猪脂肪细胞生脂及其调控研究进展

肥胖已成为严重威胁人类健康的流行病,猪作为研究肥胖及相关疾病的动物模型已引起人们的关注.通过介绍碳水化合物、蛋白质、激素等因素对猪脂肪生成的调控,期待为预防和治疗威胁人类健康的疾病提供有益的帮助.     

Extinction and Stationary Distribution of a Stochastic SIR Epidemic Model with Jumps

A stochastic susceptible-infective-recovered(SIR)epidemic model with jumps was considered.The contributions of this paper are as follows.(1) The stochastic differential equation(SDE)associated with the model has a unique global positive solution;(2) the results reveal that the solution of this epidemic model will be stochastically ultimately bounded,and the non-linear SDE admits a unique stationary distribution under certain parametric conditions;(3) the coefficients play an important role in the extinction of the diseases.     

Dynamics of fat cell turnover in humans

Obesity is increasing in an epidemic manner in most countries and constitutes a public health problem by enhancing the risk for cardiovascular disease and metabolic disorders such as type 2 diabetes. Owing to the increase in obesity, life expectancy may start to decrease in developed countries for the first time in recent history. The factors determining fat mass in adult humans are not fully understood, but increased lipid storage in already developed fat cells (adipocytes) is thought to be most important. Here we show that adipocyte number is a major determinant for the fat mass in adults. However, the number of fat cells stays constant in adulthood in lean and obese individuals, even after marked weight loss, indicating that the number of adipocytes is set during childhood and adolescence. To establish the dynamics within the stable population of adipocytes in adults, we have measured adipocyte turnover by analysing the integration of 14C derived from nuclear bomb tests in genomic DNA. Approximately 10% of fat cells are renewed annually at all adult ages and levels of body mass index. Neither adipocyte death nor generation rate is altered in early onset obesity, suggesting a tight regulation of fat cell number in this condition during adulthood. The high turnover of adipocytes establishes a new therapeutic target for pharmacological intervention in obesity.     

在脉冲免疫和脉冲隔离作用下的SIQR模型全局分析

本文讨论了在脉冲免疫和脉冲隔离作用下的SIQR模型．假定在每次免疫期有m次脉冲隔离发生，利用脉冲微分方程解的比较定理^[1]证明了无病周期解在一定条件下是全局渐近稳定的．     

A central role for JNK in obesity and insulin resistance

Obesity is closely associated with insulin resistance and establishes the leading risk factor for type 2 diabetes mellitus, yet the molecular mechanisms of this association are poorly understood. The c-Jun amino-terminal kinases (JNKs) can interfere with insulin action in cultured cells and are activated by inflammatory cytokines and free fatty acids, molecules that have been implicated in the development of type 2 diabetes. Here we show that JNK activity is abnormally elevated in obesity. Furthermore, an absence of JNK1 results in decreased adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signalling capacity in two different models of mouse obesity. Thus, JNK is a crucial mediator of obesity and insulin resistance and a potential target for therapeutics.     

Global and societal implications of the diabetes epidemic.

Changes in human behaviour and lifestyle over the last century have resulted in a dramatic increase in the incidence of diabetes worldwide. The epidemic is chiefly of type 2 diabetes and also the associated conditions known as 'diabesity' and 'metabolic syndrome'. In conjunction with genetic susceptibility, particularly in certain ethnic groups, type 2 diabetes is brought on by environmental and behavioural factors such as a sedentary lifestyle, overly rich nutrition and obesity. The prevention of diabetes and control of its micro- and macrovascular complications will require an integrated, international approach if we are to see significant reduction in the huge premature morbidity and mortality it causes.     

Central nervous system control of food intake and body weight

The capacity to adjust food intake in response to changing energy requirements is essential for survival. Recent progress has provided an insight into the molecular, cellular and behavioural mechanisms that link changes of body fat stores to adaptive adjustments of feeding behaviour. The physiological importance of this homeostatic control system is highlighted by the severe obesity that results from dysfunction of any of several of its key components. This new information provides a biological context within which to consider the global obesity epidemic and identifies numerous potential avenues for therapeutic intervention and future research.     

长期应用重组人睫状神经因子(rhCNTF)对谷氨酸钠肥胖大鼠血脂的影响

目的研究长期应用rhCNTF对谷氨酸钠(MSG)肥胖大鼠血脂的影响。方法建立MSG肥胖大鼠模型。3月龄时将肥胖动物随机分5组:分别皮下注射rhCNTF300μg·kg-1·d-1(高剂量组)、100μg·kg-1·d-1(中剂量组)、30μg·kg-1·d-1(低剂量组);西布曲明灌胃8 mg·kg-1·d-1(阳性对照组);模型组和对照组均给予生理盐水1 mL·kg-1·d-1,连续给药33 d。末次给药后24 h,同时动物禁食过夜后,在水合氯醛麻醉下测体重、身长,计算LI;断头后取腹部脂肪称重计算脂肪系数;腹主动脉取血离心后测血清总胆固醇、甘油三酯、高密度脂蛋白、血糖和血清胰岛素水平。结果(1)造模:正常大鼠189.40±38.72 g,谷氨酸钠肥胖大鼠平均体重(246.72±36.67)g,(P<0.001);LI(Lee’s指数)分别为289.27±9.05和304.42±9.64(P<0.001),说明造模成功。(2)药物实验结果高、中剂量给药组LI、脂肪系数、血总胆固醇、甘油三酯、血糖明显下降,高剂量组胰岛素水平也有所下降,达到统计学要求的显著性。结论rhCNTF30～300μg·kg-1·d-1皮下注射连续用药33 d,对谷氨酸钠肥胖大鼠具有明显的降脂作用,可能对Ⅱ型糖尿病肥胖有效。     

