内抗Fos蛋白(标记神经元)和抗胶质原纤维酸性蛋白(标记星形胶质细胞)的单一或双重标记的免疫荧光染色.结果:福尔马林灌胃后大鼠出现烦躁易激惹,呼吸变快,持续1h;而预先侧脑室注射CBX则动物疼痛行为学反应明显减轻.免疫组织化学染色发现福尔马林灌胃后大鼠VSC中的Fos免疫反应数目增强;大鼠预先侧脑室注射CBX后VSC中的Fos免疫反应数目明显减弱.结论:延髓VSC中的星形胶质细胞和神经元参与福尔马林灌胃致内脏痛的调节,星形胶质细胞可能通过缝隙连接影响神经元对内脏痛的调节功能.     

禁食不同时段下丘脑穹窿周区orexin-A的表达

目的探讨禁食不同时段大鼠下丘脑穹窿周区orexin—A的表达及是否与摄食有关。方法观察禁食前后大鼠体重变化,采用免疫组织化学染色法观察禁食不同时段下丘脑穹窿周区orexin-A的表达变化,灰度值测量观察各组orexin—A的染色强度。结果大鼠体重随禁食时间的延长而逐渐降低,各组大鼠禁食前后体重变化有统计学差异（P〈O．01）;Orexin-A主要分布于下丘脑穹窿周区,禁食组orexin—A阳性神经元计数明显多于对照组（P〈O．05）,但不同禁食组间orexin-A阳性神经元计数比较没有统计学差异（P〉O．05）;禁食48h组染色强度最深,与对照组和禁食24h、72h组有明显统计学差异（P〈0．05）。结论禁食可以促进orexin-A的表达,禁食48h应该是一种理想的促进orexin-A活化的刺激方式,orexin-A系统可能参与摄食及能量代谢的调节。     

大鼠延髓背侧迷走复合体注射ghrelin激活弓状核神经肽Y/刺鼠色蛋白相关蛋白神经元而诱发多食(英文)

Ghrelin是生长素促分泌受体的内源性配体,刺激摄食并增加体重。已有研究证实ghrelin刺激摄食的作用靶点主要是下丘脑弓状核(hypothalamic arcuate nucleus,ARC)内的神经肽Y(neuropeptide Y,NPY)/刺鼠色蛋白相关蛋白(agouti-related peptide,AgRP)神经元。除下丘脑外,脑干尾部迷走复合体具有ghrelin受体,是ghrelin调控摄食活动的另一靶点。本实验旨在验证ghrelin作用于脑干尾部所诱发的摄食增加是否需要下丘脑NPY/AgRP神经元参与。在大鼠延髓背侧迷走复合体(dorsal vagalcomplex,DVC)微量注射20pmol的ghrelin,用摄食自动分析仪测量大鼠的摄食反应,用荧光定量PCR技术测定ARC的NPY/AgRP mRNA的表达水平,同时利用免疫组化技术测定ARC的NPY阳性神经元数量及光密度。结果显示,与对照组(DVC微量注射生理盐水)相比,ghrelin微注射组大鼠摄食量增加,其累积摄食量在注射后2h达最高峰;ARC处NPY/AgRP mRNA的表达水平、NPY免疫阳性神经元的数量及光密度也明显增加,且均在ghrelin注射后2h增高达到高峰。以上结果提示,大鼠DVC注射ghrelin可能通过上行纤维激活弓状核NPY/AgRP神经元,介导大鼠的多食反应。     

马桑内酯激活的星形胶质细胞条件培养液对正常大鼠脑内谷氨酸和GABA的影响

目的探讨星形胶质细胞对大鼠脑内谷氨酸(Glu)和γ-氨基丁酸(GABA)的影响及其在癫痫发病中的作用。方法将马桑内酯激活的星形胶质细胞条件培养液(astrocyte-conditioned medium,ACM)注射入正常SD大鼠侧脑室,观察大鼠的行为变化,运用免疫组织化学及HPLC的方法,观察大鼠大脑皮质、海马内Glu和GABA免疫反应的变化及脑组织匀浆、脑脊液内Glu和GABA含量的变化。结果ACM组大鼠在注射ACM后30min出现癫痫行为,2h恢复正常。免疫组织化学显示:ACM作用后2h,大鼠大脑皮质及海马内Glu免疫反应阳性神经元数和平均光密度值明显增高,4h达高峰(P<0.05),12h恢复正常水平;ACM作用后2h,大鼠大脑皮质及海马GABA免疫反应阳性神经元数和平均光密度值明显减弱(P<0.05),12h恢复正常水平。HPLC方法显示:ACM作用后2h大鼠大脑皮质、海马及脑脊液中Glu含量均开始增加,4h达高峰(P<0.05);ACM作用后2h大脑皮质、海马及脑脊液中GABA含量均开始降低,4h达最低(P<0.05)。结论马桑内酯激活的星形胶质细胞条件培养液可影响大鼠脑内Glu和GABA的表达,并导致动物痫性发作。     

