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。     

Leptin receptor-deficient obese Zucker rats reduce their food intake in response to hypobaric hypoxia

Exposure to hypoxia induces anorexia in humans and rodents, but the role of leptin remains under discussion and that of orexigenic and anorexigenic hypothalamic neuropeptides remains unknown. The present study was designed to address this issue by using obese (Lepr(fa)/Lepr(fa)) Zucker rats, a rat model of genetic leptin receptor deficiency. Homozygous lean (Lepr(FA)/Lepr(FA)) and obese (Lepr(fa)/Lepr(fa)) rats were randomly assigned to two groups, either kept at ambient pressure or exposed to hypobaric hypoxia for 1, 2, or 4 days (barometric pressure, 505 hPa). Food intake and body weight were recorded throughout the experiment. The expression of leptin and vascular endothelial growth factor (VEGF) genes was studied in adipose tissue with real-time quantitative PCR and that of selected orexigenic and anorexigenic neuropeptides was measured in the hypothalamus. Lean and obese rats exhibited a similar hypophagia (38 and 67% of initial values at day 1, respectively, P < 0.01) and initial decrease in body weight during hypoxia exposure. Hypoxia led to increased plasma leptin levels only in obese rats. This resulted from increased leptin gene expression in adipose tissue in response to hypoxia, in association with enhanced VEGF gene expression. Increased hypothalamic neuropeptide Y levels in lean rats 2 days after hypoxia exposure contributed to accounting for the enhanced food consumption. No significant changes occurred in the expression of other hypothalamic neuropeptides involved in the control of food intake. This study demonstrates unequivocally that altitude-induced anorexia cannot be ascribed to anorectic signals triggered by enhanced leptin production or alterations of hypothalamic neuropeptides involved in anabolic or catabolic pathways.     

Litter size variation in hypothalamic gene expression determines adult metabolic phenotype in Brandt's voles (Lasiopodomys brandtii)

Background

Early postnatal environments may have long-term and potentially irreversible consequences on hypothalamic neurons involved in energy homeostasis. Litter size is an important life history trait and negatively correlated with milk intake in small mammals, and thus has been regarded as a naturally varying feature of the early developmental environment. Here we investigated the long-term effects of litter size on metabolic phenotype and hypothalamic neuropeptide mRNA expression involved in the regulation of energy homeostasis, using the offspring reared from large (10–12) and small (3–4) litter sizes, of Brandt''s voles (Lasiopodomys brandtii), a rodent species from Inner Mongolia grassland in China.

Methodology/Principal Findings

Hypothalamic leptin signaling and neuropeptides were measured by Real-Time PCR. We showed that offspring reared from small litters were heavier at weaning and also in adulthood than offspring from large litters, accompanied by increased food intake during development. There were no significant differences in serum leptin levels or leptin receptor (OB-Rb) mRNA in the hypothalamus at weaning or in adulthood, however, hypothalamic suppressor of cytokine signaling 3 (SOCS3) mRNA in adulthood increased in small litters compared to that in large litters. As a result, the agouti-related peptide (AgRP) mRNA increased in the offspring from small litters.

Conclusions/Significance

These findings support our hypothesis that natural litter size has a permanent effect on offspring metabolic phenotype and hypothalamic neuropeptide expression, and suggest central leptin resistance and the resultant increase in AgRP expression may be a fundamental mechanism underlying hyperphagia and the increased risk of overweight in pups of small litters. Thus, we conclude that litter size may be an important and central determinant of metabolic fitness in adulthood.     

根田鼠母体捕食应激效应与Trivers-Willard 模型的关系

本研究了根田鼠母体捕食应激对其子代出生、断乳和成体体重、窝性比及死亡率的作用,检验Trivers—Willard模型的2个前提条件、母体应激激素在母体投资中的作用,以及母体捕食应激效应与该模型的关系。将妊娠根田鼠母体暴露于其捕食艾鼬,母体应激子代的出生和断乳体重均显降低;到成体,雄性体重有此效应,而雌性体重则接近对照。出生窝性比无变化,但成体窝性比向雌性偏斜。不同年龄阶段的死亡率无显变化,但累计死亡率明显增大。处理雄性子代在断乳和成体时的皮质酮含量显增高,而雌性子代则无显变化,从而验证了Trivers-Willard模型的2个前提条件,提出应激母体激素参与母体对子代的投资观点,并认为,母体捕食应激使根田鼠子代成体窝性比向雌性偏斜的生理投资符合进化稳定对策。     

