Energy metabolism and the evolution of reproductive suppression in the human female

Reproduction places severe demands on the energy metabolism in human females. When physical work entails higher energy expenditure, not enough energy will be left for the support of the reproductive processes and temporal suppression of the reproductive function is expected. While energy needed for reproduction may be obtained by increases in energy intake, utilization of fat reserves, or reallocation of energy from basal metabolism, several environmental or physiological constraints render such solutions unlikely. For human ancestors increases in energy intake were limited by availability of food, by labor of food preparation and by metabolic ceilings to energy assimilation. Energy stored as fat may support only a fraction of the requirements for reproduction (especially lactation). Effects of intense physical activity on basal metabolism may also interfere with fat accumulation during pregnancy. Finally, the female physiology may experience demands on increasing the basal metabolism as a consequence of physical activity and, at the same time, on decreasing the basal metabolism, when energy to support the ongoing pregnancy or lactation is inadequate. The resulting metabolic dilemmas could constitute a plausible cause for the occurrence of reproductive suppression in response to physical activity. It is, therefore, likely that allocating enough energy to the reproductive processes during periods when energy expenditure rises may be difficult due to physiological and bioenergetic constraints. Females attempting pregnancy in such conditions may compromise their lifetime reproductive output. A reproductive suppression occurring in low energy availability situations may thus represent an adaptive rather then a pathological response.     

Meeting the energy demands of reproduction in female koalas,<Emphasis Type="Italic"> Phascolarctos cinereus</Emphasis>: evidence for energetic compensation

Koalas are generally considered to be limited by their ability to acquire energy from their diet of Eucalyptus foliage and have the lowest mass-specific peak lactational energy output measured in any mammal to date. This study considered the energetics and sources of energy utilised for reproduction in free-ranging female koalas. Energy requirements and foliage intake were greater in both lactating and non-lactating females in winter than summer, presumably due to demands of thermoregulation. Koalas met the peak energy requirements of lactation primarily by a 36% increase in their intake of foliage. Metabolic energy expenditure (field metabolic rate, 1778 kJ.day^–1 for a 6.25-kg female at the time of peak lactation) was not elevated during lactation. This was due to compensation for part of their lactational demands by reduction of another, non-reproductive, component of their energy budget. The observed energetic compensation was probably due primarily to substitution of the waste heat from the metabolic costs of milk production and increased heat increment of feeding for thermoregulatory energy expenditure. There may also have been energetic compensation by reduction of some aspect of maintenance metabolism. Such energetic compensation, together with the strategy of spreading lactation over a long period, minimises the magnitude of lactational energy demands on koalas, and thus the increase in daily food intake required during lactation. As the nutritional requirements of females at peak lactation are the highest of any members of the population, low reproductive requirements effectively increase the types and amount of habitat able to support koala populations.Abbreviations FMR field metabolic rate - HIF heat increment of feeding - RMR resting metabolic rate - _O2 rate of oxygen consumptionCommunicated by I.D. Hume     

Energy budget during four successive bouts of lactation in striped hamsters exposed to decreases in ambient temperature

A prediction of the seasonal investment hypothesis is that overall energy investment needs to be greater for young being produced at colder temperatures. Then, that energy cost is lower as temperature becomes warmer. To evaluate this assumption, I performed a series of measures of food intake and reproductive output throughout four successive bouts of lactation in striped hamsters (Cricetulus barabensis) exposed to a constant warm temperature (Warm, 21°C) or exposed to consecutive decreases in ambient temperatures from warm to cold (Warm-Cold, 30-0°C). Warm hamsters showed similar asymptotic food intake, litter size and mass over the course of four successive bouts of lactation. Warm-Cold females consumed more food, but raised lighter litters during the third bout than first bout of lactation. Ambient temperatures had significant effects on energy budget and reproductive output, by which resting metabolic rate, nonshivering thermogenesis and activity of cytochrome c oxidase (EC 1.9.3.1) of brown adipose tissue were increased, but reproductive output was decreased with declines of temperatures. These findings suggest that a trade-off occurs between different components of energy expenditure during the successive course of four bouts of lactation. Seasonal hamsters decrease their reproductive output, but increase the energy spent on thermogenesis as the ambient temperature becomes colder. It may also indicate that temperature has a direct effect on metabolism, leading to an increase in overall energy expenditure at lower temperatures.     