中枢注射Nesfatin-1与Exendin(9-39)对大鼠摄食和胃肠动力调节的影响

目的:探讨下丘脑室旁核注射GLP-1R拮抗剂Exendin(9-39)对Nesfatin-1所致大鼠摄食和胃肠动力改变的影响及作用机制。方法:选择40只雄性Wistar大鼠,随机分成正常对照组(NC组)、Nesfatin-1组(NS组)、Exendin(9-39)组(ES组)、Nesfatin-1联合Exendin(9-39)组(NE组)。采用下丘脑室旁核(PVN)埋置套管并分别给予以上药物干预,干预前和干预后的12小时、24小时记录和比较各组大鼠的摄食、饮水及体重变化。2天后,采用甲基纤维素-酚红溶液灌胃法测各组大鼠胃排空率,实时荧光定量法(RT-PCR)检测下丘脑及胃组织GLP-1Rm RNA的表达。结果:与基础摄食量比较,NS组大鼠给药后12 h、24 h的摄食量减少(P0.05),NE组大鼠给药后12 h、24 h的摄食量减少(P0.05),但较NS组增加(P0.05);与基础饮水量比较,NS组、NE组给药后12 h饮水量减少(P0.05);与基础体重比较,NS组大鼠给药后12 h、24 h的体重降低(P0.05),NE组大鼠给药后12 h的体重降低(P0.05),但较NS组增加(P0.05);NS组大鼠给药后胃排空率较NC、NE组大鼠显著下降(P0.05),NS组大鼠下丘脑GLP-1Rm RNA的表达量较NC组增加(P0.05)。结论:中枢给予GLP-1R拮抗剂能减弱Nesfatin-1引起的摄食抑制、胃排空延迟及体重下降效应,Nesfatin-1可能通过与GLP-1的协同作用参与摄食及胃肠动力的调节。     

Aβ25～35诱导大鼠记忆减退与星形胶质细胞及NOS阳性细胞变化

目的探讨Aβ25～35诱导模拟人类Alzheimer`s病(AD)的大鼠病理模型中星形胶质细胞变化与一氧化氮合酶神经元损伤引起的老年性记忆减退之间的关系.方法双侧海马内注射β-淀粉样多肽25～35片段(Aβ25～35)制作大鼠AD模型,注射一周后采用NOS组化染色、GFAP免疫组化染色及NOS组化和GFAP双重染色分析大鼠海马GFAP与NOS的表达.结果海马内注射Aβ25～35后出现海马星形胶质细胞增生、肥大、数目明显多于对照组(P<0.05),并出现一氧化氮阳性星形胶质细胞;海马一氧化氮神经元数量较对照组显著减少(P<0.05).结论 AD模型大鼠学习记忆功能低下与Aβ神经毒性导致NOS阳性神经元损伤、死亡直接相关,反应性星形胶质细胞参与Aβ导致NOS神经元细胞毒性损伤作用,间接导致学习记忆能力减退.     

Orexin 和P物质对顺铂诱发大鼠异食癖的影响

目的:观察食欲素(Orexin)和P物质(SP)对顺铂诱发大鼠异食癖的影响。方法:雄性Wistar大鼠被随机分为对照组和顺铂处理组,顺铂处理组给予大鼠顺铂(3或6 mg/kg,腹腔注射),对照组给予等量生理盐水。记录顺铂大鼠摄食高岭土量、摄食量的改变;Real-time PCR法观察顺铂对大鼠下丘脑Orexin和延髓中SP前体-前速激肽原A(PPT-A)m RNA表达的影响;分别和联合应用SP受体(NK1受体)拮抗剂阿瑞匹坦和Orexin-A对顺铂大鼠异食癖和摄食量的作用。结果:皮下注射3 mg/kg(低剂量组)的顺帕后大鼠高岭土摄入量和摄食量与对照组相比无明显差异(P0.05),而注射6 mg/kg(高剂量组)顺铂后,大鼠高岭土摄入量与对照组和低剂量组相比显著增加(P0.05);高剂量的顺铂作用12 h时,大鼠延髓内PPT-A的m RNA表达有轻微增加,但无统计学差异(P0.05),24 h后,延髓内PPT-A的m RNA表达量显著增加(P0.05)。在此后持续观察的5天中,顺铂可持续引起延髓中PPT-A的mRNA表达增高,在第5天时PPT-A的m RNA仍维持166.23±16.92%的高表达。高剂量顺铂抑制大鼠下丘脑中Orexin的mRNA表达,24 h时Orexin降低幅度最明显,为对照组的34.81±7.22%(P0.05)。此后检测的5天,Orexin浓度均低于对照组;将阿瑞匹坦和orexin联合应用,大鼠高岭土摄入量较单独应用阿瑞匹坦或orexin明显减少,摄食量显著增加(P0.05)。结论:P物质和orexin通路对顺铂化疗大鼠的异食癖和摄食量调控具有协同作用。     