Energy metabolism, thermogenesis and body mass regulation in Brandt's voles (Lasiopodomys brandtii) during cold acclimation and rewarming

Environmental cues play important roles in the regulation of an animal's physiology and behavior. The purpose of the present study was to test the hypothesis that ambient temperature was a cue to induce adjustments in body mass, energy intake and thermogenic capacity, associated with changes in serum leptin levels in Brandt's voles (Lasiopodomys brandtii). We found that Brandt's voles increased resting metabolic rate (RMR) and energy intake and kept body mass stable when exposed to the cold while showed a significant increase in body mass after rewarming. The increase in body mass after rewarming was associated with the higher energy intake compared with control. Uncoupling protein 1 (UCP1) content in brown adipose tissue (BAT) increased in the cold and reversed after rewarming. Serum leptin levels decreased in the cold while increased after rewarming, associated with the opposite changes in energy intake. Further, serum leptin levels were positively correlated with body mass and body fat mass. Together, these data supported our hypothesis that ambient temperature was a cue to induce changes in body mass and metabolism. Serum leptin, as a starvation signal in the cold and satiety signal in rewarming, was involved in the processes of thermogenesis and body mass regulation in Brandt's voles.     

Photoperiod and temperature can regulate body mass, serum leptin concentration, and uncoupling protein 1 in Brandt's voles (Lasiopodomys brandtii) and Mongolian gerbils (Meriones unguiculatus)

Environmental factors play an important role in the seasonal adaptation of body mass and thermogenesis in wild small mammals. In this study, we performed a factorial experiment (temperature x photoperiod) in which Brandt's voles and Mongolian gerbils were acclimated to different photoperiods (long photoperiod, 16L : 8D; short photoperiod, 8L : 16D) and temperatures (warm, 23 degrees C; cold, 5 degrees C) to test the hypothesis that photoperiod, temperature, or both together can trigger seasonal changes in serum leptin level, body mass, thermogenesis, and energy intake. Our data demonstrate that Brandt's voles showed a remarkable decrease in body mass in both the cold and a short photoperiod. However, no significant changes in body mass were found for gerbils exposed to similar conditions. The short photoperiod induced a decrease in serum leptin levels for both voles and gerbils that might contribute to an increase in energy intake. Furthermore, the short photoperiod induced an increase of uncoupling protein 1 (UCP1) content for both voles and gerbils, and cold can further enhance the increase in voles. No interactions between photoperiod and temperature were detected for the two species. Brandt's voles can decrease their body mass through changes in energy intake and expenditure, while Mongolian gerbils can keep body mass relatively stable by balancing energy metabolism under winterlike conditions. Leptin was potentially involved in the regulation of body mass and thermogenic capacity for the two species.     

Temporal progression of anaerobic fungal communities in dairy calves from birth to maturity

Establishment of microbial communities in neonatal calves is vital for their growth and overall health. While this process has received considerable attention for bacteria, our knowledge on temporal progression of anaerobic gut fungi (AGF) in calves is lacking. Here, we examined AGF communities in faecal samples from six dairy cattle collected at 24 different time points during the pre-weaning (days 1–48), weaning (days 48–60), and post-weaning (days 60–360) phases. Quantitative polymerase chain reaction indicated that AGF colonisation occurs within 24 h after birth, with loads slowly increasing during pre-weaning and weaning, then drastically increasing post-weaning. Culture-independent amplicon surveys identified higher alpha diversity during pre-weaning/weaning, compared to post-weaning. AGF community structure underwent a drastic shift post-weaning, from a community enriched in genera commonly encountered in hindgut fermenters to one enriched in genera commonly encountered in adult ruminants. Comparison of AGF community between calves day 1 post-birth and their mothers suggest a major role for maternal transmission, with additional input from cohabitating subjects. This distinct pattern of AGF progression could best be understood in-light of their narrower niche preferences, metabolic specialisation, and physiological optima compared to bacteria, hence eliciting a unique response to changes in feeding pattern and associated structural GIT development during maturation.     

