运动与瘦素的研究进展

瘦素（ leptin）是脂肪组织分泌的一种蛋白质类激素,主要作用在下丘脑,具有调节体脂代谢、能量平衡等功能,瘦素水平的高低对肥胖、2-型糖尿病等疾病起到调节作用。血清瘦素可通过血脑屏障与下丘脑的瘦素受体结合,激活 JAK2-STAT3等信号转导通路,进而改变中枢神经系统中一系列神经肽的表达。通过收集大量近年来关于不同运动形式、运动强度、运动时间等情况对血浆瘦素水平影响的文献,总结分析出一次性运动、非一次性运动对血浆瘦素水平和能量代谢的影响,以及目前研究存在的问题,加深对瘦素功能和机理的分子水平认知,并展望了今后的研究前景。     

肥胖与减肥的分子生物学进展

肥胖已成为社会公共健康问题.随着细胞与分子生物学技术的发展和应用,ob基因、瘦素、瘦素受体及瘦素作用机制,解耦联蛋白分子及其解耦联作用机理,抵抗素基因、抵抗素分子及抵抗素的生物学效应等方面取得了重要进展,为运动减肥提供了新的科学理论依据.     

脂肪组织血管重塑及其与慢性炎症的相互作用

肥胖机体胰岛素抵抗会引起血管并发症已得到认同,但新近关于肥胖机体慢性炎症的研究发现,在出现胰岛素抵抗前脂肪组织脉管系统已发生功能障碍。本研究分析脂肪组织毛细血管发生变化与缺氧的关系和缺氧与慢性炎症的关系,认为肥胖机体脂肪组织毛细血管发生变化,引起脂肪组织缺氧;缺氧诱导慢性炎症,肥胖关联的炎症又引起脂肪组织血管重塑,加剧脂肪组织功能障碍和胰岛素抵抗;提出在肥胖者体内,脂肪组织血管重塑能够调控慢性炎症和全身胰岛素敏感性。     

脂肪组织功能紊乱与肥胖和糖尿病

脂肪组织是机体的重要器官,主要负责能量的储存和代谢,同时分泌多种激素和细胞因子,参与机体生理功能的调控。近年来的研究表明脂肪组织的功能紊乱与肥胖和糖尿病密切相关,为进一步探讨两者的关系,综述了脂肪组织的生理和内分泌功能以及脂肪组织功能紊乱与胰岛素抵抗、肥胖和糖尿病发生、发展的关系。     

肥胖低通气综合征患者血清瘦素水平的变化及意义

为了研究血清瘦素在肥胖低通气综合征(OHS)患者体内的变化及其意义,通过酶联免疫吸附测定(ELISA)法测定了所有受试者的血清瘦素水平,选取OHS组23例、肥胖OSA组40例、非肥胖OSA组14例、单纯肥胖组6例和正常对照组10例。比较所有受试者的一般资料、血清瘦素水平和多导睡眠参数,分析肥胖各组的血气分析结果。对瘦素与其他参数进行相关性分析,并分析其对OHS的诊断预测。结果表明OHS组BMI、颈围明显高于其他组。OHS组血清瘦素水平高于其他各组,且各组之间均存在明显差异(P 0.05)。血清瘦素水平与BMI、颈围、腰围、臀围、Pa CO_2、动脉血HCO_3~-呈正相关,与Pa O_2呈负相关。BMI、颈围、腰围和血清瘦素水平对OHS具有诊断预测作用。可见OHS组血清瘦素水平较肥胖OSA组、单纯肥胖组明显升高,除了肥胖因素外,OHS本身也可成为血清瘦素水平升高的原因,血清瘦素水平的升高可以作为OHS的诊断预测指标之一。     

多基因突变小鼠模型与动脉粥样硬化研究

目前己知人类有近 2 0 0 0 0种疾病 ,其发生与发展都与基因受损有着直接或间接的关系 ,其中相当一部分疾病的发病涉及到两个以上的基因功能异常。动脉粥样硬化 (AS)、肥胖、糖尿病、高血压等多基因疑难疾病是目前严重影响人类健康的重大疾病。在AS的发病过程中 ,血脂代谢异常是其重要原因之一。在载脂蛋白E(apoE)通过与低密度脂蛋白受体 (LDLR)和乳糜微粒受体的特异性结合 ,介导血浆脂蛋白的转运与清除 ,在脂质的代谢中起着非常重要的作用。瘦素受体 (OB R)在体内介导瘦素的信号传导 ,调节能量代谢与平衡与肥胖以及血脂代谢有关。通过…     

