乳清蛋白与老年肌肉衰减征研究进展

肌肉衰减征(Sarcopenia)是伴随衰老而出现的一种以肌肉质明显减少、肌肉力量下降为特点的常见病征,同时伴随功能下降和多种慢性病发生。摄入充足的膳食蛋白质和能量,以及加强抗阻力运动和有氧运动是防治老年人肌肉衰减征的重要措施。乳清蛋白富含亮氨酸等支链氨基酸和谷氨酰胺,在防治老年肌肉衰减征中具有独特而重要的作用。     

老年肌肉减少症防治中的营养干预

肌肉减少症是与年龄相关的肌肉质量、力量和体能的下降。减缓或推迟其发生、发展的唯一途径就是运动营养干预。老年人的消化吸收功能减退,给膳食营养补充带来困难,而特殊营养品的使用成为必不可少的有效途径。本文主要针对防治老年肌少症的蛋白质、氨基酸、维生素D、钙、抗氧化剂、植物调理剂等营养品补充作详尽的阐述。     

运动和膳食干预对久坐人群的健康影响研究

目的:分析运动和膳食干预对久坐人群的健康影响。方法:2020年1—7月在北京市招募久坐人群108人,根据其近期健康检查数据和血脂数据,将其分肌肉功能减退组和脂肪代谢异常组(干预组、对照组各27人),开展12周的运动和膳食干预。肌肉功能减退组中的膳食方案中供能营养素比例为碳水化合物50%、蛋白质30%、脂肪20%,膳食纤维每天摄入量不少于30 g。脂肪代谢异常组中的膳食方案中供能营养素比例为碳水化合物60%、蛋白质20%、脂肪20%,并分组制定相应的运动干预方案,比较干预前后身体质量情况和血脂数据。结果:肌肉功能减退组,干预组中体重、腰围和BMI显著降低,骨骼肌含量、体脂肪率、内脏脂肪率显著改善(P<0.05);脂肪代谢异常组,干预组中体重、腰围和BMI显著下降,血液中CHO、TG、HDL-C均有显著改善(P<0.05)。结论:运动和膳食干预能有效提高久坐人群健康状况,并且通过设定个性化、专业的干预方案能有效增加肌肉量,提高肌肉功能,调整机体代谢水平,减少脂肪蓄积。     

老年人肌肉衰减情况及肉类饮食对其影响的研究

将60~69岁、70~79岁、≥80岁三个年龄阶段的老年人分为肌肉衰减组、正常组,调查分析了老年人肌肉衰减与肉类饮食等影响因素的关系,揭示肉类饮食、运动状况和老年人肌肉衰减的关系,从食品摄入角度为干预老年人肌肉衰减提供依据。结果表明:从总体上看,与正常组比较发现,肌肉衰减组老年人在性别、BMI(身体质量指数)上差异极显著(P<0.01);组内比较发现,肌肉衰减组三个年龄段老年人随年龄增长其肌肉衰减程度呈上升趋势,SMI(骨骼肌质量指数)下降;膳食状况与运动状况分析发现,肌肉衰减组三个年龄段中部分年龄段老年人在肉类及其蛋白摄入量、畜禽类及其蛋白摄入量、运动量分类上与正常组老年人有显著差异(P<0.05),并且其肌肉衰减率随着肉类及其蛋白摄入量、畜禽类及其蛋白摄入量、运动量分类值的增加而呈递减趋势(P<0.05);肌肉衰减与肉类及其蛋白摄入量有关(β=-2.633、P<0.05;β=-2.216、P<0.05),肉类及其蛋白摄入量为老年人肌肉衰减的保护因素(OR<1);主成分分析发现肉类、抗阻运动量的排序(2、3)和肉类蛋白、抗阻运动量(2、1)排序均靠前,SMI与肉类及其蛋白摄入量、畜禽肉及其蛋白摄入量有较强的相关性,指标之间距离较近。结论:老年人肌肉衰减受年龄、性别、BMI、肉类饮食、运动状况等因素影响,适当增加老年人肉类摄入量(特别是畜禽肉)、抗阻运动量,有助于改善老年人的肌肉衰减。     