Turning Shy on a Winter's Day: Effects of Season on Personality and Stress Response in Microtus arvalis

Animal personalities are by definition stable over time, but to what extent they may change during development and in adulthood to adjust to environmental change is unclear. Animals of temperate environments have evolved physiological and behavioural adaptations to cope with the cyclic seasonal changes. This may also result in changes in personality: suites of behavioural and physiological traits that vary consistently among individuals. Winter, typically the adverse season challenging survival, may require individuals to have shy/cautious personality, whereas during summer, energetically favourable to reproduction, individuals may benefit from a bold/risk‐taking personality. To test the effects of seasonal changes in early life and in adulthood on behaviours (activity, exploration and anxiety), body mass and stress response, we manipulated the photoperiod and quality of food in two experiments to simulate the conditions of winter and summer. We used the common voles (Microtus arvalis) as they have been shown to display personality based on behavioural consistency over time and contexts. Summer‐born voles allocated to winter conditions at weaning had lower body mass, a higher corticosterone increase after stress and a less active, more cautious behavioural phenotype in adulthood compared to voles born in and allocated to summer conditions. In contrast, adult females only showed plasticity in stress‐induced corticosterone levels, which were higher in the animals that were transferred to the winter conditions than to those staying in summer conditions. These results suggest a sensitive period for season‐related behavioural plasticity in which juveniles shift over the bold–shy axis.     

Maternal tobacco smoke exposure during lactation inhibits catecholamine production by adrenal medullae in adult rat offspring

Previously, we have shown that maternal smoke exposure during lactation, even when pups are not exposed, affects biochemical profiles in the offspring at weaning, eliciting lower body adiposity, hyperinsulinemia, hypocorticosteronemia and lower adrenal catecholamine content. However, the future impact of tobacco exposure is still unknown. As postnatal nicotine exposure causes short- and long-term effects on pups' biochemistry and endocrine profiles, we have now evaluated some endocrine and metabolic parameters of the adult offspring whose mothers were tobacco exposed during lactation. For this, from day 3 to 21 of lactation, rat dams were divided in: 1) SE group, cigarette smoke-exposed (1.7 mg nicotine/cigarettes for 1 h, 4 times/day, daily), without their pups, and 2) C group, exposed to air, in the same conditions. Offspring were killed at 180-days-old. Body weight and food intake were evaluated. Blood, white adipose tissue, adrenal, and liver were collected. All significant data were p<0.05. The adult SE offspring showed no change in body weight, cumulative food intake, serum hormone profile, serum lipid profile, or triglycerides content in liver. However, in adrenal gland, adult SE offspring showed lower catecholamine content ( - 50%) and lower tyrosine hydroxylase protein expression ( - 56%). Despite the hormonal alterations during lactation, tobacco smoke exposure through breast milk only programmed the adrenal medullary function at adulthood and this dysfunction can have consequence on stress response. Thus, an environment free of smoke during lactation period is essential to improve health outcomes in adult offspring.     

Hypothalamic Neuroendocrine Circuitry is Programmed by Maternal Obesity: Interaction with Postnatal Nutritional Environment

Objective

Early life nutrition is critical for the development of hypothalamic neurons involved in energy homeostasis. We previously showed that intrauterine and early postnatal overnutrition programmed hypothalamic neurons expressing the appetite stimulator neuropeptide Y (NPY) and suppressor proopiomelanocortin (POMC) in offspring at weaning. However, the long-term effects of such programming and its interactions with post-weaning high-fat-diet (HFD) consumption are unclear.

Research Design and Methods

Female Sprague Dawley rats were exposed to chow or HFD for 5 weeks before mating, throughout gestation and lactation. On postnatal day 1, litters were adjusted to 3/litter to induce postnatal overnutrition (vs. 12 in control). At postnatal day 20, half of the rats from each maternal group were weaned onto chow or HFD for 15 weeks. Hypothalamic appetite regulators, and fuel (glucose and lipid) metabolic markers were measured.

Results

Offspring from obese dams gained more weight than those from lean dams independent of post-weaning diet. Maternal obesity interacted with post-weaning HFD consumption to cause greater levels of hyperphagia, adiposity, hyperlipidemia, and glucose intolerance in offspring. This was linked to increased hypothalamic NPY signaling and leptin resistance in adult offspring. Litter size reduction had a detrimental impact on insulin and adiponectin, while hypothalamic NPY and POMC mRNA expression were suppressed in the face of normal energy intake and weight gain.