运动对肥胖大鼠胰岛素抵抗、血清瘦素及饮食量的影响

文章通过对肥胖大鼠进行10周的饮食监测以及游泳运动减肥,观察运动对肥胖大鼠饮食量和胰岛素抵抗、血清瘦素指标的影响。研究结果表明,一定时间的有规律运动不仅能对肥胖大鼠的饮食量产生一定的抑制作用,而且使得肥胖大鼠胰岛素抵抗指数和血清瘦素水平得到了有效降低。     

脂联素受体与2型糖尿病

脂联素（Adiponectin）是脂肪组织分泌的一种脂肪细胞因子,具有增加脂肪酸氧化、提高葡萄糖摄取量、改善胰岛素抵抗、调控血管内皮的炎症反应等作用。正常人血浆中脂联素浓度与体质量指数（BMI）、腰臀比、空腹血糖、空腹胰岛素、甘油三酯、尿酸和瘦素呈负相关。脂联素还与肥胖、胰岛素抵抗、2型糖尿病和心血管疾病密切相关。     

从中药获取新减肥药

<正>尽管医学不断取得新的突破,但至今仍未发现能够有效治疗肥胖的药物。20年前,瘦素的发现成为了治疗肥胖的最大希望,然而,机体对高浓度瘦素的抵抗作用,成为了瘦素治疗肥胖的巨大阻碍。2015年5月,美国哈佛大学的Urnut Ozcan团队于Cell上发表了一项新的研究。通过使用生物芯     

A PPARγ-FGF1 axis is required for adaptive adipose remodelling and metabolic homeostasis

Although feast and famine cycles illustrate that remodelling of adipose tissue in response to fluctuations in nutrient availability is essential for maintaining metabolic homeostasis, the underlying mechanisms remain poorly understood. Here we identify fibroblast growth factor 1 (FGF1) as a critical transducer in this process in mice, and link its regulation to the nuclear receptor PPARγ (peroxisome proliferator activated receptor γ), which is the adipocyte master regulator and the target of the thiazolidinedione class of insulin sensitizing drugs. FGF1 is the prototype of the 22-member FGF family of proteins and has been implicated in a range of physiological processes, including development, wound healing and cardiovascular changes. Surprisingly, FGF1 knockout mice display no significant phenotype under standard laboratory conditions. We show that FGF1 is highly induced in adipose tissue in response to a high-fat diet and that mice lacking FGF1 develop an aggressive diabetic phenotype coupled to aberrant adipose expansion when challenged with a high-fat diet. Further analysis of adipose depots in FGF1-deficient mice revealed multiple histopathologies in the vasculature network, an accentuated inflammatory response, aberrant adipocyte size distribution and ectopic expression of pancreatic lipases. On withdrawal of the high-fat diet, this inflamed adipose tissue fails to properly resolve, resulting in extensive fat necrosis. In terms of mechanisms, we show that adipose induction of FGF1 in the fed state is regulated by PPARγ acting through an evolutionarily conserved promoter proximal PPAR response element within the FGF1 gene. The discovery of a phenotype for the FGF1 knockout mouse establishes the PPARγ–FGF1 axis as critical for maintaining metabolic homeostasis and insulin sensitization.     