促老年人蛋白质消化吸收方法的研究进展

蛋白质是人体重要的营养物质，蛋白质的长期缺乏会直接或间接导致人体免疫力低下、肌肉衰减、骨质疏松等病症的发生概率增加，这种现象在老年人群中更为突出，从而降低了老年人群的运动及机体代谢能力，直接影响其生活质量，这也增加了我国公共卫生及医疗系统负担，阻碍了“健康中国”战略的稳步推进。目前，对于改善老年人蛋白质摄入不足/缺乏的方式主要有改良食物特性（改变蛋白质结构）、改善身体机能（添加可促进蛋白消化酶分泌的成分）、改变饮食结构（增加寡肽的摄入）以及改变饮食习惯（增加蛋白质摄入量和种类）。本文探讨年龄增长对蛋白质消化吸收能力的影响作用，并总结现有的促进蛋白质消化吸收的方法，同时对未来改善老年人蛋白质消化吸收能力的方法进行展望，以期为促进老年人营养尤其是蛋白质吸收的研究提供参考。     

青稞提取物干预对老年小鼠骨骼肌萎缩的影响

衰老过程中氧化应激的增加与骨骼肌质量与功能的显著降低存在密切关联。青稞富含多酚、类黄酮等生物活性成分,具有较强的抗氧化活性。研究表明,膳食中的天然抗氧化成分可以有效缓解骨骼肌增龄性萎缩。为探讨青稞水提物和醇提物是否对老年小鼠骨骼肌萎缩产生影响,测定了12周青稞提取物干预对老年小鼠骨骼肌年龄相关生理变化的影响,并利用反转录聚合酶链反应和免疫蛋白印记测定了肌萎缩标志基因、氧化应激相关基因的表达。实验结果表明:与衰老的对照小鼠相比,两种青稞提取物干预均有效抑制了衰老小鼠骨骼肌肌肉质量的减少,并增强了衰老小鼠的运动能力；青稞提取物在mRNA和蛋白水平均显著降低了肌肉环状指基因1和肌肉萎缩盒F基因的表达；青稞提取物激活了SIRT3蛋白的表达,并显著抑制了衰老小鼠骨骼肌中的氧化应激。研究结果表明,青稞提取物可以通过激活SIRT3信号的表达有效抑制衰老诱导的氧化应激,从而缓解衰老导致的骨骼肌萎缩。     

大豆蛋白在体重管理上出奇制胜

按照世界卫生组织(WTO)的统计数据,全球超重/肥胖人口不断上升,预计到2015年全球超重成年人将达到23亿,肥胖成年人将达到7亿.导致超重与肥胖的因素有若干,比如基因、新陈代谢、行为、环境等等.然而,对于大多数人来说,热量摄入过剩或/和体能锻炼不足是导致超重与肥胖的主要原因. 蛋白质-抵抗脂肪的强大武器 控制体重需要减少热量的摄入.有数据显示,蛋白质能够影响饱腹感.蛋白质的饱和脂肪含量低,可作为是热量限制饮食的一部分.研究表明,用蛋白质代替碳水化合物,尤其是精制碳水化合物,能够增加饱腹感和脂肪消耗,减少去脂体重的损耗.此外,研究还表明,和低蛋白饮食相比,高蛋白摄入量的饮食更能增加饱腹感,从而减少其他食物的摄入.     

运动性疲劳的机制与大豆多肽对其调控的研究进展

健康已经日益成为人们所关注的话题,越来越多人开始通过各种运动方式提升自己的身体机能,运动也在人们生活中占据越来越重的份量。不管是年轻人群还是老年人群,由于自身条件的不同以及运动量的不合理,经常因为过度运动导致身体不适,引起身体疲劳,从而影响工作效率,甚至造成各种运动性损伤,危及身体健康。本文从分子水平阐述运动性疲劳相关信号通路,综述运动性疲劳与骨骼肌蛋白质的合成、活性氧介导的骨骼肌蛋白质分解以及骨骼肌糖代谢的相互关联。针对大豆多肽易吸收、营养丰富、抗氧化能力强、快速恢复血糖等优点,根据已有的实验结论阐述了大豆多肽营养补充剂缓解运动性疲劳的理论依据。     