繁殖经历对黑线仓鼠哺乳期能量收支的影响

为探讨繁殖经历与哺乳期最大持续能量收支的关系,对连续4 次繁殖的黑线仓鼠哺乳期的能量收支情况进行了测定。结果显示:1)不同繁殖组哺乳高峰期的摄食量、泌乳能量支出(MEO)、胎仔数和胎仔重差异不显著,静止代谢率(RMR)、非颤抖性产热(NST)、褐色脂肪组织(BAT)线粒体细胞色素c 氧化酶(COX)活性、血清甲状腺激素(T3 、T4 )和催乳素水平也无明显变化;2)摄食量与MEO、胎仔重和RMR 呈显著正相关。结果表明,不同繁殖经历的黑线仓鼠主要通过降低产热和增加能量摄入来满足哺乳高峰期的能量需求;哺乳期最大持续代谢率(SusMR)可能受乳腺组织泌乳能力的限制,与“外周限制假说” 的预测一致,不支持“中心限制假说”;SusMR 限制因素和哺乳期能量收支策略可能与繁殖经历无关。     

Effect of Intermittent Cold Exposure on Brown Fat Activation,Obesity, and Energy Homeostasis in Mice

Homeotherms have specific mechanisms to maintain a constant core body temperature despite changes in thermal environment, food supply, and metabolic demand. Brown adipose tissue, the principal thermogenic organ, quickly and efficiently increases heat production by dissipating the mitochondrial proton motive force. It has been suggested that activation of brown fat, via either environmental (i.e. cold exposure) or pharmacologic means, could be used to increase metabolic rate and thus reduce body weight. Here we assess the effects of intermittent cold exposure (4°C for one to eight hours three times a week) on C57BL/6J mice fed a high fat diet. Cold exposure increased metabolic rate approximately two-fold during the challenge and activated brown fat. In response, food intake increased to compensate fully for the increased energy expenditure; thus, the mice showed no reduction in body weight or adiposity. Despite the unchanged adiposity, the cold-treated mice showed transient improvements in glucose homeostasis. Administration of the cannabinoid receptor-1 inverse agonist AM251 caused weight loss and improvements in glucose homeostasis, but showed no further improvements when combined with cold exposure. These data suggest that intermittent cold exposure causes transient, meaningful improvements in glucose homeostasis, but without synergy when combined with AM251. Since energy expenditure is significantly increased during cold exposure, a drug that dissociates food intake from metabolic demand during cold exposure may achieve weight loss and further metabolic improvements.     

黑线仓鼠断乳后能量代谢和脂肪累积的适应性调节

小型哺乳动物能量代谢和脂肪累积的适应性调节是其应对自然环境变化的主要能量学策略,但在不同的生活史阶段,脂肪组织适应性调节的特征和能量机理尚不清楚。为探讨不同繁殖阶段能量代谢和脂肪累积的变化及其内分泌机理,本文测定了黑线仓鼠哺乳期和断乳后摄食量、脂肪重量,以及血清瘦素水平、下丘脑瘦素受体（Ob-Rb）和相关神经肽的基因表达。结果显示,哺乳高峰期黑线仓鼠的脂肪重量几乎降低至零,断乳后显著增加;与非繁殖对照组相比,皮下脂肪、肾周脂肪与腹腔脂肪重量分别增长了1.5倍、37.1倍和1.9倍。断乳后摄食量、血清瘦素水平显著高于非繁殖对照组,Ob-Rb基因表达显著下调,而促食与抑食神经肽的基因表达均未发生显著变化。哺育不同胎仔数的黑线仓鼠在断乳后能量摄入、静止代谢率、身体组分未出现显著差异。研究表明,在不同的繁殖阶段脂肪累积呈现显 著的适应性调节,瘦素抵抗是断乳后脂肪累积补偿性增长的重要内分泌机制之一。这对迅速恢复脂肪累积,以应对将来的能量需求增加或者食物资源短缺的环境,进而提高自身的适合度具有重要意义。     