Food restriction selectively increases hypothalamic orexin-B levels in lactating rats

Orexins are hypothalamic peptides implicated in the regulation of ingestive and other behaviours. Here we investigated prepro-orexin expression and hypothalamic orexin-A and -B levels in lactating rats, which display marked hyperphagia, with or without food restriction for 2 days or treatment with bromocriptine, which inhibits milk production and thus reduces the energy losses of lactation. Neither prepro-orexin gene expression nor hypothalamic orexin-A peptide levels were changed in any of these lactating groups compared with age-matched virgin controls. However, hypothalamic orexin-B levels were significantly higher in lactating rats that were food-restricted for 2 days (P<0.05) compared with non-lactating controls and with lactating rats that were either freely-fed or bromocriptine-treated. Thus, food restriction superimposed on lactation selectively increases hypothalamic orexin-B levels, suggesting that orexin-A and -B may be differentially released or cleared. Changes in orexin-B availability may influence physiological activities other than energy homeostasis, perhaps inducing arousal.     

Upregulation of astrocytic basic fibroblast growth factor in the cingulate cortex of lactating rats: time course and role of suckling stimulation

Previous work from our laboratory has shown that there is a much higher level of bFGF and GFAP immunoreactivity in area 2 of the cingulate cortex (Cg2) of rats on day 16 of lactation than in cycling or late pregnant females. To examine the time course of this change, in the first of the current studies, we compared bFGF and GFAP immunoreactivity in the brains of lactating females on postpartum day 4 (PP4), day 10 (PP10), day 16 (PP16), and day 24 (PP24) with that of cycling and ovariectomized (OVX) females. In the second study, we investigated whether the maintenance of these changes in bFGF and GFAP depended on suckling stimulation by removing litters on day 1 or day 16 postpartum and examining the brains of the dams on day 4 (Pr4) or day 24 (Pr24) postpartum, respectively. bFGF and GFAP immunoreactivity within Cg2 and the medial preoptic area (MPOA) were measured. In both experiments astrocytic bFGF and GFAP surface density in the Cg2 varied significantly across groups. All postpartum rats, regardless of stage of lactation or presence of the litter, had significantly higher levels of bFGF and GFAP immunoreactivity than cycling animals. Thus, the maintenance of this upregulation in bFGF and GFAP immunoreactivity does not depend on suckling stimulation. Consistent with our previous report, astrocytic bFGF was also elevated in the MPOA of PP16 animals. These data suggest a robust, long-lasting, postpartum change in bFGF and GFAP immunoreactivity in Cg2 and a role for this area of the cortex in the physiological and behavioral adaptations that accompany reproductive experience.     

Changes in leptin levels during lactation: implications for lactational hyperphagia and anovulation

In these studies we investigated the time course of changes in circulating leptin levels in lactating rats and the dependence of these changes on the energetic cost of lactation and evaluated the contribution of changes in leptin levels to lactational hyperphagia and infertility. In the first experiment, plasma leptin levels were measured on Days 5, 10, 15, 20, and 25 postpartum in freefeeding lactating rats and age-matched virgin females. Retroperitoneal and parametrial fat pads weights were obtained from the same females. In the second experiment the same measures, together with plasma insulin and prolactin levels, were taken on Days 15 and 20 postpartum from galactophore-cut and sham-operated females. In Experiments 3 and 4, the effects of exogenous leptin administration, either subcutaneously (sc) or intracerebroventricularly (icv), on lactational anovulation, maternal food intake, and dam and litter weights were examined. Circulating leptin levels decreased in lactating rats. Leptin levels were highly positively correlated with fat pad weight. Eliminating the energetic costs of lactation by preventing milk delivery induced dramatic increases in plasma leptin and insulin levels and also increased adiposity. Exogenous leptin administration did not affect length of lactational anovulation but reduced food intake, maternal body weight, and litter weight gain when given centrally and maternal body weight when given systemically. Together, these data show that the energetic costs of lactation are associated with a fall in circulating leptin levels but that these do not make a major contribution to the suppression of reproduction in lactating rats; however, they may be permissive to the hyperphagia of lactation.     