平衡蛋白饮食能够延缓衰老导致的肌肉流失

正伯明翰大学的一项新研究发现,在早餐或午餐时间吃更多的蛋白质可以帮助老年人维持肌肉量。人体产生新肌肉的机制是需要定期刺激。这种刺激往往发生在我们吃蛋白质的时候。老年人肌肉再生的效率较低,因此他们需要吃更多的蛋白质才能获得与年轻人相同的效果。但是,仅仅吃更多的蛋白质是不够的——老年人还需要在所有膳食中平均分配摄入量,以确保他们最大限度地利用蛋白质对肌肉质量的益处。对此,伯明翰大学的研究人员研究了年轻人,中年人和老年人的饮食摄入,并且特别调查了蛋白质的摄入     

1-脱氧野尻霉素对肥胖小鼠甲状腺激素稳态的影响

甲状腺激素在调节脂代谢方面发挥着十分重要的作用,本实验探究肥胖对甲状腺激素稳态的影响以及1-脱氧野尻霉素(1-deoxynojirimycin,DNJ)的干预作用。饲喂高脂饲料建立肥胖小鼠模型,继续饲喂高脂饲料的同时灌胃剂量分别为2.0、4.0、8.0 mg/(kg mb·d)的DNJ 45 d,测定血脂水平及甲状腺激素相关指标水平。结果表明,与肥胖对照组相比,高剂量DNJ能够抑制小鼠体质量的增加,改善高脂饮食引起的血脂异常;高剂量DNJ使雌、雄小鼠血清总甲状腺素水平分别上升22.03%、15.99%,总三碘甲状腺原氨酸水平分别上升66.86%、47.79%(P0.05),促甲状腺激素水平分别下降9.65%、9.73%(P0.05),肝脏1型脱碘酶活力分别上升40.99%、24.40%(P0.05),肝脏1型脱碘水平分别上升35.68%、29.50%(P0.05),肝脏甲状腺激素β受体蛋白水平分别上升37.53%、27.81%(P0.05);并能显著上调肝脏1型脱碘酶、甲状腺激素β受体及脂代谢相关甲状腺激素靶基因脂肪甘油三酯脂酶、肉毒碱棕榈酰转移酶1α、胆固醇7α-羟化酶mRNA表达。结论:DNJ能够改善肥胖引起的甲状腺激素功能紊乱,进而上调脂代谢相关甲状腺激素靶基因mRNA表达,促进脂类分解代谢,抑制体质量增加。     

New insights into body composition and health through imaging analysis. 2007 Ryley-Jeffs memorial lecture.

From calipers to magnetic resonance imaging (MRI), we have come a long way in our ability to analyze body composition. Some historical milestones are a reminder that many concepts in muscle and fat metabolism, and their measurement, have stood the test of time. However, newer imaging technology has improved our understanding of population heterogeneity in body composition, and the potential health problems associated with certain body composition phenotypes. Imaging analyses, such as dual energy X-ray absorptiometry, computed tomography, and MRI, have provided detailed characterization of the type and amount of fat deposited centrally (abdominal adipose tissue), the trajectory of losses in muscle tissue (sarcopenia), and the combination of low muscle mass/high fat mass (sarcopenic obesity). The last is a new emerging health concern because the presence of these two disproportionate tissue depots may have an additive effect on increasing morbidity. Ongoing measurement of body composition is needed, and preliminary research suggests this may have important nutritional implications.     

肥胖诊断标准及其临床应用的研究进展

肥胖是目前世界范围内最受瞩目的公共健康问题,它不仅是一种由多因素引起的慢性代谢性疾病,还作为一种高危因素广泛应用于慢性病的临床筛查与疾病防治.肥胖的分型方法各异,诊断标准也不再是单一的体质指数（BMI）法,能客观反映脂肪分布和含量的腰围（WC）、体脂量（BF）、内脏脂肪面积（VFA）等新标准正逐渐渗入到临床诊断和治疗评估中.本文就近年来临床常用的肥胖诊断标准及其应用领域、优缺点进行综述,为肥胖及脂肪相关疾病的诊断、防治提供依据.     

