随机限食和重喂食小鼠能量收支和生长发育的可塑性

为阐明能量收支和生长发育的可塑性对动物适应食物资源变化的作用和意义,将断乳后的雄性KM小鼠40只随机限食4周,再重喂食4周。采用封闭式流体压力呼吸计测定基础代谢率(BMR)。限食使摄食量显著增加,BMR和活动行为降低,胴体和生殖腺重量显著降低。重喂食后上述指标均恢复到对照组水平,表现出显著的可塑性变化。结果表明,KM小鼠能通过摄食量、BMR、活动行为和身体组成的可塑性调节以适应难以预测的食物资源变化。     

随机饥饿和重喂食对小鼠能量代谢和行为的影响

为阐明能量代谢和行为的可塑性对动物适应食物资源变化的意义,将成年雄性KM 小鼠随机饥饿驯化4
周,再重喂食驯化4 周。采用食物平衡法测定摄食量、封闭式流体压力呼吸计测定基础代谢率(BMR) 和非颤
抖性产热(NST)、观察法测定行为。随机饥饿使摄食量、消化道重量显著增加,BMR 和NST 显著降低。与对照
组相比,饥饿组休息行为显著增加,活动显著降低。重喂食后,上述指标均恢复到对照组水平,表现出显著的
可塑性。研究结果表明,动物适应难以预测的食物资源短缺的主要策略包括:增加自由取食期间的摄食量;降
低BMR、NST 和活动行为,从而保存身体贮存的能量。能量代谢和活动行为在较短的时间尺度内表现出显著的
可塑性对小鼠适应不可预测的食物资源短缺的应激环境具有重要意义。     

食物限制对高山姬鼠能量代谢和内脏器官形态的影响

为探讨栖息于横断山区高山姬鼠对食物匮乏的适应策略,在实验室条件下,以每日能量需求为标准,测定了饲喂食量为130%每日能量需求(DER)和70%DER两组高山姬鼠的体重、体温、基础代谢率(BMR)、非颤抖性产热(NST)等的变化,并在限食28d后,测定了肝脏鲜重和消化道形态的变化。结果显示:限食组高山姬鼠的体温、体重、BMR、NST显著降低,比0d分别下降了4.4%、23.6%、38.6%、20.3%。肝脏鲜重显著下降,小肠长度和小肠含内容物重显著增加。在限食条件下,高山姬鼠主要通过降低体重、体温、减少肝脏重量和能量代谢水平及消化器官适应性变化来减少能量支出,以适应食物资源短缺的外部环境。     

限食及重喂食对雄性长爪沙鼠生理指标的影响

限食通常会显著影响鼠类的营养及内分泌等生理指标,但限食后重喂食其生理指标是否能得以恢复尚不
清楚。本文采取70% 的限食水平,研究了限食及重喂食对雄性长爪沙鼠生理指标的影响。将雄性长爪沙鼠分为
限食组、重喂食组和对照组。限食组先自由饮食4 周,后70% 限食4 周;重喂食组先70% 限食4 周,后恢复自
由饮食4 周。对照组自由饮食8 周。实验结束时,检测各组肥满度及血清白蛋白和总蛋白含量、血清甲状腺素
T3 和T4 水平、睾酮和皮质醇含量等各项生理指标的变化。研究结果表明,4 周限食显著降低了雄性长爪沙鼠的肥满度和血清甲状腺素T4 含量,显著升高了其血液皮质醇含量;限食后重喂食4 周后可使上述指标恢复或接近正常,但血清白蛋白含量比对照组低,其他指标与对照组无明显差异,长爪沙鼠的一些生理指标在限食重喂食
后能得以恢复,但其内分泌调节可能存在新的变化,值得进一步研究。     

随机限食和重喂食对小鼠体重、能量收支及瘦素的影响

为阐明限食和重喂食(SFR-Re)诱导的体重"补偿性增长"生理机制,该文测定了SFR-Re驯化的KM小鼠能量摄入与支出、身体成分以及血清瘦素水平。结果显示,随机限食使体重显著降低,重喂食后体重增加至对照组水平。驯化结束后,SFR-Re驯化小鼠基础代谢率增加,产热降低,褐色脂肪组织(BAT)细胞色素c氧化酶(COX)活性和解偶联蛋白1(UCP1)水平显著降低,摄入能、消化率和脂肪重量均显著高于自由取食的对照组小鼠,但血清瘦素水平组间差异不显著。即在食物资源丰富的条件下,经历食物短缺的动物将增加能量摄入和消化吸收效率以及脂肪组织能量贮存,从而导致体重的"补偿性增长",同时,血清瘦素可能在该过程中发挥重要作用。     