Resistance to high-fat diet in the female progeny of obese mice fed a control diet during the periconceptual, gestation, and lactation periods

With the worldwide epidemic of metabolic syndrome (MetS), the proportion of women that are overweight/obese and overfed during pregnancy has increased. The resulting abnormal uterine environment may have deleterious effects on fetal metabolic programming and lead to MetS in adulthood. A balanced/restricted diet and/or physical exercise often improve metabolic abnormalities in individuals with obesity and type 2 diabetes mellitus (T2D). We investigated whether reducing fat intake during the periconceptual/gestation/lactation period in mothers with high-fat diet (HFD)-induced obesity could be used to modify fetal/neonatal MetS programming positively, thereby preventing MetS. First generation (F1) C57BL/6J female mice with HFD-induced obesity and T2D were crossed with F1 males on control diet (CD). These F1 females were switched to a CD during the periconceptual/gestation/lactation period. At weaning, both male and female second generation (F2) mice were fed a HFD. Weight, caloric intake, lipid parameters, glucose, and insulin sensitivity were assessed. Sensitivity/resistance to the HFD differed significantly between generations and sexes. A similar proportion of the F1 and F2 males (80%) developed hyperphagia, obesity, and T2D. In contrast, a significantly higher proportion of the F2 females (43%) than of the previous F1 generation (17%) were resistant (P<0.01). Despite having free access to the HFD, these female mice were no longer hyperphagic and remained lean, with normal insulin sensitivity and glycemia but mild hypercholesterolemia and glucose intolerance, thus displaying a "satiety phenotype." This suggests that an appropriate dietary fatty acid profile and intake during the periconceptual/gestation/lactation period helps the female offspring to cope with deleterious intrauterine conditions.     

Bioenergetics of reproduction and pup development in a subterranean rodent (Ctenomys talarum)

The objective of this study was to evaluate the maternal costs of reproduction and pup development in the subterranean rodent Ctenomys talarum (Thomas 1898). Statistical differences were detected in whole-animal metabolic rates between nonreproductive and pregnant or lactating females. Whole-animal metabolic rates during pregnancy and lactation were 128% and 151% of the resting metabolic rate (RMR) observed in nonreproductive females. The total additional energy cost of reproduction (above the nonreproductive level) was similar for both the gestation and lactation periods. Mass-specific RMR revealed an upregulation of cell or tissue metabolism during lactation but not during gestation. The mass-specific metabolic rate of pups was 237% of the adults' metabolic rates. No differences were observed in body temperature among nonreproductive, pregnant, or lactating females. No differences were detected in body mass at birth among pups from litters with different numbers of nestlings. Pups increased their body temperature, reaching adult temperature at 30 d of age, when they were near weaning. Milk constituted the exclusive food for pups until they started eating solid food at 10 d old. Suckling time decreased with age of pups, and at the same time, mother chases directed toward their pups increased. These reproductive characteristics may contribute to successful existence in a subterranean habitat.     

Perigestational suppression of weight gain with central leptin gene therapy results in lower weight F1 generation