Conclusions

Maternal obesity, postnatal litter size reduction and post-weaning HFD consumption caused obesity via different neuroendocrine mechanims. There were strong additive effects of maternal obesity and post-weaning HFD consumption to increase the metabolic disorders in offspring.     

Effects of pre-weaning housing in a multi-suckling system on performance and carbohydrate absorption of relatively light and heavy piglets around weaning

The low feed intake and stress associated with abrupt weaning in conventional pig farming often result in poor post-weaning performance, which is related to impaired intestinal function. We investigated effects of housing conditions before weaning on performance around weaning of relatively light and heavy piglets. Before weaning, piglets were housed either with five sows and their litters in a multi-suckling (MS) system or in pens with individually housed sows in farrowing crates (FC). After weaning at 4 weeks of age (day 0), 16 groups of four piglets (two light and two heavy litter-mates) were housed under equal conditions in enriched pens. Mannitol (day −5 and day 5) and galactose (day 5) were orally administered as markers for gastrointestinal carbohydrate absorption, and after 20 min a blood sample was taken (sugar absorption test). In addition, BW, feed intake and faecal consistency as an indicator for diarrhoea, were assessed frequently during 2 weeks post-weaning. Pre-weaning housing, weight class and their interaction did not affect post-weaning faecal consistency scores. Weight gain over 2 weeks did not differ between pre-weaning housing treatments, but MS piglets gained more (0.67±0.12 kg) than FC piglets (0.39±0.16 kg) between days 2 and 5 post-weaning, P=0.02), particularly in the ‘heavy’ weight class (interaction, P=0.04), whereas feed intake was similar for both treatments. This indicates a better utilisation of the ingested feed of the MS piglets compared with the FC piglets in the early post-weaning period. Pre-weaning mannitol concentrations were unaffected by pre-weaning housing, weight class and their interaction. On day 5 post-weaning, however, MS piglets had a lower plasma concentration of mannitol (320 v. 592 nmol/ml, SEM=132, P=0.04) and galactose (91 v. 157 nmol/ml, SEM=20, P=0.04) than FC piglets, regardless of weight class. In conclusion, MS and FC piglets differed in aspects of post-weaning gastrointestinal carbohydrate absorption and in weight gain between days 2 and 5 after weaning, but pre-weaning housing did not affect feed intake, weight gain and measures of faecal consistency over the first 2 weeks after weaning.     

Postnatal early overfeeding induces hypothalamic higher SOCS3 expression and lower STAT3 activity in adult rats

Postnatal early overnutrition (EO) is a risk factor for future obesity and metabolic disorders. Rats raised in small litters (SLs) develop overweight, hyperphagia, hyperleptinemia, hyperinsulinemia and hypertension when adults. As obesity is related to hyperleptinemia, leptin resistance and metabolic syndrome, we aimed to investigate body composition, plasma hormone levels, glucose tolerance and the leptin signaling pathway in hypothalamus from early overfed animals at weaning and adulthood. To induce postnatal EO, we reduced litter size to three pups/litter (SL), and the groups with normal litter size (10 pups/litter) were used as control. Rats had free access to standard diet and water postweaning. Body weight and food intake were monitored daily, and offspring were killed at 21 (weaning) and 180 days old (adulthood). Postnatal EO group had higher body weight and total and visceral fat mass at both periods. Lean mass and serum high-density lipoprotein cholesterol (HDL-C) were higher at 21 days and lower at 180 days. Small litter rats presented higher levels of globulins at both periods, while albumin levels were higher at weaning and lower at adulthood. There was higher leptin, insulin and glucose serum concentrations at 21 days old, while no glucose intolerance was observed in adulthood. Leptin signaling pathway was unaffected at weaning. However, postnatal EO induced lower JAK2 and p-STAT3, and higher SOCS3 expression in adult animals, indicating central leptin resistance in adulthood. In conclusion, postnatal EO induces obesity, higher total and visceral fat mass, lower HDL-C and central leptin resistance in adult life.     