The effect of cholecystokinin, bombesin and calcitonin on food intake in virgin, lactating and postweaning female rats

During lactation food intake increases greatly without an accompanying large increase in body weight; therefore, this physiological state is an excellent example of non-obese hyperphagia. In the present study, we found that cholecystokinin (CCK-8) decreased food intake in lactating and virgin female rats. However, female rats were more resistant to the effect of CCK on eating following weaning of the pups. Bombesin (BB) suppressed food intake in virgin female rats and in lactating rats during early and mid lactation. Rats were resistant to its satiating effect during late lactation and during the postweaning period. Calcitonin potently suppressed food intake in virgin, lactating and postweaning rats. The present findings suggest that CCK and bombesin decrease food intake more effectively in virgin female rats and during earlier phases of lactation than during late lactation or postweaning.     

Lactational performance, consummatory behavior, and suppression of estrous cyclicity in rats suckling underfed pups

The role of pups' appetite in the regulation of maternal consummatory behavior (food intake of nursing mothers), lactational performance and postpartum diestrus was studied over a period of 45 days postpartum in rats chronically exposed to either underfed or normally fed pups. Experimental rats (n = 10) daily received 5 pups, 4-10-days-old, that had been deprived of food for the preceding 24 h while under the care of nonlactating foster mothers. Control rats (n = 10) received normally fed pups obtained daily from lactating foster mothers. Throughout the experimental period, the daily milk yield (estimated by litter weight gain), the intake of food and water by the mother, as well as the ratio of litter weight gain to mother's intake of food and water were all markedly higher in rats nursing underfed pups than in rats nursing normally fed pups. After a peak in lactation around Day 15 postpartum, experimental rats produced the same amount of milk during extended lactation as they did in the beginning of lactation, while control rats produced only half the amount of milk during extended lactation as they did in early lactation. Regardless of the nutritional state of the suckling pups, maternal body weight increased progressively over the first four weeks of lactation and remained unchanged during the time of extended lactation. The postpartum diestrus and the subsequent diestrous phase in the time of extended lactation were considerably longer in duration in rats that nursed underfed pups. On Day 45 of lactation, prolactin levels were higher and the adrenal glands were larger in experimental rats than in controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Leptin and the adaptations of lactation in rodents and ruminants.

Lactation markedly increases nutrient requirements in both rodents and ruminants. This is met mostly by increased food intake, but there are also adaptations to increase metabolic efficiency. Despite such changes, lactating animals usually experience periods of negative energy balance. This is not due to a physical constraint on food intake, at least in the rat. Leptin, a hormone secreted by adipocytes, plays an important role in the regulation of appetite and energy balance. During lactation, serum leptin concentration is decreased in both rodents and ruminants, and the nocturnal rise in concentration is lost in rats. Hypoleptinaemia in lactation is primarily a result of negative energy balance. There is also increased clearance of serum leptin, and the attenuation of the nocturnal rise in leptin in rats is at least partly due to the suckling stimulus. Hypoleptinaemia is not the major factor driving hyperphagia in lactating rats, but it probably facilitates the increased food intake. Leptin may play a more important role in this respect in lactating ruminants. Leptin is probably involved in other adaptations that increase metabolic efficiency during lactation. The ability of hypothalamic neuropeptides to respond to leptin does not appear to be altered by lactation in either rodents or ruminants. The reason why lactating animals do not respond to hypoleptinaemia with a further increase in appetite, thereby achieving energy balance, appears to be due to a failure to respond to changes in neuropeptides which mediate the effects of leptin.     

Interaction of late pregnancy and lactation in rats.

The effect of pregnancy on lactation was studied during the third week of lactational pregnancy in postpartum pregnant rats with a delay in implantation of only 1 day (1d-LP rats). In an experimental design in which the suckling litter was prevented from consuming solid food, lactational performance was estimated by weighing the ten-pup suckling litters on days 16-21 of lactation or by measuring maternal weight loss after a nursing spell on day 21. In 1d-LP rats, food consumption as well as lactational performance was lower than it was in nonpregnant lactating rats (L rats) and pregnant-lactating rats with a normal long delay of implantation of at least 6 days (LP rats). The time spent by the pups sucking at the nipples was not different among the three groups, but the number of milk ejections was diminished in 1d-LP dams. Restriction of daily food supply during days 16 to 21 of lactation diminished lactational performance more strongly in 1d-LP rats than it did in L rats; 1d-LP rats conserved protein stores and mobilized fewer minerals than did L rats. The weight and composition of the litter in vitro were not affected by the food restriction. In pregnant-lactating rats (LP and 1d-LP rats), the number of early resorptions was increased in comparison with pregnant rats, showing that lactation can affect the earlier stages of pregnancy. It was concluded that late pregnancy does not affect nursing behaviour, but suppresses lactation by restricting maternal food intake and mobilization of maternal stores. Measurements in serum indicate a causative role for oestradiol, but not for leptin.     