The efficacy of central leptin therapy on weight homeostasis through various phases of reproduction, pregnancy outcome and postnatal, prepubertal and pubertal growth of offspring was assessed. Enhanced leptin transgene expression after a single intracerebroventricular injection of recombinant adeno-associated virus vector encoding the leptin gene (rAAV-lep) decreased calorie intake and weight in adult nulliparous female rats. rAAV-lep treated rats conceived normally, displayed unremarkable pregnancy rate, parturition and delivered normal sized litters. Significantly lower weight was maintained through gestation, lactation, and post-lactation periods. The maintenance of a modest weight reduction was accompanied by voluntarily reduced calorie intake, increased thermogenic energy expenditure, decreased adiposity as reflected by drastically reduced leptin levels, and suppressed insulin and insulin-like growth factor 1 levels through lactation and post-lactation in rAAV-lep treated dams. The offspring at birth weighed significantly less than those of controls and this lower weight range was sustained during postnatal, prepubertal, pubertal and adult (3 months old) periods, contemporaneous with metabolic circulating hormones in the normal range. For the first time we show the persistent efficacy of central leptin gene therapy to suppress weight gain through all phases of reproduction, lactation and post-lactation in dams and reveal the potential imprinting link to producing lower weight in the F1 generation.     

Nutritional modulation of leptin expression and leptin action in obesity and obesity-associated complications

In obesity, an elevated accumulation and dysregulation of adipose tissue, due to an imbalance between energy intake and energy expenditure, usually coexists with the loss of responsiveness to leptin in central nervous system, and subsequently with hyperleptinemia. Leptin, a peptide hormone mainly produced by white adipose tissue, regulates energy homeostasis by stimulating energy expenditure and inhibiting food intake. Human obesity is characterized by increased plasma leptin levels, which have been related with different obesity-associated complications, such as chronic inflammatory state (risk factor for diabetes, cardiovascular and autoimmune diseases), as well as infertility and different types of cancer. Besides, leptin is also produced by placenta, and high leptin levels during pregnancy may be related with some pathological conditions such as gestational diabetes. This review focuses on the current insights and emerging concepts on potentially valuable nutrients and food components that may modulate leptin metabolism. Notably, several dietary food components, such as phenols, peptides, and vitamins, are able to decrease inflammation and improve leptin sensitivity by up- or down-regulation of leptin signaling molecules. On the other hand, some food components, such as saturated fatty acids may worsen chronic inflammation increasing the risk for pathological complications. Future research into nutritional mechanisms that restore leptin metabolism and signals of energy homeostasis may inspire new treatment options for obesity-related disorders.     

Metabolic compensation during high energy output in fasting, lactating grey seals (Halichoerus grypus): metabolic ceilings revisited

Lactation is the most energetically expensive period for female mammals and is associated with some of the highest sustained metabolic rates (SusMR) in vertebrates (reported as total energy throughput). Females typically deal with this energy demand by increasing food intake and the structure of the alimentary tract may act as the central constraint to ceilings on SusMR at about seven times resting or standard metabolic rate (SMR). However, demands of lactation may also be met by using a form of metabolic compensation such as reducing locomotor activities or entering torpor. In some phocid seals, cetaceans and bears, females fast throughout lactation and thus cannot offset the high energetic costs of lactation through increased food intake. We demonstrate that fasting grey seal females sustain, for several weeks, one of the highest total daily energy expenditures (DEE; 7.4 x SMR) reported in mammals, while progressively reducing maintenance metabolic expenditures during lactation through means not explained by reduction in lean body mass or behavioural changes. Simultaneously, the energy-exported in milk is progressively increased, associated with increased lipoprotein lipase activity in the mammary gland, resulting in greater offspring growth. Our results suggest that females use compensatory mechanisms to help meet the extraordinary energetic costs of lactation. Additionally, although the concepts of SusMR and ceilings on total DEE may be somewhat different in fasting lactating species, our data on phocid seals demonstrate that metabolic ceilings on milk energy output, in general, are not constrained by the same kind of peripheral limitations as are other energy-consuming tissues. In phocid seals, the high ceilings on DEE during lactation, coupled with metabolic compensation, are undoubtedly important factors enabling shortened lactation.     