Ontogenesis of hepatic growth hormone receptors in the rat

Detailed ontogenic studies of the binding of human (hGH) and bovine growth hormone (bGH) have been performed in liver preparations from male and female rats during the neonatal, weanling, pre- and post-pubertal periods. Specific binding of both hormones was readily detected at all ages, with no apparent interference due to occupancy by endogenous hormones. No sex difference in binding was observed prior to weaning (22 days) for hGH, which binds to both somatotrophic and lactogenic sites. However, after weaning a marked sex-related dissociation in the pattern of binding did occur, with female rats binding 3-4 times more hGH than in the pre-weaning period and male rats binding hGH to only half their pre-weaning levels. A very similar pattern was seen for binding of bGH (which binds only to somatotrophic sites) except that in male rats, the post-weaning levels did not fall. Binding patterns for either hGH or bGH prior to weaning did not mirror the known age-related pattern of circulating rat GH levels, suggesting the absence of a definitive auto-regulation system for the GH-GH receptor system under normal circumstances in vivo. The possible role of the weaning process per se in the post-weaning changes of GH binding seen in male and female rats still requires elucidation.     

Cold exposure does not decrease serum leptin concentration,but increases energy intake and thermogenic capacity in pregnant Brandt's voles (Lasiopodomys brandtii)

In most mammals, maternal body mass and fat mass increase during pregnancy due to hyperphagia. These physiological changes provide the fetus with energy and nutrients and prepare the mother for the high energetic demands of lactation. In the present study, metabolic changes in response to cold and pregnancy were examined in female Brandt's voles (Lasiopodomys brandtii). At 23±1 °C, the voles increased body mass and deposited body fat during pregnancy. However, at 5±1 °C pregnant voles did not deposit body fat even though energy intake increased above the level in the warm. Serum leptin concentration increased during pregnancy and was not influenced by cold exposure. Thermogenic capacity, as indicated by uncoupling protein 1 (UCP1) content in brown adipose tissue (BAT), increased in cold-exposed pregnant voles. The number and mass of fetuses were not affected by cold exposure. Our data may indicate the importance of an increased serum leptin concentration for a successful outcome of the pregnancy and also the independence of leptin secretion from body fat in pregnant voles. It also implies the need to develop central leptin resistance with respect to control of energy balance for pregnant voles.     

Intrauterine ethanol exposure results in hypothalamic oxidative stress and neuroendocrine alterations in adult rat offspring

Prenatal ethanol (EtOH) exposure is associated with low birth weight, followed by increased appetite, catch-up growth, insulin resistance, and impaired glucose tolerance in the rat offspring. Because EtOH can induce oxidative stress, which is a putative mechanism of insulin resistance, and because of the central role of the hypothalamus in the regulation of energy homeostasis and insulin action, we investigated whether prenatal EtOH exposure causes oxidative damage to the hypothalamus, which may alter its function. Female rats were given EtOH by gavage throughout pregnancy. At birth, their offspring were smaller than those of non-EtOH rats. Markers of oxidative stress and expression of neuropeptide Y and proopiomelanocortin (POMC) were determined in hypothalami of postnatal day 7 (PD7) and 3-mo-old (adult) rat offspring. In both PD7 and adult rats, prenatal EtOH exposure was associated with decreased levels of glutathione and increased expression of MnSOD. The concentrations of lipid peroxides and protein carbonyls were normal in PD7 EtOH-exposed offspring, but were increased in adult EtOH-exposed offspring. Both PD7 and adult EtOH-exposed offspring had normal neuropeptide Y and POMC mRNA levels, but the adult offspring had reduced POMC protein concentration. Thus only adult offspring preexposed to EtOH had increased hypothalamic tissue damage and decreased levels of POMC, which could impair melanocortin signaling. We conclude that prenatal EtOH exposure causes hypothalamic oxidative stress, which persists into adult life and alters melanocortin action during adulthood. These neuroendocrine alterations may explain weight gain and insulin resistance in rats exposed to EtOH early in life.     

Leptin-programmed rats respond to cold exposure changing hypothalamic leptin receptor and thyroid function differently from cold-exposed controls