鸟类基础产热的可塑性

基础代谢率(basal metabolic rate,BMR)是动物在清醒时维持身体各项基本功能所需的最小能量值,能反映出鸟类对环境独特的适应机制和进化对策。鸟类的BMR具有一定的可塑性,包括实验室适应、迁徙和季节性驯化期间的变化。鸟类BMR可塑性变化的形态学、生理学及生化分子生物学基础包括:调整代谢活性器官的重量、特殊器官的代谢强度及组织器官内氧含量和底物的转运能力等。     

短期持续限食对树麻雀体重和基础代谢率的影响及生态学意义

为探讨短期持续限食对树麻雀(Passer monanus)体重和基础代谢率的影响,及其生理适应的调节机制。以正常饲喂树麻雀为对照组(0D组,D为饥饿天数),以进食量相同和持续限食时间不同的4组(1D、3D、5D和7D)树麻雀为研究对象进行限食驯养。结果显示,体重与个体BMR间存在极显著的线性关系(r=0.512,P=0.001);5组树麻雀单位体重的基础代谢率(BMR)差异不显著,5D和7D组树麻雀的个体BMR组间差异显著(P0.05);树麻雀的体重驯养前后变化为对照组增加而4个实验组降低,驯养后,1D和7D组与对照组相比体重降低分别为显著(P0.05)和极显著(P0.01),3D和5D组相对于1D、7D组出现小幅度的上调,1～7d持续限食树麻雀的体重出现降升降的趋势。结论是:当摄食量不足时,消耗体内的能量储备和降低个体的基础能耗对缓解短期持续限食的生存压力有利,但个体适合度随之降低。体内能量储备和个体基础能耗的相应增加是树麻雀应对饥饿环境的关键,也是其重要的生存策略之一。     

黑线仓鼠的BMR个体差异及其应对高脂食物的能量学对策

为探讨高脂食物对小型哺乳动物能量代谢的影响及其与基础代谢率(Basal metabolic rate, BMR)的关系,将成年雌性黑线仓鼠(Cricetulus barabensis)分为高、低BMR组,每组再随机分为低脂、高脂食物组,驯化6周后,测定体重、摄入能和代谢率,以及消化酶活力、褐色脂肪组织(Brown adipose tissue, BAT)和主要内脏器官与肌肉的细胞色素c氧化酶(Cytochrome c oxidase, COX)活性、解偶联蛋白(Uncoupling protein, UCP) mRNA表达等。结果显示,高脂食物对高、低BMR组动物体重均无显著影响。与低脂食物组相比,高脂食物组的摄食量、摄入能和消化能显著下降,小肠脂肪酶活力显著增强,消化率明显增加,但高、低BMR组的组间差异不显著。夜间代谢水平显著高于昼间,高脂食物使高BMR组的夜间代谢率显著升高。BAT、肌肉和内脏器官COX活性不受高脂食物的影响,高、低BMR组的组间差异也不显著。高脂食物组仅肝脏UCP2表达显著上调。结果表明,能量摄入和消化系统形态及功能的可塑性调节是黑线仓鼠应对高脂食物的主要策略;黑线仓鼠的代谢率具有显著的昼夜节律,既受高脂食物的影响,也与动物自身的BMR水平有关,但UCP表达具有组织特异性,这可能不是导致BMR个体差异的因素。     

白头鹎的代谢率与器官重量在季节驯化中的可塑性变化

动物能量代谢的生理生态特征与物种的分布和丰富度密切相关,基础代谢率(BMR)是恒温动物维持正常生理机能的最小产热速率,是动物在清醒时维持身体各项基本功能所需的最小能量值,是内温动物能量预算的重要组成部分.本研究测定了白头鹎(Pycnonotus sinensis)的BMR、内部器官(肝、心、肌胃、小肠、肾和整体消化道)和肌肉的重量,分析了白头鹎内部器官和肌肉重量的季节性变化及与BMR的关系.方差分析表明,白头鹎的BMR存在明显的季节性变化,冬季较高,夏季最低.其内部器官及肌肉重量的变化同样有明显的季节性.相关分析表明,白头鹎的BMR与肝、心、消化道等内部器官和肌肉重量存在明显的相关性.     