Acutely decreased thermoregulatory energy expenditure or decreased activity energy expenditure both acutely reduce food intake in mice

Despite the suggestion that reduced energy expenditure may be a key contributor to the obesity pandemic, few studies have tested whether acutely reduced energy expenditure is associated with a compensatory reduction in food intake. The homeostatic mechanisms that control food intake and energy expenditure remain controversial and are thought to act over days to weeks. We evaluated food intake in mice using two models of acutely decreased energy expenditure: 1) increasing ambient temperature to thermoneutrality in mice acclimated to standard laboratory temperature or 2) exercise cessation in mice accustomed to wheel running. Increasing ambient temperature (from 21°C to 28°C) rapidly decreased energy expenditure, demonstrating that thermoregulatory energy expenditure contributes to both light cycle (40±1%) and dark cycle energy expenditure (15±3%) at normal ambient temperature (21°C). Reducing thermoregulatory energy expenditure acutely decreased food intake primarily during the light cycle (65±7%), thus conflicting with the delayed compensation model, but did not alter spontaneous activity. Acute exercise cessation decreased energy expenditure only during the dark cycle (14±2% at 21°C; 21±4% at 28°C), while food intake was reduced during the dark cycle (0.9±0.1 g) in mice housed at 28°C, but during the light cycle (0.3±0.1 g) in mice housed at 21°C. Cumulatively, there was a strong correlation between the change in daily energy expenditure and the change in daily food intake (R² = 0.51, p<0.01). We conclude that acutely decreased energy expenditure decreases food intake suggesting that energy intake is regulated by metabolic signals that respond rapidly and accurately to reduced energy expenditure.     

High-protein nutrition during pregnancy and lactation programs blood pressure, food efficiency, and body weight of the offspring in a sex-dependent manner

Maternal low-protein diet during pregnancy is a risk factor for cardiovascular disease of the offspring in later life. The impact of high-protein diet during pregnancy on the cardiovascular phenotype of the offspring, however, is still unknown. We examined the influence of a high-protein diet during pregnancy and lactation on the renal, hemodynamic, and metabolic phenotype of the F1 generation. Female Wistar rats were either fed a normal protein diet (20% protein: NP) or an isocaloric high-protein diet (40% protein: HP) throughout pregnancy and lactation. At weaning, the offspring were fed with standard diet, and they were allocated according to sex and maternal diet to four groups: normal-protein male (NPm, n = 25), normal-protein female (NPf, n = 19), high-protein male (HPm, n = 24), high-protein female (HPf, n = 29). During the experiment (22 wk), the animals were characterized by repeated measurement of body weight, food intake, blood pressure, glucose tolerance, energy expenditure, and kidney function. At the end of the study period histomorphological analyses of the kidneys and weight measurement of reproductive fat pads were conducted. There were no differences in birth weight between the study groups. No influence of maternal diet on energy expenditure, glucose tolerance, and plasma lipid levels was detected. Blood pressure and glomerulosclerosis were elevated in male offspring only, whereas female offspring were characterized by an increased food efficiency, higher body weight, and increased fat pads. Our study demonstrates that a high-protein diet during pregnancy and lactation in rats programs blood pressure, food efficiency, and body weight of the offspring in a sex-dependent manner.     

布氏田鼠哺乳期低温经历抑制成年期神经再生

哺乳动物在出生前后所经历的环境条件对其成年后的行为和生理等具有重要影响。环境温度是影响动物后代表型的重要因素之一。本研究将分娩当天的布氏田鼠母体和幼仔在常温（23℃±1℃）或低温（4℃±1℃）饲养,断乳（21日龄）时转至常温环境,至第63日龄时再随机将两组动物各分为常温组和低温暴露组,期间检测体重、摄食量、静止代谢率、认知能力和神经细胞增殖和存活等,以验证哺乳期的低温经历可影响成年动物的代谢生理、行为表型和相关脑区神经再生的假说。结果发现：哺乳期低温经历导致成年布氏田鼠摄食量显著降低,与代谢有关的下丘脑以及学习记忆有关的海马区细胞增殖和存活数量减少。当动物在成年期面临冷暴露时,与哺乳期常温经历的动物相比,哺乳期低温经历的动物摄食量较低,在Y迷宫新异臂中的穿梭次数和停留时间显著降低,但海马和下丘脑部分核团的细 胞增殖以及海马CA的细胞存活明显升高。这表明哺乳期低温经历对布氏田鼠的能量代谢、行为和相关脑区的成体神经再生产生了持久的抑制效应,但成年后再次面对低温时,动物的代谢能力和代谢及学习记忆相关脑区的神经细胞可塑性优于哺乳期未曾经历低温的动物。     

