Autonomic nervous system activity and the state and development of obesity in Japanese school children

OBJECTIVE: The autonomic nervous system (ANS) plays an important role in regulating energy expenditure and body fat content; however, the extent to which the ANS contributes to pediatric obesity remains inconclusive. The aim of this study was to evaluate whether sympathetic and/or the parasympathetic nerve activities were altered in an obese pediatric population. We further examined a physiological association between the duration of obesity and the sympatho-vagal activities to scrutinize the nature of ANS alteration as a possible etiologic factor of childhood obesity. RESEARCH METHODS AND PROCEDURES: Forty-two obese and 42 non-obese healthy sedentary school children were carefully selected from 1080 participants initially recruited to this study. The two groups were matched in age, gender, and height. The clinical records of physical characteristics and development of the obese children were retrospectively reviewed to investigate the onset and progression of obesity. The ANS activities were assessed during a resting condition by means of heart rate variability power spectral analysis, which enables us to identify separate frequency components, i.e., total power (TP), low-frequency (LF) power, and high-frequency (HF) power. The spectral powers were then logarithmically transformed for statistical testing. RESULTS: The obese children demonstrated a significantly lower TP (6.77 +/- 0.12 vs. 7.11 +/- 0.04 ln ms(2), p < 0.05), LF power (6.16 +/- 0.12 vs. 6.42 +/- 0.05 ln ms(2), p < 0.05), and HF power (5.84 +/- 0.15 vs. 6.34 +/- 0.07 ln ms(2), p < 0.01) compared with the non-obese children. A partial correlation analysis revealed that the LF and HF powers among 42 obese children were negatively associated with the duration of obesity independent of age (LF: partial r = -0.55, p < 0.001; HF: partial r = -0.40, p < 0.01). The obese children were further subdivided into two groups based on the length of their obesity. All three spectral powers were significantly reduced in the obese group with obesity of >3 years (n = 18) compared to the group with obesity of <3 years. DISCUSSION: Our data indicate that obese children possess reduced sympathetic as well as parasympathetic nerve activities. Such autonomic depression, which is associated with the duration of obesity, could be a physiological factor promoting the state and development of obesity. These findings further imply that preventing and treating obesity beginning in the childhood years could be an urgent and crucial pediatric public health issue.     

Energy metabolism in human obesity

Summary Obesity results from a chronic imbalance between energy intake and expenditure. Accurate measurements of total energy expenditure of lean and obese individuals with a respiration chamber have clearly shown that obese individuals expend more energy than lean sedentary subjects. Studies on the body composition of obese individuals reveal that not only the fat mass is enlarged, but the fat-free mass is also increased as compared with that of lean subjects. Since basal metabolic rate is proportional to the fat-free mass, obese subjects have a greater basal metabolic rate than lean controls. The energy cost of weight bearing activities such as walking and standing is related to body weight, and is therefore increased in obese individuals.The thermogenic response to food ingestion, the diet-induced thermogenesis, has been found to be reduced in some groups of obese people, but not in all obese individuals. The thermic effect of glucose or to meal ingestion is blunted in obese subjects with insulin resistance. Any alteration in thermogenic responses to a caloric excess can be important to store or to oxidize part of the excessive energy intake. After weight reduction in obese subjects due to a hypocaloric diet, the total 24-hour energy expenditure decreases by 20 to 25 kcal/day for each kilogram of weight loss. Failure to adapt the every day energy intake accordingly will result in body weight gain and relapse of obesity.

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Energieumsatz bei Fettleibigen

Zusammenfassung Fettleibigkeit wird durch ein gestörtes Gleichgewicht zwischen Energiezufuhr und -verbrauch erzeugt. Exakte Messungen mit Hilfe einer kalometrischen Kammer haben deutlich ergeben, dass adipöse Personen einen höheren Energieverbrauch verzeichnen als normalgewichtige Personen mit passiven Lebensgewohnheiten.Untersuchungen über die Körperzusammensetzung haben gezeigt, dass Fettleibige nicht nur mehr Fettgewebe besitzen, sondern auch mehr fettfreies Gewebe haben. Da sich der Grundenergieumsatz proportional zur Fettmasse verhält, haben adipöse Personen einen höheren Grundenergieumsatz. Der Energieverbrauch gewichttragender Körperleistungen, wie Gehen und Stehen, steht in direktem Verhältnis zum Körpergewicht und ist somit bei Fettleibigen erhöht. Bei gewissen, jedoch nicht bei allen adipösen Personen wurde eine verringerte, auf die Mahlzeit folgende Wärmeerzeugung, diätindi-zierte Thermogenese gefunden. Bei insulinresistenten Patienten konnte eine verminderte Wärmereaktion auf Glukose- oder Nahrungszufuhr nachgewiesen werden. Jede änderung der Wärmereaktion auf eine übertriebene Kalorienzufuhr kann entweder die Ablagerung oder die Verbrennung eines Teils der überflüssigen Energiezufuhr beeinflussen. Nach Gewichtsverlust adipöser Personen durch kalorienarme Kost fällt der 24stündige Gesamtenergieverbrauch um 20 bis 25 kcal/Tag und pro verlorenes Kilogramm. Die Unfähigkeit, die Nahrungseinnahme dem neuen Zustand anzupassen, hat unvermeidlich eine Gewichtszunahme zur Folge und erklärt die häufigen Rückfälle zur Fettleibigkeit.