食物限制对雄性大绒鼠能量代谢特征的影响

为探讨横断山区大绒鼠适应食物匮乏的适应对策,将成年雄性大绒鼠随机分为自由取食组和饲喂正常摄食量的80% 限食组。测定了自由取食组和限食组雄性大绒鼠的体重、静止代谢率、非颤抖性产热以及体脂含量、血清瘦素含量、肝脏鲜重、褐色脂肪组织重量和消化道形态。结果显示:限食使雄性大绒鼠的体重、体脂含量、静止代谢率、非颤抖性产热、褐色脂肪组织重量和大肠、小肠长度显著降低,使盲肠内容物重量显著增加。血清瘦素含量与体重、体脂含量呈极显著正相关。在限食条件下,大绒鼠主要通过降低体重、基础代谢和产热的能量支出以及动用体内脂肪以应对食物资源短缺的环境条件,瘦素可能参与了能量代谢和体重的适应性调节。     

Body mass and behavior in Swiss mice subjected to continuous or discontinuous food restriction and refeeding

Food restriction (FR) is hypothesized to decrease body fat content of an animal and thus prevent obesity. However, the response of energy budget to a continuous (CFR) or discontinuous FR (DFR) remains inconsistent. In the present study, effects of CFR or DFR and refeeding on energy budget and behavior were examined in male Swiss mice. CFR significantly decreased the energy expenditure associated with basal metabolic rate (BMR) and activity behavior, but not sufficiently to compensate for energy deficit and thus resulted in lower body mass and fat content. DFR mice had a significantly higher food intake on ad libitum days and showed increases in BMR and activity after 4 weeks’ DFR, which might resulted in lower body mass and less body fat than controls. After being refed ad libitum, both CFR and DFR mice had similar body mass, BMR, and behavioral patterns to controls but had 95% and 75% higher fat content. This suggested that not only CFR but also DFR would be a significant factor in the process of obesity for animals that were refed ad libitum. It also indicated that food restriction interrupted many times by periods of ad libitum feeding had the same long-term effects like continuous underfeeding.     

食物限制对黑线仓鼠能量代谢和产热的影响

为阐明动物应对食物短缺的能量学对策与其自身的代谢水平的关系,测定了不同限食程度下黑线仓鼠的体重、基础代谢率和非颤抖性产热。结果发现,限食使基础代谢率、非颤抖性产热、褐色脂肪组织细胞色素c氧化酶活性降低。90% 限食驯化4 周后,存活率为80% ,60% 限食驯化4 周后,存活率为30% 。低温驯化使黑线仓鼠基础代谢率和非颤抖性产热显著增加,使80% 限食动物的体重和存活率显著降低。高基础代谢率组的摄食量比低基础代谢率组多23.8% ,80% 限食后两组体重降低的幅度和存活率差异不显著。结果表明:高水平的代谢率使黑线仓鼠对食物资源短缺的敏感性增加;支持“代谢率转换假说”,符合“具有储食习性的动物对食物短缺的生理耐受性较低” 的预测。     

黑线仓鼠繁殖输出与基础代谢率的关系

为了解黑线仓鼠繁殖输出与基础代谢率(BMR)的关系,阐明最大持续能量收支(SusMR)的限制水平, 揭示哺乳期能量收支对策,本文测定了哺乳期黑线仓鼠的体重、摄食量、BMR 和身体组成,以及哺乳期的胎仔数、胎仔重和泌乳能量支出(MEO)。结果显示,黑线仓鼠哺乳期体重降低了15.0 ± 0.8% , 摄食量显著增加, 哺乳高峰期平均摄食量为13.9 ± 0.3 g /d, 摄入能为222.1 ± 5.3 kJ/ d, 比哺乳初期增加121% , 比对照组高288% ;哺乳高峰期MEO 为62.4 ± 2.3 kJ/ d, 哺乳末期BMR 为49.7 ± 1.1 kJ/ d; 断乳时平均胎仔数4.7 ± 0.2、窝胎仔重50.5 ±1.6 g; 哺乳末期BMR 比对照组增加48% ,BMR 与消化系统各器官的相关性高于对照组; BMR 与胎仔数、胎仔重、乳腺重量和MEO 显著正相关。结果表明:初次繁殖的黑线仓鼠哺乳期SusMR 限制为4.47 ×BMR, 在自身维持和繁殖输出之间采取了“权衡分配”的原则,通过体重降低以减少BMR 的增加幅度, 从而有利于繁殖输出。     

Trade-off between energy budget, thermogenesis and behavior in Swiss mice under stochastic food deprivation

(1) The role of metabolic rate, thermogenesis and behavior in trade-off strategy was examined in Swiss mice under stochastic food deprivation (FD).

(2) For the mice under severe FD, food intake on feeding days increased, and basal metabolic rate (BMR) and nonshivering thermogenesis decreased significantly. The duration of activity decreased but resting behavior increased significantly on feeding days.

(3) It suggested that a trade-off between increased food intake and decreased energy expenditure related to lower BMR, thermogenesis and activity might be employed to meet reduced calorie intake caused by unpredictable FD.

