名刊封面

《国际肥胖症期刊》2010.11 多动症与肥胖症 为了解青少年注意力不足多动症与成年肥胖症的关系,美国杜克大学医学中心的研究人员分析了1.5万多名美国青少年的医疗数据,并于1995年至2009年间对他们进行了跟踪调查。     

肥胖症的药物治疗进展

肥胖症是指能量的摄入大于消耗,造成体内脂肪过度积聚而引发的疾病,肥胖症已成为一种发病率逐年增加的流行疾病,许多代谢性疾病均与肥胖密切相关。目前对于肥胖症的治疗主要有药物、手术和行为学治疗三方面,本文介绍肥胖的药物治疗。     

肥胖症的药物治疗进展

肥胖症是指能量的摄入大于消耗,造成体内脂肪过度积聚而引发的疾病,肥胖症已成为一种发病率逐年增加的流行疾病,许多代谢性疾病均与肥胖密切相关。目前对于肥胖症的治疗主要有药物、手术和行为学治疗三方面,本文介绍肥胖的药物治疗。     

名刊封面

<正>《国际肥胖症期刊》2010.11多动症与肥胖症为了解青少年注意力不足多动症与成年肥胖症的关系,美国杜克大学医学中心的研究人员分析了1.5万多名美国青少年的医疗数据,并于1995年至2009年间对     

GDF15及其受体GFRAL在肥胖治疗上的相关研究进展

肥胖症是一种由于营养物质过剩导致体内脂肪堆积而引起的代谢性疾病,与糖尿病、心脏病等一系列疾病相关。近年来肥胖症的发病率不断攀升,严重威胁人类健康。药物是治疗肥胖症的重要手段,目前治疗肥胖症的药物多为小分子化学药物,存在较严重的副反应,亟待开发更加安全有效的新型药物。生长与分化因子15(GDF15)属于TGF-β超家族,是一类具有抗炎和抗细胞凋亡效应的细胞因子,近年来被发现具有强大的改善能量代谢和控制体重的作用,从而成为潜在治疗肥胖症的新型药物。简要综述了GDF15及其特异性受体——胶质细胞源性神经营养因子家族受体α相似蛋白(GFRAL)在治疗肥胖症中的研究进展。     

代谢组学在肥胖症中的研究进展

肥胖症病因复杂,其发病机制目前尚未完全明确。代谢组学可以从分子水平对代谢途径中的终端产物进行研究,更系统全面地揭示肥胖症的发病机制。文章总结了与肥胖相关的糖、脂、氨基酸、磷脂类及肠道菌群代谢途径及其代谢标志物的变化,以期为肥胖症的临床治疗提供参考。     

我国科学家发现导致肥胖症新基因

正中国科学院遗传与发育生物学研究所李巍课题组领衔的研究发现,位于人类6号染色体长臂D6S1009位点旁侧的SLC35D3基因是人类肥胖症和代谢综合征的致病基因。相关研究于2013年2月13日发表于美国《科学公共图书馆—遗传学》。肥胖症的发生与遗传和环境两种因素有关,其中,遗传因素的贡献约占2/3。不过,研究人员虽已发现了一些单基因肥胖症的致病基因,如瘦素基因(LEP)等,还通过全基因组关联或连锁分析发现了150多个与肥胖症相关的基因位点,     

单纯性肥胖症与血液流变学摘要

单纯性肥胖症与血液流变学摘要第二十九医院颉元文,陶志清为探讨单纯性肥胖症的血液流变学的变化,本文观察５０例,现报告如下：１一般情况１．１肥胖症判断标准,体重超过标准体重的２０％以上,最重为３５％。１．２年龄,男肥胖组５０例,最小年龄４５岁,最大年龄６...     

蛋白质组学在肥胖症研究中的应用

在世界范围内,肥胖及其相关代谢性疾病的发生率逐年增加,尤其是儿童肥胖症的普遍存在引起了广泛关注。过度肥胖是2型糖尿病、心血管疾病和一些肿瘤的重要危险因素。有关肥胖症的研究过去主要集中在脂肪组织功能改变,脂肪细胞分化,棕色脂肪转化,线粒体功能失调,以及肠道营养物质吸收这些方面的分子生物学研究。肥胖作为一种复杂的代谢紊乱性疾病,基因层面的探索并不能全面体现肥胖的机体内各种参与能量代谢的蛋白质功能的变化。高通量蛋白质组学的应用为研究肥胖的机体蛋白质表达和功能变化提供了可能,并为进一步理解肥胖症的发病机理,寻找疾病相关干预靶点提供了重要的帮助。本综述,总结了近年来关于蛋白质组学在肥胖症病理生理变化中的相关研究,并讨论参与肥胖症发生的可能机制和干预作用靶点。     