Role of thermogenesis in the regulation of energy balance in relation to obesity

Obligatory thermogenesis is a necessary accompaniment of all metabolic processes involved in maintenance of the body in the living state, and occurs in all organs. It includes energy expenditure involved in ingesting, digesting, and processing food (thermic effect of food (TEF]. At certain life stages extra energy expenditure for growth, pregnancy, or lactation would also be obligatory. Facultative thermogenesis is superimposed on obligatory thermogenesis and can be rapidly switched on and rapidly suppressed by the nervous system. Facultative thermogenesis is important in both thermal balance, in which control of thermoregulatory thermogenesis (shivering in muscle, nonshivering in brown adipose tissue (BAT] balances neural control of heat loss mechanisms, and in energy balance, in which control of facultative thermogenesis (exercise-induced in muscle, diet-induced thermogenesis (DIT) in BAT) balances control of energy intake. Thermal balance (i.e., body temperature) is much more stringently controlled than energy balance (i.e., body energy stores). Reduced energy expenditure for thermogenesis is important in two types of obesity in laboratory animals. In the first type, deficient DIT in BAT is a prominent feature of altered energy balance. It may or may not be associated with hyperphagia. In a second type, reduced cold-induced thermogenesis in BAT as well as in other organs is a prominent feature of altered thermal balance. This in turn results in altered energy balance and obesity, exacerbated in some examples by hyperphagia. In some of the hyperphagic obese animals it is likely that the exaggerated obligatory thermic effect of food so alters thermal balance that BAT thermogenesis is suppressed. In all obese animals, deficient hypothalamic control of facultative thermogenesis and (or) food intake is implicated.     

The arrangement of the heart chambers and associated blood vessels in the Devonian osteostracan Norselaspis glacialis. A reinterpretation based on recent studies of the circulatory system in lampreys

Food intake and digestion were investigated at four stages in the first 218 days of lactation in tammar wallabies ( Macropus eugenii ) carrying litters of one, and in non-lactating females as a control. This period of lactation in tammars, which includes the phase of exponential growth of the young, is comparable to gestation plus early lactation in ruminant placentals. Food and energy intakes by mothers remained at the non-lactating level while rate of growth of young was slow (up to Day 105 of lactation) but then rose as the growth rate of young increased, keeping pace with the predicted requirements for milk synthesis and export. There was no indication of the energy deficit seen in late gestation and early lactation in many herbivorous placental mammals. The gross efficiency of utilization of ME for growth of offspring was estimated as 13–15%, which is at least as high as values for placentals during gestation. The mean intake of metabolizable energy (ME) at 218 days was 603 kJ.kg^-0.75.d^-1, which represented 136% of ME intake by nonlactating females, or an increment of 159 kJ.kg^-0.75.d^-1. It was estimated that ME intake may rise to 773 kJ.kg^-0.75.d^-1 at peak lactation, which would be 174% of the non-lactating level or an increment of 329 kJ.kg^-0.75. d^-1. This allometrically-scaled increment is similar to values for some ruminants that use body reserves extensively to offset peak lactational food requirements. These and previously-reported trends suggest that ecologically comparable herbivorous marsupials and placentals utilize different physiological strategies to minimize demands on food resources during reproduction, but that both daily and overall demands can be similar.     