Nutrient-rich meat proteins in offsetting age-related muscle loss

From a health perspective, an underappreciated consequence of the normal aging process is the impacts that the gradual loss of skeletal muscle mass, termed sarcopenia, has on health beyond an effect on locomotion. Sarcopenia, refers to the loss of muscle mass, and associated muscle weakness, which occurs in aging and is thought to proceed at a rate of approximately 1% loss per year. However, periods of inactivity due to illness or recovery from orthopedic procedures such as hip or knee replacement are times of accelerated sarcopenic muscle loss from which it may be more difficult for older persons to recover. Some of the consequences of age-related sarcopenia are easy to appreciate such as weakness and, eventually, reduced mobility; however, other lesser recognized consequences include, due to the metabolic role the skeletal muscle plays, an increased risk for poor glucose control and a predisposition toward weight gain. What we currently know is that two stimuli can counter this age related muscle loss and these are physical activity, specifically resistance exercise (weightlifting), and nutrition. The focus of this paper is on the types of dietary protein that people might reasonably consume to offset sarcopenic muscle loss.     

Cyanidin-3-O-β-glucoside improves obesity and triglyceride metabolism in KK-Ay mice by regulating lipoprotein lipase activity

BACKGROUND: Cyanidin‐3‐O‐β‐glucoside (Cy‐3‐g)‐rich foods have been reported to inhibit the onset of obesity, but whether the pure anthocyanin supplementation affects obesity remains uncertain. RESULTS: Cy‐3‐g supplementation significantly reduced obesity, accumulation of fat in visceral adipose and liver tissues, and plasma triglyceride levels. Furthermore, adenosine monophosphate (AMP)‐activated protein kinase phosphorylation (pAMPK) in the skeletal muscle and visceral adipose were significantly increased by Cy‐3‐g consumption. This was followed by the activation of lipoprotein lipase (LPL) in plasma and skeletal muscle but the suppression of this enzyme in visceral adipose. LPL activation in skeletal muscle cells and its suppression in adipocytes by Cy‐3‐g were blocked by inhibition of pAMPK. CONCLUSION: Our present data thus demonstrate that Cy‐3‐g improves obesity and triglyceride metabolism in KK‐Ay mice. The underlying mechanism is found to be partly related to the activation of LPL in plasma and skeletal muscle, and inhibition of LPL in adipose tissue following the activation of pAMPK. Copyright © 2011 Society of Chemical Industry     

Effects of level of nutrient intake and age on mammalian target of rapamycin,insulin, and insulin-like growth factor-1 gene network expression in skeletal muscle of young Holstein calves

The molecular mechanisms by which level of nutrient intake enhances skeletal muscle growth in young ruminants are not fully understood. We examined mammalian target of rapamycin (mTOR), insulin, and insulin-like growth factor-1 (IGF-1) gene network expression in semitendinosus muscle tissue of young male Holstein calves fed a conventional milk replacer plus conventional starter (CON) or an enhanced milk replacer plus high-protein starter (ENH) for 5 wk followed by a conventional starter or a high-protein starter until 10 wk of age. Feeding ENH led to greater concentration of plasma IGF-1 and leptin and greater carcass protein and fat mass throughout the study. Despite the greater plasma IGF-1 and protein mass at wk 5, calves fed ENH had lower expression of IGF1R, INSR, and RPS6KB1 but greater expression of IRS1 and PDPK1 in muscle tissue. Except for IGF1R expression, which did not differ at wk 10, these differences persisted at wk 10, suggesting a long-term effect of greater nutrient intake on physiological and molecular mechanisms. Components of mTOR complex (mTORC)1 and mTORC2 (RICTOR and RPTOR) and FOXO1 expression decreased by wk 10 regardless of diet. Overall, the present data revealed that greater nutrient intake throughout the milk-fed and early postweaning phase alters body mass composition partly by altering hormonal and molecular profiles of genes associated with glucose and amino acid signaling. Those networks may play a crucial role in coordinating neonatal muscle growth and metabolism in response to level of nutrient intake.     