抗肥胖症和抗糖尿病新药

4 个新药——Contrave、Saxenda、Xultophy 和 Trulicity 在 2014 年 9 月份相继获批或推荐批准,分别用于治疗肥胖症和 2 型糖尿病,可见糖尿病和肥胖症治疗领域迎来长足进展。分别介绍这 4 个新药及其开发历程与市场前景。     

Assessing Life Stress: A Critical Priority in Obesity Research and Treatment

Significant childhood adversity and chronic life stress are highly prevalent in patients with severe obesity. Such stress has been found to increase risk of adulthood obesity by up to 50%, and it can also substantially degrade the effectiveness of evidence‐based treatments for this chronic disease condition. Despite general appreciation of these facts, though, stress is not frequently measured in obesity research or routinely assessed during treatment for obesity or obesity‐related complications. To address this important issue, we describe several validated tools that can be used for assessing life stress and discuss how information obtained from these instruments can be integrated into obesity treatment and research. Given the documented relevance of stress for obesity, we argue that stress assessment and management should be included in clinical treatments for obesity and that stress should be routinely measured in studies examining the long‐term effects of obesity and obesity treatment.     

Obesity Level and Attrition: Support for Patient-Treatment Matching in Obesity Treatment

Obesity treatment studies report attrition rates front 20% to 45%. To reduce attrition, researchers have proposed matching patients to treatment based upon level of obesity. The current study attempted to validate the commonly held assumption that a mismatch between obesity level and treatment will promote attrition. The level of obesity and attrition rates of 39 adults who enrolled in a 12-session behavior therapy program were examined. As obesity level increased, so did attrition. Sixty-nine percent of subjects with mild obesity, 43% of subjects with moderate obesity and 0% of subjects with severe obesity completed treatment.     

Molecular basis of obesity: current status and future prospects

Obesity is a global health problem that is gradually affecting each continent of the world. Obesity is a heterogeneous disorder, and the biological causes of obesity are complex. The rapid increase in obesity prevalence during the past few decades is due to major societal changes (sedentary lifestyle, over-nutrition) but who becomes obese at the individual level is determined to a great extent by genetic susceptibility. In this review, we evidence that obesity is a strongly heritable disorder, and provide an update on the molecular basis of obesity. To date, nine loci have been involved in Mendelian forms of obesity and 58 loci contribute to polygenic obesity, and rare and common structural variants have been reliably associated with obesity. Most of the obesity genes remain to be discovered, but promising technologies, methodologies and the use of "deep phenotyping" lead to optimism to chip away at the 'missing heritability' of obesity in the near future. In the longer term, the genetic dissection of obesity will help to characterize disease mechanisms, provide new targets for drug design, and lead to an early diagnosis, treatment, and prevention of obesity.     

Stigmatizing attitudes toward obesity in a representative population-based sample

Objective: The aim of this study was to determine stigmatizing attitudes toward obesity in the population, and its related psychological and sociodemographic determinants. Methods and Procedures: In a representative population‐based survey (N = 1,000), computer‐assisted telephone interviewing was used to assess stigmatizing attitudes toward obesity, causal attributions of obesity, the labeling of obesity as an illness, perceptions about prevalence, severity, and chronicity of obesity, support of obesity prevention, and sociodemographic characteristics. Results: Of the 1,000 participants, 23.5% (n = 235) had stigmatizing attitudes toward obesity, 21.5% (n = 215) did not have stigmatizing attitudes toward obesity, and 55.0% (n = 550) had attitudes that were undetermined with respect to stigmatization. Predictors of greater stigmatization were more causal attributions of obesity to individual behavior, less education, and older age, while causal attributions of obesity to heredity and labeling obesity as an illness predicted less stigmatization. Stigmatizing attitudes were significantly associated with stronger overall support of obesity prevention, but less readiness to support prevention financially. Discussion: Our results indicate that stigmatizing attitudes toward obesity are prevalent in the population. Information about the etiology of obesity and the clinical relevance of this condition could prove useful for destigmatization efforts.     

Dealing With Obesity as a Chronic Disease

There are major efforts underway to educate the primary care physician about the health risks of obesity. Obesity is a chronic disease that requires chronic management. We must establish models that allow primary care physicians to participate in the chronic management of obesity, while recognizing that the interest and ability of primary care physicians to participate in obesity management will vary. Three general models of obesity management are proposed for the primary care physician, ranging from minimal evaluation to complete evaluation and treatment. In order for the models to be implemented, we must consider establishing a category of obesity specialists who can develop comprehensive treatment programs to which patients with obesity can be referred, and who can provide leadership and guidance for primary care physicians who are involved in obesity management. The North American Association for the Study of Obesity (NAASO) could help establish obesity specialists and provide a structure to allow them to provide leadership for obesity treatment.     