Role of resting metabolic rate and energy expenditure in hunger and appetite control: a new formulation

A long-running issue in appetite research concerns the influence of energy expenditure on energy intake. More than 50 years ago, Otto G. Edholm proposed that “the differences between the intakes of food [of individuals] must originate in differences in the expenditure of energy”. However, a relationship between energy expenditure and energy intake within any one day could not be found, although there was a correlation over 2 weeks. This issue was never resolved before interest in integrative biology was replaced by molecular biochemistry. Using a psychobiological approach, we have studied appetite control in an energy balance framework using a multi-level experimental system on a single cohort of overweight and obese human subjects. This has disclosed relationships between variables in the domains of body composition [fat-free mass (FFM), fat mass (FM)], metabolism, gastrointestinal hormones, hunger and energy intake. In this Commentary, we review our own and other data, and discuss a new formulation whereby appetite control and energy intake are regulated by energy expenditure. Specifically, we propose that FFM (the largest contributor to resting metabolic rate), but not body mass index or FM, is closely associated with self-determined meal size and daily energy intake. This formulation has implications for understanding weight regulation and the management of obesity.     

Different physiological roles of serum leptin in the regulation of energy intake and thermogenesis between pregnancy and lactation in primiparous Brandt's voles (Lasiopodomys brandtii)

Reproduction, especially lactation, is associated with major metabolic adaptive changes. In this study, we investigated the metabolic changes and the roles of leptin during different periods of reproduction in primiparous Brandt's voles (Lasiopodomys brandtii). Energy intake, thermogenic capacity and serum leptin levels were examined in non-reproductive, mid pregnant, late pregnant, early lactating and peak lactating voles. Voles increased body mass by nearly 70% during late pregnancy compared to the non-breeding controls. The increase in body mass was mainly due to the increase in body fat mass which increased by 56%, and the growth of the reproductive tissues and digestive organs. Lactating voles decreased body fat by nearly 27% at peak lactation compared to the controls, and 53% compared to late pregnant voles. At the same time they increased food intake significantly. Uncoupling protein 1 (UCP1) content in brown adipose tissue (BAT) decreased significantly at peak lactation. Serum leptin increased significantly in the mid pregnancy, at a time when there was no increase in body fat, and remained at this high level in late pregnancy. Leptin levels decreased after parturition and reached a nadir at peak lactation. Serum leptin was negatively correlated with energy intake during lactation, but not during pregnancy. These data suggest that Brandt's voles adjust energy intake, thermogenic capacity and body reserves to match the high energy demands for reproduction. Hyperleptinemia, without decreased energy intake suggests a state of leptin resistance during pregnancy, and hypoleptinemia during lactation might act as a signal to stimulate energy intake.     

高纤维食物对海南社鼠能量代谢的影响

自然界中食物质量常存在季节性变化,可影响小型哺乳动物的生理特征及其生存和分布。为研究高纤维(低质量)食物对栖息于贵州遵义的海南社鼠(Niviventer lotipes)能量代谢的影响,通过饲喂标准兔饲料(高纤维)或鼠饲料(低纤维)处理海南社鼠4周,实验期间测定动物的体重和能量摄入,使用开放式代谢仪测定动物的能量消耗,并在实验处理结束后解剖动物进行身体成分分析。研究发现,饲喂兔饲料的海南社鼠实验期间体重持续下降,到实验结束时为饲喂鼠饲料动物(对照组)体重的62.8%。饲喂兔饲料4周后,动物的整体基础代谢率和非颤抖性产热显著下降,分别为对照组的55.1%和63.4%。饲喂兔饲料的海南社鼠干物质摄入、消化能和消化率显著降低,分别为对照组的63.7%、38.8%和71.8%;身体成分分析显示,主要内脏器官重量以及消化道的重量和长度也显著下降。研究结果表明,饲喂高纤维的兔饲料后海南社鼠没有增加食物摄入来补偿消化率的下降,消化道形态尤其是小肠和盲肠的重量和长度没有适应性增加,虽然动物可通过降低基础代谢率和非颤抖性产热节约能量,但动物能量利用效率太低不能维持能量平衡而体重显著下降,海南社鼠对高纤维...     

Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis

Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the 'metabolic syndrome'). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis.