炎症转录因子C/EBPβ在间质细胞分化中作用与机制

免疫炎症性转录因子C/EBPβ在多种细胞的分化过程中起着重要作用.如在间充质细胞中,决定着间充质干细胞(MSCs)的分化方向,诱导脂肪细胞的分化,调节成骨细胞和软骨细胞分化.了解C/EBPβ及其不同亚型的在不同的间充质细胞中的作用,尤其是在成纤维细胞、脂肪细胞、软骨细胞和成骨细胞分化过程中的调控机制很有必要,随着间充质干细胞被再生医学重视,转录因子C/EBPβ有望成为未来研究的热点.     

Rosiglitazone balances insulin-induced exo- and endocytosis in single 3T3-L1 adipocytes

Rosiglitazone (Rosi) improves insulin sensitivity and increases the translocation of glucose transporter 4 (GLUT4) to the plasma membrane (PM). This involves the fusion of membrane-bound compartments with the plasma membrane, thus increasing the plasma membrane area. However, recent work has shown that in Rosi-pretreated 3T3-L1 adipocytes membrane area did not increase following insulin application, suggesting that the rates of exo- and endocytosis are balanced. Here we examined whether Rosi differentially affects the rates of exo- and endocytosis in 3T3-L1 adipocytes. The immunolabelling of GLUT4 revealed the 3.1-fold increase in PM-resident GLUT4 in Rosi-pretreated, insulin-stimulated cells. By monitoring cumulative exocytosis and endocytosis we found that in Rosi-pretreated cells insulin substantially stimulated the rate of exocytosis and to a similar extent also the rate of endocytosis. We conclude that Rosi-pretreatment balances insulin-stimulated exocytosis and endocytosis, which may prevent insulin-mediated adipocyte cell size increase.     

脂肪细胞线粒体功能与肥胖

线粒体主要存在于能量需求高、代谢强的组织,被认为是细胞的"动力工厂",为细胞的代谢活动提供能量.肥胖的发生主要是脂质积聚过多,而脂肪细胞线粒体是脂肪酸β氧化的场所之一,脂肪细胞线粒体的脂肪酸氧化功能对于维持脂肪细胞内甘油三酯代谢有重要作用,其功能失调与肥胖的关系成为新的研究热点.

Abstract：

Mitochondria are usually described as the "powerhouse unit" of the cell, which exist in tissues with a high energy demand and a high metabolic activity, and provide energy for the metabolic activity of cell. More lipid accumulation can lead to obesity. Mitochondria are the main sites of fatty acid β oxidization which are very important to adipocyte triglyceride metabolism. The relationship between mitochondrial dysfunction and obestiy has become the new research derection.     

骨关节炎患者髌下脂肪垫前脂肪细胞成脂诱导模型的建立

目的 观察骨关节炎患者髌下脂肪垫前脂肪细胞的原代培养及成脂诱导过程.方法 采用酶消化法分离得到前脂肪细胞,进行细胞形态学观察、CCK-8法测定生长曲线;成脂诱导过程中,油红O染色方法鉴定脂肪细胞、酶联免疫吸附法测定细胞上清脂联素.结果 原代培养的前脂肪细胞呈梭形,与成纤维细胞类似.成脂诱导第3天胞质内出现反光脂质小滴,第21天80%以上的前脂肪细胞可分化为脂肪细胞.细胞上清脂联素随脂肪细胞数量的增多而升高,3周时达到稳定,证实成脂诱导的细胞为功能活跃的脂肪细胞.结论 成功建立了骨关节炎患者髌下脂肪垫前脂肪细胞的原代培养及成脂诱导方法,为研究髌下脂肪垫的内分泌代谢功能及其在骨关节炎发病机制中的作用提供较为理想的细胞模型.

Abstract：

Objective To investigate the primary culture and adipogenic process of pre-adipocytes from infrapatellar fat pad of osteoarthritic patients. Methods The pre-adipocytes were isolated by enzymatic digestion. The morphological changes of cultured cells were observed and the growth curve was drawn by CCK-8 method. During the adipogenic process, the intracytoplasmic lipid of differentiated cells was determined by oil red O staining. And the adiponectin levels in the culture supernatants were measured by ELISA (enzyme-linked immunosorbent assay). Results The primary cultured fibroblast-like cells were spindle-shaped. In the process of adipogenesis, the intracytoplasmic lipid droplets were observed at Day 3and over 80% of the cells differentiated into adipocytes at Day 21. With the increasing number of adipocytes, the adiponectin levels in the culture supemant elevated and peaked at Week 3. The differentiated cells were proven to be adipocytes functioning actively. Conclusion The primary culture and adipogenic process of pre-adipocytes in infrapatellar fat pad of osteoarthritic patients has been successfully established. Thus it may provide an ideal model for the study of endocrine function of infrapatellar fat pad and understanding its role in the pathogenesis of osteoarthritis.     

