肥胖患者血清瘦素水平性别差异的临床分析

瘦素(leptin)是体内脂肪组织分泌的一种16KDa的血浆蛋白，1994年，美国洛克菲勒大学的Zhang等利用位点克隆技术成功地克隆了小鼠的肥胖基因(ob基因)，并阐明ob基因编码的蛋白质产物即瘦素的主要生理功能是抑制进食、增加代谢，从而使脂肪消耗，调节能量代谢和体重。本文探讨了瘦素分泌在肥胖患者中的性别差异。     

吡格列酮提高肥胖小鼠脂肪组织内脂素的基因表达

目的观察吡格列酮对营养性肥胖小鼠内脏脂肪和皮下脂肪组织内脂素基因表达的影响。方法高脂饮食喂养刚断乳雄性 c57BL/6小鼠8周,诱导出营养性肥胖模型。8周后,筛选肥胖小鼠,随机分为营养性肥胖组和吡格列酮治疗组[100 mg/(kg·d);治疗两周],普通饲料作为正常对照(正常体质量对照组),实时荧光定量RT-PCR 方法检测内脂素的基因表达。结果吡格列酮治疗组内脏脂肪量、腹部皮下脂肪量虽较正常体质量对照组增加(P<0.01),但较肥胖组降低(P<0.05)。以正常体质量组内脂素基因表达为1,吡格列酮治疗组内脏脂肪组织内脂素基因表达比正常体质量对照组和肥胖组明显升高(吡格列酮:7.6比肥胖组:4.8比正常体质量组:1,P<0.01),腹部皮下脂肪组织内脂素基因表达也比正常体质量对照组和肥胖组明显升高(吡格列酮:5.4比肥胖组:1.3比正常体质量组:1,P<0.01)。结论吡格列酮能够促进内脏脂肪与皮下脂肪的再分布,上调内脏脂肪组织和皮下脂肪组织内脂素的基因表达。     

瘦素、瘦素抵抗与阻塞型睡眠呼吸暂停综合征

瘦素是肥胖基因编码的蛋白产物,可调控体重和脂肪分布。阻塞型睡眠呼吸暂停综合征(OSAS)患者具有更多的颈部及内脏脂肪,这种脂肪选择性分布可能与瘦素、瘦素抵抗有关。     

瘦素的主要功能是什么

瘦素(leptin)又称脂肪抑制素(adipostatic hormon),是肥胖基因所编码的蛋白质,瘦素是由脂肪细胞所合成和分泌的一种激素。     

谈谈肥胖糖尿病临床方案的选择及临床操作

美国糖尿病协会(ADA)报告,约85％的肥胖患者患有2型糖尿病,在轻、中、重度肥胖者中发生糖尿病的危险性分别是正常体重的2.5、5和10倍.因此,对于肥胖糖尿病的治疗应兼顾减重和降糖.1肥胖和糖尿病的共同发病机制 "节约基因"可能决定了肥胖及其不良后果.在人类进化过程中,这类基因型通过保证过多热量如脂肪的有效储存而有...     

高脂血症人群血清瘦素水平与胰岛素敏感性的相关性分析

瘦素(Lep)是由肥胖基因编码、由脂肪细胞表达的蛋白激素，主要生理功能是调节脂肪沉积。有文献报道大多数成年人群中存在胰岛素抵抗(IR)。本研究旨在探索Lep是否与和肥胖密切相关的高脂血症和IR相关。     

单纯性肥胖患者脂蛋白脂酶基因多态性

目的 探讨脂蛋白脂酶(LPL)基因HindⅢ多态性与单纯性肥胖患者体脂分布、脂质代谢的关系。方法 采用PCR-RFLP对98例单纯性肥胖患者和51名正常对照组LPL基因第8内含子HindⅢ酶切位点进行多态性分析,并测定体脂分布指标与血脂水平。结果LPL HindⅢ位点在两组中均以H+等位基因为主。两组等位基因频率及基因型差异均无显著性,但肥胖组H+H+基因型者血浆甘油三酯水平明显增高、高密度脂蛋白胆固醇明显降低(P均<0.05),腰围、腹腔内脏脂肪面积也显著高于非H+H+基因型者(P<0.05)。结论LPL HindⅢ基因多态性对肥胖患者的血脂水平及脂肪分布有影响。具有HindⅢ酶切位点的H+等位基因可能是单纯性肥胖患者出现腹型肥胖和脂代谢紊乱的遗传易感因素之一。     