Macrophage-specific PPARgamma controls alternative activation and improves insulin resistance

Obesity and insulin resistance, the cardinal features of metabolic syndrome, are closely associated with a state of low-grade inflammation. In adipose tissue chronic overnutrition leads to macrophage infiltration, resulting in local inflammation that potentiates insulin resistance. For instance, transgenic expression of Mcp1 (also known as chemokine ligand 2, Ccl2) in adipose tissue increases macrophage infiltration, inflammation and insulin resistance. Conversely, disruption of Mcp1 or its receptor Ccr2 impairs migration of macrophages into adipose tissue, thereby lowering adipose tissue inflammation and improving insulin sensitivity. These findings together suggest a correlation between macrophage content in adipose tissue and insulin resistance. However, resident macrophages in tissues display tremendous heterogeneity in their activities and functions, primarily reflecting their local metabolic and immune microenvironment. While Mcp1 directs recruitment of pro-inflammatory classically activated macrophages to sites of tissue damage, resident macrophages, such as those present in the adipose tissue of lean mice, display the alternatively activated phenotype. Despite their higher capacity to repair tissue, the precise role of alternatively activated macrophages in obesity-induced insulin resistance remains unknown. Using mice with macrophage-specific deletion of the peroxisome proliferator activated receptor-gamma (PPARgamma), we show here that PPARgamma is required for maturation of alternatively activated macrophages. Disruption of PPARgamma in myeloid cells impairs alternative macrophage activation, and predisposes these animals to development of diet-induced obesity, insulin resistance, and glucose intolerance. Furthermore, gene expression profiling revealed that downregulation of oxidative phosphorylation gene expression in skeletal muscle and liver leads to decreased insulin sensitivity in these tissues. Together, our findings suggest that resident alternatively activated macrophages have a beneficial role in regulating nutrient homeostasis and suggest that macrophage polarization towards the alternative state might be a useful strategy for treating type 2 diabetes.     

Complete protein sequence and identification of structural domains of human apolipoprotein B

Epidemiological, pathological and genetic studies show a strong positive correlation between elevated plasma concentrations of low-density lipoprotein (LDL) cholesterol and the risk of premature coronary heart disease. Apolipoprotein (apo) B-100 is the sole protein component of LDL and is the ligand responsible for the receptor-mediated uptake and clearance of LDL from the circulation. Apo B-100 is made by the liver and is essential for the assembly of triglyceride-rich very low-density lipoproteins (VLDL) in the cisternae of the endoplasmic reticulum and for their secretion into the plasma. VLDL transports triglyceride to peripheral muscle and adipose tissue, where the triglyceride is hydrolysed by lipoprotein lipase. The resultant particle, relatively enriched in cholesteryl ester, constitutes LDL. LDL delivers cholesterol to peripheral tissues where it is used for membrane and steroid hormone biosynthesis and to the liver, the only organ which can catabolize and excrete cholesterol. Plasma LDL levels are therefore determined by the balance between their rate of production from VLDL and clearance by the hepatic LDL (apo B/E) receptor pathway. Here we report the complete 4,563-amino-acid sequence of apo B-100 precursor (relative molecular mass (Mr) 514,000 (514K] determined from complementary DNA clones. Numerous lipid-binding structures are distributed throughout the extraordinary length of apo B-100 and must underlie its special functions as a nucleus for lipoprotein assembly and maintenance of plasma lipoprotein integrity. A domain enriched in basic amino-acid residues has been identified as important for the cellular uptake of cholesterol by the LDL receptor pathway.     

心肌肥厚大鼠血管膜周脂肪组织对血管舒缩功能的影响

目的:观察正常大鼠及部分结扎腹主动脉致心肌肥厚大鼠的血管膜周脂肪组织对血管舒缩功能的影响。方法:手术部分结扎腹主动脉致心肌肥厚模型,采用血管张力记录法,观察正常大鼠及模型大鼠血管膜周脂肪组织对血管舒缩功能的影响。结果:对于正常大鼠,血管膜周脂肪组织可显著降低血管对苯肾上腺素的反应性;对于模型鼠,血管膜周脂肪组织可显著升高血管对苯肾上腺素的反应性。结论:血管膜周脂肪组织对于血管的舒缩功能有重要的调节作用。     

棕色脂肪组织银染实验

通过改进龙桂开银染方法对休眠期刺猬褐色脂肪组织进行染色实验,结果表明适当改进的龙桂开银染方法能够使褐色脂肪组织染出良好的效果,并在银染的休眠期刺猬褐色脂肪组织观察中发现,休眠期刺猬褐色脂肪组织细胞内有核仁,并多为1～4个,这与常规描述不一致。