Mild Calorie Restriction Induces Fat Accumulation in Female C57BL/6J Mice

This study investigated the effects of mild calorie restriction (CR) (5%) on body weight, body composition, energy expenditure, feeding behavior, and locomotor activity in female C57BL/6J mice. Mice were subjected to a 5% reduction of food intake relative to baseline intake of ad libitum (AL) mice for 3 or 4 weeks. In experiment 1, body weight was monitored weekly and body composition (fat and lean mass) was determined at weeks 0, 2, and 4 by dual energy X‐ray absorptiometry. In experiment 2, body weight was measured every 3 days and body composition was determined by quantitative magnetic resonance weekly, and energy expenditure, feeding behavior, and locomotor activity were determined over 3 weeks in a metabolic chamber. At the end of both experiments, CR mice had greater fat mass (P < 0.01) and less lean mass (P < 0.01) compared with AL mice. Total energy expenditure (P < 0.05) and resting energy expenditure (P < 0.05) were significantly decreased in CR mice compared with AL mice over 3 weeks. CR mice ate significantly more food than AL mice immediately following daily food provisioning at 1600 hours (P < 0.01). These findings showed that mild CR caused increased fat mass, decreased lean mass and energy expenditure, and altered feeding behavior in female C57BL/6J mice. Locomotor activity or brown adipose tissue (BAT) thermogenic capacity did not appear to contribute to the decrease in energy expenditure. The increase in fat mass and decrease in lean mass may be a stress response to the uncertainty of food availability.     

小鼠基础代谢率与繁殖输出和繁殖期末器官的关系

以封闭式流体压力呼吸计测定KM小鼠(Mus musculus)的基础代谢率(BMR);采用残差分析和Pearson相关分析检验BMR与繁殖输出、内脏器官的相关性。哺乳末期BMR显著高于繁殖前,繁殖前BMR与繁殖输出不相关,但哺乳末期BMR与体重、摄食量、胎仔数和胎仔重、内脏器官和消化道显著正相关;与消化道器官的相关性高于其他内脏器官。研究结果支持"哺乳期较高的BMR有利于消化系统增强消化和吸收能力,以增加能量摄入用于繁殖输出"的假设。     

The role of leptin in striped hamsters subjected to food restriction and refeeding

Food restriction(FR) and refeeding(Re) have been suggested to impair body mass regulation and thereby making it easier to regain the lost weight and develop over-weight when FR ends. However, it is unclear if this is the case in small mammals showing seasonal forging behaviors. In the present study, energy budget, body fat and serum leptin level were measured in striped hamsters that were exposed to FR-Re. The effects of leptin on food intake, body fat and genes expressions of several hypothalamus neuropeptides were determined. Body mass, fat content and serum leptin level decreased during FR and then increased during Re. Leptin supplement significantly attenuated the increase in food intake during Re, decreased genes expressions of neuropepetide Y(NPY) and agouti-related protein(AgRP) of hypothalamus and leptin of white adipose tissue(WAT). Hormone-sensitive lipase(HSL) gene expression of WAT increased in leptin-treated hamsters that were fed ad libitum, but decreased in FR-Re hamsters. This indicates that the adaptive regulation of WAT HSL gene expression may be involved in the mobilization of fat storage during Re, which partly contributes to the resistance to FR-Re-induced overweight. Leptin may be involved in the down regulations of hypothalamus orexigenic peptides gene expression and consequently plays a crucial role in controlling food intake when FR ends.     

Heparanase affects food intake and regulates energy balance in mice

Mutation of the melanocortin-receptor 4 (MC4R) is the most frequent cause of severe obesity in humans. Binding of agouti-related peptide (AgRP) to MC4R involves the co-receptor syndecan-3, a heparan sulfate proteoglycan. The proteoglycan can be structurally modified by the enzyme heparanase. Here we tested the hypothesis that heparanase plays a role in food intake behaviour and energy balance regulation by analysing body weight, body composition and food intake in genetically modified mice that either lack or overexpress heparanase. We also assessed food intake and body weight following acute central intracerebroventricular administration of heparanase; such treatment reduced food intake in wildtype mice, an effect that was abolished in mice lacking MC4R. By contrast, heparanase knockout mice on a high-fat diet showed increased food intake and maturity-onset obesity, with up to a 40% increase in body fat. Mice overexpressing heparanase displayed essentially the opposite phenotypes, with a reduced fat mass. These results implicate heparanase in energy balance control via the central melanocortin system. Our data indicate that heparanase acts as a negative modulator of AgRP signaling at MC4R, through cleavage of heparan sulfate chains presumably linked to syndecan-3.