We showed that neonatal leptin treatment programmes for hyperleptinemia and central leptin resistance both at 30days-old and adulthood, while programmes for lower serum T3 at 30days-old, but higher thyroid hormones (TH) at adulthood. As in these animals, acute cold at 30days-old normalized leptinemia and restored the expression of hypothalamic leptin receptor (OBR), here we evaluate the effect of cold exposure on the thyroid function and OBR in adult rats programmed by neonatal hyperleptinemia. Pups were divided into 2 groups: Lep-injected with leptin (8μg/100g/BW, sc) for the first 10days of lactation, and C-injected with saline. At 150days, both groups were subdivided into: LepC and CC, which were exposed to 8°C for 12h. Serum leptin, TH, TSH, liver type I and brown adipose tissue (BAT) type II deiodinases (D1 and D2) activities, liver mitochondrial alpha-glycerol-3-phosphate dehydrogenase (mGPD) activity and adrenal catecholamine content were measured. Hypothalamic and thyroid OBR protein contents were evaluated. Differences were significant when p<0.05. Lep group had hyperleptinemia (+19%), higher T4 (+20%) and T3 (+30%) with lower TSH (-55%), higher liver D1 (1.4 fold-increase), lower BAT D2 (-44%) and liver mGPD activities (-55%), higher adrenal catecholamines (+44%), lower hypothalamic OBR (-51%) and normal thyroid OBR. Cold exposure normalized leptinemia, D1, mGPD, catecholamine and hypothalamic OBR. However, cold exposure further increased TH and decreased D2. Thus, cold exposure normalizes most of the changes programmed by neonatal hyperleptinemia, at the expense of worsening the hyperthyroidism and BAT thermogenesis.     

Early hypothalamic FTO overexpression in response to maternal obesity--potential contribution to postweaning hyperphagia

Background

Intrauterine and postnatal overnutrition program hyperphagia, adiposity and glucose intolerance in offspring. Single-nucleotide polymorphisms (SNPs) of the fat mass and obesity associated (FTO) gene have been linked to increased risk of obesity. FTO is highly expressed in hypothalamic regions critical for energy balance and hyperphagic phenotypes were linked with FTO SNPs. As nutrition during fetal development can influence the expression of genes involved in metabolic function, we investigated the impact of maternal obesity on FTO.

Methods

Female Sprague Dawley rats were exposed to chow or high fat diet (HFD) for 5 weeks before mating, throughout gestation and lactation. On postnatal day 1 (PND1), some litters were adjusted to 3 pups (vs. 12 control) to induce postnatal overnutrition. At PND20, rats were weaned onto chow or HFD for 15 weeks. FTO mRNA expression in the hypothalamus and liver, as well as hepatic markers of lipid metabolism were measured.

Results

At weaning, hypothalamic FTO mRNA expression was increased significantly in offspring of obese mothers and FTO was correlated with both visceral and epididymal fat mass (P<0.05); body weight approached significance (P = 0.07). Hepatic FTO and Fatty Acid Synthase mRNA expression were decreased by maternal obesity. At 18 weeks, FTO mRNA expression did not differ between groups; however body weight was significantly correlated with hypothalamic FTO. Postnatal HFD feeding significantly reduced hepatic Carnitine Palmitoyltransferase-1a but did not affect the expression of other hepatic markers investigated. FTO was not affected by chronic HFD feeding.

Significance

Maternal obesity significantly impacted FTO expression in both hypothalamus and liver at weaning. Early overexpression of hypothalamic FTO correlated with increased adiposity and later food intake of siblings exposed to HFD suggesting upregulation of FTO may contribute to subsequent hyperphagia, in line with some human data. No effect of maternal obesity was observed on FTO in adulthood.     

Sucrose exposure in early life alters adult motivation and weight gain

The cause of the current increase in obesity in westernized nations is poorly understood but is frequently attributed to a 'thrifty genotype,' an evolutionary predisposition to store calories in times of plenty to protect against future scarcity. In modern, industrialized environments that provide a ready, uninterrupted supply of energy-rich foods at low cost, this genetic predisposition is hypothesized to lead to obesity. Children are also exposed to this 'obesogenic' environment; however, whether such early dietary experience has developmental effects and contributes to adult vulnerability to obesity is unknown. Using mice, we tested the hypothesis that dietary experience during childhood and adolescence affects adult obesity risk. We gave mice unlimited or no access to sucrose for a short period post-weaning and measured sucrose-seeking, food consumption, and weight gain in adulthood. Unlimited access to sucrose early in life reduced sucrose-seeking when work was required to obtain it. When high-sugar/high-fat dietary options were made freely-available, however, the sucrose-exposed mice gained more weight than mice without early sucrose exposure. These results suggest that early, unlimited exposure to sucrose reduces motivation to acquire sucrose but promotes weight gain in adulthood when the cost of acquiring palatable, energy dense foods is low. This study demonstrates that early post-weaning experience can modify the expression of a 'thrifty genotype' and alter an adult animal's response to its environment, a finding consistent with evidence of pre- and peri-natal programming of adult obesity risk by maternal nutritional status. Our findings suggest the window for developmental effects of diet may extend into childhood, an observation with potentially important implications for both research and public policy in addressing the rising incidence of obesity.     