Constitutively active Stat5A and Stat5B promote adipogenesis

Objective  

The metabolic syndrome is an important social problem affecting many people in developed countries. Obesity is a leading cause of this syndrome, hence understanding molecular mechanisms underlying obesity is of prime importance for preventive medicine to develop novel methods to alleviate the corresponding social cost as well as for pharmaceutical companies to develop antimetabolic drugs.     

一种新的脂肪细胞源性血管舒张因子

血压调节的研究多年来经过许多变革,最初的工作多集中在各种具有血管活性的神经、内分泌因子及其受体、受体亚型上。上世纪80年代起,随着人们发现内皮源性的一氧化氮可扩张血管,便开始将研究兴趣转向血管内皮的调节作用。此间,研究者并未重视血管外周组织可能具有分泌功能,研究     

单纯性肥胖儿童和非肥胖儿童脂肪细胞基础凋亡率的研究

目的　探讨单纯性肥胖儿童和非肥胖儿童脂肪细胞的基础凋亡状况及其相关因素。方法　应用DNA原位末端标记技术 (terminaldeoxynucleotidyltransferase mediateddUTPnickendlabeling,TUNEL)检测 15例单纯性肥胖儿童 (男 11例 ,女 4例 )和 15例非肥胖儿童 (男 9例 ,女 6例 )腹壁皮下脂肪细胞的基础凋亡状况 ,计算凋亡指数 (apoptosisindex,AI)并进行对比和相关性分析。结果　单纯性肥胖儿童和非肥胖儿童腹壁皮下脂肪细胞存在很低的凋亡率 ,肥胖组AI为 (0 2 3± 0 18) % ,非肥胖组为 (0 6 5± 0 5 9) %。单纯性肥胖儿童脂肪细胞的凋亡率明显低于非肥胖儿童 (P <0 0 2 ) ;儿童腹壁皮下脂肪细胞的AI与体块指数 (bodymassindex ,BMI)、体脂百分数 (percentbodyfat,BF % )和体脂含量(fatmass,FM)呈负相关 ,与性别和年龄则无明显相关性。结论　儿童腹壁皮下脂肪细胞的AI与BMI和FM呈负相关 ,单纯肥胖儿童脂肪细胞的凋亡率明显低于非肥胖儿童 ,这种异常有可能参与了肥胖症的发生过程     

Effects of interferon alpha on insulin binding and glucose transport in human adipocytes

We have previously demonstrated that interferon administration impairs glucose tolerance and causes insulin resistance in healthy man. Whether this is a direct effect of interferon is not known. The present study was undertaken to examine directly the effect of interferon alpha on insulin binding and action on glucose transport in isolated human adipocytes. Different concentrations of interferon alpha (range 10(-3)-10(5) IU ml-1) and different incubation times (0-5-24 h) with interferon were employed. Acute and 5-h and 24-h exposure of human adipocytes to 10(-2)-10 IU ml-1 of interferon increased the high affinity binding of 125I-insulin (P less than 0.05). In contrast, human interferon alpha had no effect on insulin binding in rat adipocytes. In short-term studies interferon had no effect on 14C-glucose transport clearance. 24-h preincubation of human adipocytes with 10(-2), 10, 10(4) IU ml-1 interferon increased maximally-insulin stimulated 14C-glucose transport clearance (P less than 0.05) and glucose transport responsiveness to insulin was enhanced by 24% (P less than 0.05) in cells exposed to 10(-2) IU ml-1 interferon. After 5 and 24-h preincubations with interferon we observed modest changes in glucose transport sensitivity to moderate concentrations of insulin (50-100 pM) with upregulation in the presence of 10(-2)-10 IU ml-1 interferon and downregulation in the presence of 10(4)-10(5) IUm ml-1 interferon (P less than 0.05). The insulin sensitivity index (ED50) did not change.(ABSTRACT TRUNCATED AT 250 WORDS)     

Differentiation with elaidate tends to impair insulin-dependent glucose uptake and GLUT4 translocation in 3T3-L1 adipocytes

Development of type 2 diabetes mellitus and insulin resistance is associated with a quality of dietary fatty acids such as saturated and unsaturated fatty acids. Dietary fatty acids also include transform of unsaturated fatty acids and intake of transform of oleate (elaidate) is associated with cardiovascular disease. However, little is known about the roles of elaidate in insulin responsiveness. We show here that elaidate impairs insulin-dependent glucose uptake in adipocytes. Differentiation with 10?μM elaidate, which is close to physiological plasma concentration, reduces insulin-dependent glucose uptake. Furthermore, insulin-dependent GLUT4 translocation is disturbed in adipocytes differentiated with elaidate. In addition, analysis of lipolysis and gene expression shows that deteriorative effects of elaidate on insulin responsiveness are limited but not general. Thus, our findings reveal that differentiation with elaidate tends to affect insulin-dependent glucose uptake through alternation of GLUT4 translocation from cytosol to the plasma membrane.