Effect of intraperitoneal CCK-8 on food intake and brain orexin-A after 48 h of fasting in the rat

We investigated the interactions of the peripheral satiety peptide cholecystokinin and the brain orexin-A system in the control of food intake. The effect of an intraperitoneal (i.p.) injection of sulfated cholecystokinin octapeptide (in this article called CCK) (5 microg/kg, 4.4 nmol/kg) or of phosphate-buffered saline (PBS, vehicle control) on 48 h fasting-induced feeding and on orexin-A peptide content was analyzed in diverse brain regions innervated by orexin neurons and involved in the control of food intake. Administration of CCK after a 48 h fast reduced fasting-induced hyperphagia (P<0.05). I.p. CCK increased the orexin-A content in the posterior brainstem of 48 h fasted rats by 35% (P<0.05). Fed animals receiving CCK had 48% higher orexin-A levels in the posterior brainstem than fasted rats (P<0.05). In the lateral hypothalamus, fasting decreased orexin-A levels by 50% as compared to fed rats (P<0.05). In the septal nuclei, the combination of fasting and CCK administration reduced orexin-A contents compared to fed PBS and CCK animals by 13% and 17%, respectively (P<0.05). These results suggest a convergence of pathways activated by peripheral CCK and by fasting on the level of orexin-A released in the posterior brainstem and provide evidence for a novel interaction between peripheral satiety signaling and a brain orexigen in the control of food intake.     

Regulation of ghrelin secretion during pregnancy and lactation in the rat: possible involvement of hypothalamus

We investigated the plasma concentration of ghrelin peptide during pregnancy and lactation in rats. Plasma ghrelin levels on days 10 and 15 of pregnancy were significantly lower than those of the non-pregnant rats. Thereafter, the plasma ghrelin levels on day 20 of pregnancy sharply increased to levels comparable with those in non-pregnant rats. Ghrelin peptide concentrations in the stomach did not change significantly during pregnancy. In the hypothalamus, ghrelin mRNA levels were significantly lower on day 15 of pregnancy than in the non-pregnant rats. Also, plasma ghrelin levels were significantly lower in lactating dams than non-lactating controls on days 3 and 8 of lactation. We examined the possible involvement of prolactin and oxytocin in the regulation of plasma ghrelin concentrations during lactation. Although plasma prolactin levels were decreased by the administration of bromocriptine, plasma ghrelin levels did not differ significantly between vehicle- and drug-treated lactating rats. Administration of haloperidol produced a marked increase in plasma prolactin levels as compared with the non-lactating controls. However, plasma ghrelin levels were not significantly different between vehicle- and drug-treated rats. Administration of an oxytocin antagonist into the lateral ventricle significantly inhibited the increase in the plasma oxytocin level induced by acute suckling. However, plasma ghrelin levels did not significantly between the groups. These observations indicated that the decrease in serum ghrelin is caused by a loss of the contribution of hypothalamic ghrelin. Furthermore, the present results suggested that the suckling stimulus itself, but the release of prolactin or oxytocin, is the factor most likely to be responsible for the suppression of ghrelin secretion during lactation.     

The energetics of lactation in cooperatively breeding meerkats Suricata suricatta

Species may become obligate cooperative breeders when parents are unable to raise their offspring unassisted. We measured the daily energy expenditure of mothers, helpers and offspring during peak lactation in cooperatively breeding meerkats Suricata suricatta using the doubly labelled water technique. Lactating mothers expended more energy per day than allo-lactating subordinate females, non-lactating females or suckling offspring. Metabolizable energy intakes of lactating mothers were calculated from isotope-based estimates of offspring milk energy intake, and were not significantly different from the previously suggested maximal limit for mammals. Allo-lactating females were the only category of animals that lost weight during the period of study, probably because they spent more time babysitting than non-lactating females. Daily energy expenditure (DEE) of lactating mothers increased with litter size but decreased with the number of helpers. Calculations show that for every 10 helpers, even in the absence of allo-lactators, mothers are able to reduce their DEE during peak lactation by an amount equivalent to the energy cost of one pup. These results indicate that helpers have beneficial energetic consequences for lactating mothers in an obligate cooperatively breeding mammal.