Effects of physical forms of starter feed on growth,nutrient digestibility,gastrointestinal enzyme activity,and morphology of pre- and post-weaning lambs

The physical form of starter feed may affect the gastrointestinal development and the performance of ruminant. However, little information is available on how changes in the physical forms of starter feed influence the performance of lambs, especially during the pre- and post-weaning periods. The aim of this study was to investigate the effects of different physical forms of starter feeds on growth performance, nutrient digestibility, gastrointestinal enzyme activity, and morphology of pre- and post-weaning lambs. Twenty-four 8-day-old male Hu lamb (5.04 ± 0.75 kg BW) were randomly assigned to one of two dietary treatments: 1) a pelleted starter (PS) feed and 2) a textured starter (TS) feed, which included coarse mashed steam-flaked corn. From eight to thirty-five days of age (pre-weaning), the lambs were bottle-fed milk replacer (MR) at 2% of BW measured on day 8. All lambs were weaned at day 35 when feeding of MR was stopped. Six lambs for each treatment were euthanized at 21 or 42 days of age for sampling. The following results are obtained by variance analysis: TS lambs had a greater (P < 0.05) final BW, higher apparent digestibility of starch and ether extract, activities of α-amylase pre- or post-weaning, and higher (P < 0.05) average dry matter intake and lipase post-weaning in small intestine contents and had a trend of significantly higher average daily gain post-weaning (P = 0.07). Rumen development analysis of TS lambs showed a significantly higher (P < 0.05) relative weight of rumen post-weaning, greater papillae length, increased circular and layered muscle, increased sectional area pre- and post-weaning, and increased rumen papillae width post-weaning. Textured starter treatment increased the villus height and villus width (except jejunum pre-weaning) of the whole small intestine and villus height to crypt depth ratio of jejunum and ileum during the whole period and tended to increase the relative weight of the rumen pre-weaning (P = 0.07). The results indicated that TS feeding is more beneficial to lambs over the weaning transition than PS in promoting gastrointestinal development, intestinal enzyme activities, nutrient digestibility, and growth performance. The findings provide new insights into the selection of physical forms of starter feeds in lamb production. Further research with more animals and female lambs is needed to obtain a more complete conclusion.     

Effects of isovalerate supplements on morphology and functional gene expression of rumen mucosa in pre- and post-weaning dairy calves

Isovalerate supplements could stimulate rumen development by improving morphology and function of rumen mucosa, and then promote the growth of calves. This study was done to evaluate the effects of isovalerate supplements on morphology and functional gene expression of rumen mucosa in dairy calves. In total, 48 Chinese Holstein male calves with 15 days of age and 45.1±0.36 kg of BW were randomly assigned to four groups. The treatments were: control, low-isovalerate, moderate-isovalerate and high-isovalerate with 0, 3, 6 and 9 g isovalerate per calf per day, respectively. Supplementary isovalerate was hand-mixed into milk in pre-weaning calves and into concentrate portion in post-weaning calves. The study consisted of a 15-day-adaptation period and a 60-day-sampling period. Calves were weaned at 60 days of age. Three calves were slaughtered from each of the four treatments at 30, 60 and 90 days of age. The weight of body and stomach were measured, samples of ruminal tissues and blood were analyzed. Total stomach weight, total stomach to BW ratio, rumen wall and keratinized layer thickness, serum growth hormone and IGF-1 for both pre- and post-weaning calves increased linearly with increasing isovalerate supplements. Rumen to total stomach weight ratio, the length and width of rumen papillae, and serum β-hydroxybutyrate increased linearly for post-weaning calves. However, abomasum weight to total stomach weight ratio decreased linearly for both pre- and post-weaning calves. The relative messenger RNA expression for growth hormone receptor, IGF-1 receptor and 3-hydroxy-3-methylglutaryl-CoA synthase 1 in rumen mucosa increased linearly for post-weaning calves. Our results suggested that isovalerate supplements promoted rumen development in a dose-dependent manner. The optimum dose was 6.0 g isovalerate per calf per day.