脂肪甘油三酯脂肪酶:一种新的脂肪分解基因

脂肪是人体重要的能量储存组织,脂肪组织的脂质代谢紊乱与高甘油三酯血症、2型糖尿病、肥胖密切相关.脂肪组织中脂肪代谢基因调控着脂肪生成和分解的平衡.以前脂肪生成基因研究很多,但是对脂肪分解基因的认识仅仅限于激素敏感性脂肪酶(hormone-sensitive lipase,HSL),随着2000年HSL敲除小鼠的诞生[1],发现它并无肥胖或仅有甘油二酯的沉积,说明应该有更重要的酶控制着脂肪的水解.     

瘦素与冠心病的关系及其机制的研究进展

瘦素 (Leptin)又称“消脂素” ,是肥胖基因 (ob)的产物 ,由哺乳动物体内的白色脂肪细胞分泌 ,在血液中有游离态、结合态两种存在形式 ,其血液浓度与机体脂肪含量成正比。瘦素分泌受到体脂含量、脂肪细胞大小的影响 ,随体内脂肪储存增加而增加。它将脂肪组织中能量储存状况的信息传递至神经中枢 ,使机体适当调整食欲 ,维持机体能量平衡 ,诱导体重下降。瘦素需要与特异的瘦素受体结合方能发挥生物学效应。瘦素及其受体基因发生突变可导致肥胖、不育和胰岛素抵抗等症状。瘦素与肥胖、胰岛素抵抗的密切关系已从大量研究中得到证实。以下就瘦素…     

固醇调节元件结合蛋白与脂代谢的基因调控

固醇调节元件结合蛋白(SREBPs)是脂肪合成基因重要的转录调节因子.SREBP-1a、-1c主要调节与脂肪酸代谢相关的酶,SREBP-2主要调控胆固醇代谢.SREBP-1c又称脂肪细胞定向和分化因子(ADD1),在脂肪细胞的分化中发挥重要作用.SREBPs还参与脂肪合成基因的营养调控,并受胰岛素/葡萄糖和瘦素调控,而且是代谢综合征中重要的基因调控连结点.对其调控作用进行全面深入的研究,将对糖尿病、肥胖等代谢综合征的发病机理和临床治疗有更新、更全面的认识.     

New aspects of the pharmacokinetics of ethanol

In the paper a survey on new results in the pharmacokinetics of ethanol is given. Resorption follows the rules of diffusion and is influenced by a lot of factors, this results in a high interindividual variation. Distribution is influenced by a first-pass-effect and the tissue contents of water. Metabolism is performed by alcohol dehydrogenase and microsomal ethanol oxidizing system. The kinetics of ADH is undependent on concentration, the MEOS is inducible. Results of acute and chronic ethanol treatment are discussed, clinical consequences are reviewed.     

Actinomycosis of the Colon: A Rare Form of Presentation

Actinomycosis is an uncommon entity, caused by an anaerobic bacterium, Actinomyces israelii, which is a component of the human oral and gastrointestinal flora. The cervicofacial region is the commonest site of disease, and the abdomen is the second commonest. In this situation the disease is almost always unifocal and restricted to the right colon, especially to the cecum. We report here the case of a patient with a very rare form of this entity, characterized by multiple foci of abdominal involvement with the most severe lesions localized in the transverse and sigmoid colon. The clinical presentation resembled a picture of colon perforation by cancer or diverticulitis, and the diagnosis was made by histopathologic examination of the lesions removed at surgery. No predisposing factor was found. The infection was successfully treated with a prolonged course of penicillin, after the surgical removal of the lesions.     

The economic aspects of the system of organizing antitubercular measures in Tomsk Province

To reduce the cost of detection, diagnosis, and hospital stay by reasonably decreasing bed-days, by developing microbiological methods for diagnosing the disease in a general hospital, by making a differential prophylactic fluorography is a requisite measure. The DOTS strategy used by primary health care staff by the world at large is an optimal way of distribution of limited resources. Its efficiency is confirmed by practice in Tomsk Province.     