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Métabolisme énergétique dans l'obésité humaine

Résumé L'obésité résulte d'un déséquilibre chronique entre apports et dépenses d'énergie. Des mesures précises de la dépense énergétique de sujets normaux et obèses en utilisant une chambre calorimétrique ont clairement montré que les sujets obèses dépensent davantage d'énergie que les sujets non obèses sédentaires. L'étude de la composition corporelle des obèses montre que non seulement la masse adipeuse est augmentée, mais que la masse de tissus maigres est aussi plus importante que celle de sujets non obèses. Le métabolisme basal étant proportionnel à la masse de tissus maigres, il s'ensuit que les obèses ont un métabolisme basal plus élevé que celui des sujets non obèses. Le coût énergétique de plusieurs activités physiques, telles que la marche, la station debout, est fonction du poids corporel; il est donc augmenté chez l'obèse.La réponse thermogénique à la prise alimentaire est diminuée chez certains groupes de patients obèses, mais cette diminution n'est pas présente chez tous les obèses. La réponse thermogénique au glucose, ou à un repas, est diminuée chez les obèses qui se caractérisent par une résistance à l'insuline. Toute altération de la réponse thermogénique à un excès d'apports énergétiques peut influencer la part stockée ou oxydée de cet excès alimentaire. Après perte de poids chez les patients obèses consécutive à un régime hypocalorique, la dépense d'énergie totale de 24 heures diminue de 20 à 25 kcal par jour pour chaque kilogramme de poids perdu. Si l'apport alimentaire quotidien n'est pas adapté à cette diminution de la dépense, la reprise pondérale est inévitable, ce qui explique la récidive fréquente de l'obésité après traitement.

     

妊娠期铁缺乏和缺铁性贫血诊治指南

探讨总铁、补充剂铁、膳食总铁、血红素铁等不同来源铁摄入水平与妊娠期糖尿病（GDM）的关联,进一步为指导孕期合理膳食及含铁补充剂选用提供科学依据。

采用回顾性队列研究,选取2020年1月—2021年7月上海某医院分娩的668例孕中期女性为研究对象,采用自行设计的调查表,通过电子病历系统收集研究对象基本信息及孕中期含铁补充剂使用情况,应用简化的膳食频率问卷量化研究对象孕中期膳食摄入情况。确定总铁及不同来源铁摄入量,并根据摄入量五分位数和中位数进行分组,采用logistic回归分析孕中期总铁及不同来源铁摄入量对GDM发生风险的影响。

校正高龄、糖尿病家族史、孕前超重/肥胖、孕早期血红蛋白（Hb）、能量、碳水化合物供能比、蛋白质、游离糖后发现总铁摄入量与GDM风险无关（P>0.05）。与低剂量补充剂铁摄入组相比,高剂量补充剂铁摄入组GDM发生风险上升（OR=1.65,95%CI：1.14~2.39）。与低剂量膳食总铁摄入组相比,高剂量膳食总铁摄入组GDM发生风险降低（OR=0.53,95%CI：0.35~0.81）,膳食血红素铁的摄入与GDM风险无关（P>0.05）。

高膳食总铁摄入水平可能是GDM的保护因素,而高补充剂铁摄入水平则可能是GDM的危险因素,提示在无妊娠期铁缺乏的情况下,妊娠期女性宜谨慎选用高剂量含铁补充剂,建议优先保证膳食铁摄入。

     

Occasional physical inactivity combined with a high-fat diet may be important in the development and maintenance of obesity in human subjects