石榴皮提取物改善肥胖大鼠糖、脂代谢紊乱的分子机制

目的:探讨高脂饮食诱发的大鼠肥胖对肝脏糖代谢的影响,揭示石榴皮提取物(EPP)改善肥胖大鼠糖、脂代谢紊乱的分子机制。方法:应用高脂饲料(D12451)和对照饲料(D12450H)分别饲养大鼠16周,复制肥胖动物模型。在造模的同时,灌胃大鼠3个剂量的EPP(50,100,200 mg/kg)进行干预。结果:高脂饲料喂养16周后大鼠体重、Lee’s指数和肝重指数显著增高;血清TC、TG、LDL-C和FFA水平增高,HDL-C水平降低;大剂量EPP干预可显著改善高脂大鼠体重、Lee’s指数、肝重指数和血脂水平,表明EPP可有效降低高脂饮食诱发的大鼠肥胖。EPP可显著改善肥胖大鼠肝脏显微结构和肝功能损伤。大鼠胰岛素抵抗和肝脏糖代谢的检测结果表明:高脂饮食大鼠存在明显的血糖增高和胰岛素抵抗现象,大剂量EPP可显著性降低血糖,改善胰岛素抵抗,提高肥胖大鼠肝脏组织IRS-2和GLUT2的蛋白水平。结论:EPP通过降低肥胖大鼠血脂和改善肝脏葡萄糖代谢紊乱发挥肝脏保护作用。     

(-)-Epigallocatechin-3-gallate increases the expression of genes related to fat oxidation in the skeletal muscle of high fat-fed mice

(-)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been shown to prevent the development of obesity in rodent models. Here, we examined the effect of EGCG on markers of fat oxidation in high fat-fed C57bl/6J mice. High fat-fed mice treated with 0.32% dietary EGCG for 16 weeks had reduced body weight gain and final body weight (19.2% and 9.4%, respectively) compared to high fat-fed controls. EGCG-treatment decreased fasting blood glucose, plasma insulin, and insulin resistance by 18.5%, 25.3%, and 33.9%, respectively. EGCG treatment also reduced markers of obesity-related fatty liver disease in high fat-fed mice. Gene expression analysis of skeletal muscle showed that EGCG increased mRNA levels of nuclear respiratory factor (nrf)1, medium chain acyl coA decarboxylase (mcad), uncoupling protein (ucp)3, and peroxisome proliferator responsive element (ppar)α by 1.4-1.9-fold compared to high fat-fed controls. These genes are all related to mitochondrial fatty acid oxidation. In addition, EGCG increased fecal excretion of lipids in high fat-fed mice. In summary, it appears that EGCG modulates body weight gain in high fat-fed mice both by increasing the expression of genes related fat oxidation in the skeletal muscle and by modulating fat absorption from the diet.     

Evidences on three relevant obesogenes: MC4R, FTO and PPARγ. Approaches for personalized nutrition

Obesity is a complex disease that results from the interaction between lifestyle (dietary patterns and sedentary habits) and genetic factors. The recognition of a genetic basis for human obesity has driven to identify putative causal genes to understand the pathways that control body mass and fat deposition in humans as well as to provide personalized treatments and prevention strategies to fight against obesity. More than 120 candidate genes have been associated with obesity-related traits. Genome-wide association study has so far identified over 20 novel loci convincingly associated with adiposity. This review is specifically focused on the study of the effects of melanocortin 4 receptor, Peroxisome proliferator-activated receptor γ and fat mass and obesity associated (FTO) gene variants and their interactions with dietary intake, physical activity or drug administration on body weight control. The advances in this field are expected to open new ways in genome-customized diets for obesity prevention and therapy following personalized approaches.     

山楂、荷叶、普洱茶膳食干预对肥胖大鼠脂质代谢的影响

摘 要: 目的 研究山楂、荷叶、普洱茶对高脂饮食诱导的肥胖大鼠脂质代谢的影响。方法 利用斯普拉-道来氏(sprague-dawley, SD)雄性大鼠制作高脂饮食诱导的肥胖模型, 通过检测体重、血脂水平、肝脏系数、体脂比等生理生化指标, 观察肝脏、肾周脂肪组织病理变化, 分析山楂、荷叶、普洱茶膳食干预对脂质代谢的影响。结果 山楂、荷叶、普洱茶及复合组均能抑制大鼠体重的增长, 调节血脂水平, 同时降低肝脏指数和体脂比, 其中复合组的效果最佳; 山楂、荷叶、普洱茶单用对肥胖大鼠受损的肝脏组织、脂肪细胞改善效果欠佳, 三者联用可明显减少肝脏炎性浸润和脂肪堆积的病变情况, 有效抑制脂肪细胞数量的增多和面积的增大。结论 山楂、荷叶、普洱茶联用可有效调节肥胖大鼠脂质代谢。