The Obesity Epidemic: Metabolic Imprinting on Genetically Susceptible Neural Circuits

The apparent obesity epidemic in the industrialized world is not explained completely by increased food intake or decreased energy expenditure. Once obesity develops in genetically predisposed individuals, their obese body weight is avidly defended against chronic caloric restriction. In animals genetically predisposed toward obesity, there are multiple abnormalities of neural function that prime them to become obese when dietary caloric density and quantity are raised. Once obesity is fully developed, these abnormalities largely disappear. This suggests that obesity might be the normal state for such individuals. Formation of new neural circuits involved in energy homeostasis might underlie the near permanence of the obese body weight. Such neural plasticity can occur during both nervous system development and in adult life. Maternal diabetes, obesity, and undernutrition have all been associated with obesity in the offspring of such mothers, especially in genetically predisposed individuals. Altered brain neural circuitry and function often accompanies such obesity. This enhanced obesity may then be passed on to subsequent generations in a feed‐forward, upward spiral of increasing body weight across generations. Such findings suggest a form of “metabolic imprinting” upon genetically predisposed neural circuits involved in energy homeostasis. Centrally acting drugs used for obesity treatment lower the defended body weight and alter the function of neural pathways involved in energy homeostasis. But they generally have no permanent effect on body weight or neural function. Thus, early identification of obesity‐prone mothers, infants, and adults and treatment of early obesity may be the only way to prevent the formation of permanent neural connections that promote and perpetuate obesity in genetically predisposed individuals.     

The genetics of childhood obesity and interaction with dietary macronutrients

The genes contributing to childhood obesity are categorized into three different types based on distinct genetic and phenotypic characteristics. These types of childhood obesity are represented by rare monogenic forms of syndromic or non-syndromic childhood obesity, and common polygenic childhood obesity. In some cases, genetic susceptibility to these forms of childhood obesity may result from different variations of the same gene. Although the prevalence for rare monogenic forms of childhood obesity has not increased in recent times, the prevalence of common childhood obesity has increased in the United States and developing countries throughout the world during the past few decades. A number of recent genome-wide association studies and mouse model studies have established the identification of susceptibility genes contributing to common childhood obesity. Accumulating evidence suggests that this type of childhood obesity represents a complex metabolic disease resulting from an interaction with environmental factors, including dietary macronutrients. The objective of this article is to provide a review on the origins, mechanisms, and health consequences of obesity susceptibility genes and interaction with dietary macronutrients that predispose to childhood obesity. It is proposed that increased knowledge of these obesity susceptibility genes and interaction with dietary macronutrients will provide valuable insight for individual, family, and community preventative lifestyle intervention, and eventually targeted nutritional and medicinal therapies.     

蔗糖诱发Sprague—Dawley雄性大鼠肥胖病高脂血症

用蔗糖作辅助铁水,饲养刚离乳的Sprague－Dawley雄性大鼠,180天后,53％大鼠肥胖成为饮食诱发肥胖型大鼠（DIO大鼠）,47％大鼠不肥胖成为饮食诱发肥胖抵抗型大鼠（DIO－R大鼠）且DIO和DIO－R大鼠均具高脂血症。说明25％蔗糖可诱发Sprague-Dawley雄性大鼠肥胖病高脂血症,但同样条件下为什么部分大鼠不肥胖还有待于进一步研究。另外,对DIO大鼠的肥胖机制作了初步探讨。     

Genetics of Obesity: What have we Learned?

Candidate gene and genome-wide association studies have led to the discovery of nine loci involved in Mendelian forms of obesity and 58 loci contributing to polygenic obesity. These loci explain a small fraction of the heritability for obesity and many genes remain to be discovered. However, efforts in obesity gene identification greatly modified our understanding of this disorder. In this review, we propose an overlook of major lessons learned from 15 years of research in the field of genetics and obesity. We comment on the existence of the genetic continuum between monogenic and polygenic forms of obesity that pinpoints the role of genes involved in the central regulation of food intake and genetic predisposition to obesity. We explain how the identification of novel obesity predisposing genes has clarified unsuspected biological pathways involved in the control of energy balance that have helped to understand past human history and to explore causality in epidemiology. We provide evidence that obesity predisposing genes interact with the environment and influence the response to treatment relevant to disease prediction.     

The timing of the rise in U.S. obesity varies with measure of fatness

There are several ways to measure fatness and obesity, each with its own strengths and weaknesses. The primary measure for tracking the prevalence of obesity has historically been body mass index (BMI). This paper compares long-run trends in the prevalence of obesity when obesity is defined using skinfold thickness instead of BMI, using data from the full series of U.S. National Health Examination Surveys. The results indicate that when one uses skinfold thickness rather than BMI to define obesity, the rise in the prevalence of obesity is detectable 10-20 years earlier. This underscores the importance of examining multiple measures of fatness when monitoring or otherwise studying obesity.