BACKGROUND: A better understanding of the environmental factors that contribute to obesity is imperative if any therapeutic effect on the increasing prevalence of overweight and obesity in the United States is to be achieved. OBJECTIVE: This study examined the effect of the interaction of diet composition and physical inactivity on energy and fat balances. DESIGN: Thirty-five normal-weight and obese subjects were randomly assigned to either a 15-d isoenergetic high-carbohydrate (HC) or high-fat (HF) diet according to a crossover design. During the first 14 d, body weight and physical activity were maintained. On day 15, subjects spent 23 h in a whole-room indirect calorimeter and were fed a diet similar to that consumed during the previous 7 d while remaining physically inactive. RESULTS: Energy intakes required to maintain body weight stability during the first 14 d were similar between diets. Normal-weight and obese subjects consuming both diets had a positive energy balance on the sedentary day (day 15), suggesting that subjects were less active in the calorimeter. There was no significant effect of diet composition on total energy balance and total protein-energy balance on day 15; however, carbohydrate balance was more positive with the HC (2497.8 +/- 301.2 kJ) than with the HF (1159 +/- 301.2 kJ) diet (P = 0.0032). Most importantly, fat balance was more positive with the HF (1790.8 +/- 510.4 kJ) than with the HC (-62.8 +/- 510.4 kJ) diet (P = 0.0011). CONCLUSION: Chronic consumption of a high-carbohydrate diet could provide some protection against body fat accumulation in persons with a pattern of physical activity that includes frequent sedentary days.     

瘦素、肥胖与青春期发育

瘦素是由肥胖基因编码的一种分泌型的蛋白质,其作用主要在于调节体重、脂肪和能量代谢。青春期的发动需要一定量的体重或是体脂的贮存,瘦素可能是脂肪组织发出的给生殖系统一种特殊的代谢信号。现就瘦素与肥胖及青春期发育关系的研究进展作以综述。     

Genetic manipulation in nutrition, metabolism, and obesity research

We summarize the current standard methods for overexpressing, inactivating, or manipulating genes, with special focus on nutritional and obesity research. These molecular biology procedures can be carried out with the maintenance of the genetic information to subsequent generations (transgenic technology) or devised to exclusively transfer the genetic material to a given target animal, which cannot be transmitted to the future progeny (gene therapy). On the other hand, the RNA interference (RNAi) approach allows for the creation of new experimental models by transient ablation of gene expression by degrading specific mRNA, which can be applied to assess different biological functions and mechanisms. The combination of these technologies contributes to the study of the function and regulation of different metabolism- and obesity-related genes as well as the identification of new pharmacologic targets for nutritional and therapeutic approaches.     

Fatty acid metabolism in obesity and type 2 diabetes mellitus

Disturbances in pathways of lipolysis and fatty acid handling are of importance in the aetiology of obesity and type 2 diabetes mellitus. There is evidence that a lowered catecholamine-mediated lipolytic response may play a role in the development and maintenance of increased adipose tissue stores. Increased adipose tissue stores, a disturbed insulin-mediated regulation of lipolysis and subnormal skeletal muscle non-esterified fatty acid (NEFA) uptake under conditions of high lipolytic rate may increase circulating NEFA concentrations, which may promote insulin resistance and cardiovascular complications. In addition, a disturbance of NEFA uptake by adipose tissue postprandially is also a critical determinant of plasma NEFA concentration. Furthermore, evidence is increasing that insulin-resistant muscle is characterised by a lowered ability to oxidise fatty acids. A dysbalance between fatty acid uptake and fatty acid oxidation may in turn be a factor promoting accumulation of lipid intermediates and triacylglycerols within skeletal muscle, which is strongly associated with skeletal muscle insulin resistance. The present review describes the reported disturbances in pathways of lipolysis and skeletal muscle fatty acid handling, and discusses underlying mechanisms and metabolic consequences of these disturbances.     

肥胖诊治的现代概念肥胖与代谢综合征

肥胖是指机体内脂肪的过度蓄积,脂肪组织绝对量增多或其比例增高.根据病因可分成原发性(单纯性)肥胖和继发性肥胖两大类,以前者多见、常见,占肥胖的绝大多数.世界卫生组织(WHO)认为肥胖是一种慢性非传染性流行性疾病,应称为肥胖症.随着我国经济的快速发展,人民生活水平的提高,近年来我国肥胖症的发病率呈逐年上升倾向,患病率已达5.4%,且呈年轻化趋势,全国肥胖者已超过7 000万,肥胖者中将有50%会发展为糖尿病,17%会患高血压,某些肿瘤、胆道疾病、胰腺疾病等患病危险性也显著增加,肥胖已成为21世纪严重的社会问题.     

Current and emerging concepts on the role of peripheral signals in the control of food intake and development of obesity

The gastrointestinal peptides are classically known as short-term signals, primarily inducing satiation and/or satiety. However, accumulating evidence has broadened this view, and their role in long-term energy homeostasis and the development of obesity has been increasingly recognised. In the present review, the recent research involving the role of satiation signals, especially ghrelin, cholecystokinin, glucagon-like peptide 1 and peptide YY, in the development and treatment of obesity will be discussed. Their activity, interactions and release profile vary constantly with changes in dietary and energy influences, intestinal luminal environment, body weight and metabolic status. Manipulation of gut peptides and nutrient sensors in the oral and postoral compartments through diet and/or changes in gut microflora or using multi-hormone 'cocktail' therapy are among promising approaches aimed at reducing excess food consumption and body-weight gain.