The hormone resistin links obesity to diabetes

Diabetes mellitus is a chronic disease that leads to complications including heart disease, stroke, kidney failure, blindness and nerve damage. Type 2 diabetes, characterized by target-tissue resistance to insulin, is epidemic in industrialized societies and is strongly associated with obesity; however, the mechanism by which increased adiposity causes insulin resistance is unclear. Here we show that adipocytes secrete a unique signalling molecule, which we have named resistin (for resistance to insulin). Circulating resistin levels are decreased by the anti-diabetic drug rosiglitazone, and increased in diet-induced and genetic forms of obesity. Administration of anti-resistin antibody improves blood sugar and insulin action in mice with diet-induced obesity. Moreover, treatment of normal mice with recombinant resistin impairs glucose tolerance and insulin action. Insulin-stimulated glucose uptake by adipocytes is enhanced by neutralization of resistin and is reduced by resistin treatment. Resistin is thus a hormone that potentially links obesity to diabetes.     

Abdominal obesity and metabolic syndrome

Metabolic syndrome is associated with abdominal obesity, blood lipid disorders, inflammation, insulin resistance or full-blown diabetes, and increased risk of developing cardiovascular disease. Proposed criteria for identifying patients with metabolic syndrome have contributed greatly to preventive medicine, but the value of metabolic syndrome as a scientific concept remains controversial. The presence of metabolic syndrome alone cannot predict global cardiovascular disease risk. But abdominal obesity - the most prevalent manifestation of metabolic syndrome - is a marker of 'dysfunctional adipose tissue', and is of central importance in clinical diagnosis. Better risk assessment algorithms are needed to quantify diabetes and cardiovascular disease risk on a global scale.     

An obesity-associated gut microbiome with increased capacity for energy harvest

The worldwide obesity epidemic is stimulating efforts to identify host and environmental factors that affect energy balance. Comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant bacterial divisions, the Bacteroidetes and the Firmicutes. Here we demonstrate through metagenomic and biochemical analyses that these changes affect the metabolic potential of the mouse gut microbiota. Our results indicate that the obese microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a significantly greater increase in total body fat than colonization with a 'lean microbiota'. These results identify the gut microbiota as an additional contributing factor to the pathophysiology of obesity.     

肥胖的机制与科学减肥

肥胖问题是严重影响人类生活的现代疾病.其病因极为复杂,涉及遗传、生理、生活方式等多种因素.肥胖可以导致众多的并发病症.控制肥胖的手段有多种选择,运动与合理的饮食是最安全、可行的方法.合理的运动可以有效地控制、调整身体成分,达到健康减肥的目的.综述了肥胖的机制及科学减肥的方法.     

减肥训练营的建立及其组织相关因素的分析

肥胖已被公认为一种全球性流行性疾病,减肥已经成为一种热潮,作为一种新型的体育产业,减肥训练营迎合了市场发展需求。运用文献资料、逻辑分析等研究方法,在审视当前减肥现状的基础上,从减肥训练营的概念入手,探讨其建立的可行性与必要性。并从科学锻炼与合理饮食两方面对减肥训练营的组织模式进行了探索,最后从教练团队、锻炼内容、锻炼方法、营销战略、服务质量等几个方面探析了其成功组织的相关影响因素,旨在为减肥训练营的开展提供可行性参考。     

考虑通信流量的复杂网络病毒传播研究

基于一维元胞自动机,考虑信息网络节点全局交互和网络通信流量不均衡的特点,提出新的susceptible -infected - susceptible (SIS)病毒传播模型,研究多种网络拓扑结构下病毒传播行为.研究表明,随着网络通信流量增大,病毒在不同拓扑结构网络中传播速度都明显加快,并在更短的时间内达到稳定的更高的感染规模.研究还发现,在考虑一定通信流量和路由协议下,病毒在节点度分布异质化程度较高的网络中最不易爆发.     

带病程的类年龄结构SIRS流行病模型的稳定性

建立了一类带病程的类年龄结构SIRS流行病模型,运用微积分方程理论和稳定性理论研究了该模型平衡点的稳定性,得到了无病平衡点的全局稳定性条件及特定条件下地方病平衡点的局部稳定性条件.     

单纯性肥胖的主要原因与运动减肥原理

单纯性肥胖是一种现代“     

具有饱和发生率的SIRS传染病模型的稳定性

研究了一类饱和发生率且各类都具有常数输入的SIRS型传染病模型,通过构造合适的Lyapunov函数,在一定条件下得到了模型地方病平衡点的全局渐近稳定性。     

一类基于心理作用的SIRS传染病模型

根据传染病动力学原理建立一类基于心理作用的SIRS传染病模型. 先通过构造Lyapunov函数, 利用常微分方程稳定性和极限系统理论, 分别获得该模型在无病平衡点和地方病平衡点全局渐近稳定性的充分条件, 再通过数值仿真验证所得结论. 数值模拟结果表明, 心理作用的积极影响在一定程度上能控制传染病的传播与流行.     

基于颜色分块全局直方图的图像检索方法及系统实现

通过比较全局颜色直方图和分块颜色直方图, 提出一种分块全局直方图的检索方法. 该方法以分块直方图的特征为基础, 在检索时, 由用户为含有重要空间信息的分块设置权值, 并将不注重空间信息的分块权值设为零. 系统将权值为零的分块重新合并为部分全局直方图, 计算所有权值非零分块的距离及部分全局直方图的距离, 再按照用户给出的权值进行加权累加作为两幅图像之间的最终距离. 结果表明, 两幅图像间 的距离越小, 则视觉差异也越小. 同时, 引入相关反馈技术以改善检索效果.