新生血管动物模型的构建

新生血管是指从已有毛细血管发展形成新血管,该过程受血管生成因子和血管抑制因子双重调控,是一个动态平衡的过程。新生血管是多种疾病的病理性改变,包括肿瘤、早产儿视网膜病变和糖尿病视网膜病变等,是严重的致残性病变。建立新生血管动物模型是研究这些疾病发病机制的重要前提,本文主要对主动脉环血管生成模型、基质胶栓动物模型、氧诱导视网膜病变模型、激光诱导脉络膜新生血管动物模型4种建模方法进行了综述。     

Pathogenesis of Selective Expansion of PNH Clones

Hemolysis, a characteristic of paroxysmal nocturnal hemoglobinuria (PNH), is caused by the expansion of an affected stem cell with a mutation of the PIG-A gene. Increasing evidence has shown that the presence of the PIG-A mutation alone does not induce the expansion. Two theories have been proposed. One, the growth advantage hypothesis, is supported by current data indicating the presence of several intrinsic alterations that might confer a proliferative advantage to PNH clones over normal cells. Alternatively, the PIG-A mutation might confer a relative survival advantage to PNH clones. This theory is supported by clinical observation indicating that PIG-A mutant cells survive immune-mediated bone marrow injury in patients with aplastic anemia, PNH, and myelodysplastic syndromes. The latter theory is also supported by current experimental data indicating that PIG-A mutant cells are relatively resistant to cytotoxic attack by natural killer cells and cytotoxic T-lymphocytes. The 2 theories appear complementary rather than mutually exclusive. Rapid progress in this field can be expected in the near future.     

The role of bacteria in the pathogenesis of inflammatory bowel disease

Crohn's disease (CD) and ulcerative colitis (UC) have features that suggest bacterial involvement, and all genetic models of inflammatory bowel disease (IBD) require the presence of commensal bacteria. CD is associated with innate immune response genes such as NOD2/CARD15 and the autophagy genes ATG16L1 and IRGM. However, IBD responds to immunosuppression, suggesting that any bacteria involved are not acting as conventional pathogens. Molecular techniques are rapidly advancing our knowledge of the gut microbiota. In CD there is reduced diversity, and notably a reduction in the probiotic Faecalibacterium prausnitzii, the presence of which in the terminal ileum is associated with a reduced risk of recurrence following surgery. There is also a consistent increase in mucosa-associated Escherichia coli with an "adherent and invasive" phenotype, which allows them to replicate inside macrophages and induce granulomas. Speculation that CD could be caused by the Mycobacterium avium subspecies paratuberculosis (MAP) continues. The response to antitumor necrosis factor treatments suggests that, if relevant at all, MAP is not acting as a conventional pathogen. However, there is increased colonization by MAP in CD, and there is evidence that it could have an indirect effect mediated by the suppression of macrophage function. UC relapse is frequently associated with infection by pathogens, but there is less evidence for involvement of a specific bacterial species. Poor barrier integrity followed by an inflammatory reaction to bacterial components, with chronicity maintained by an autoimmune process, seems a plausible pathogenic model. Bacterial theories of pathogenesis are now becoming testable by targeted therapeutic interventions.     

Social exploitation of vitellogenin

Vitellogenin is a female-specific glucolipoprotein yolk precursor produced by all oviparous animals. Vitellogenin expression is under hormonal control, and the protein is generally synthesized directly before yolk deposition. In the honeybee (Apis mellifera), vitellogenin is not only synthesized by the reproductive queen, but also by the functionally sterile workers. In summer, the worker population consists of a hive bee group performing a multitude of tasks including nursing inside the nest, and a forager group specialized in collecting nectar, pollen, water, and propolis. Vitellogenin is synthesized in large quantities by hive bees. When hive bees develop into foragers, their juvenile hormone titers increase, and this causes cessation of their vitellogenin production. This inverse relationship between vitellogenin synthesis and juvenile hormone is opposite to the norm in insects, and the underlying proximate processes and life-history reasons are still not understood. Here we document an alternative use of vitellogenin by showing that it is a source for the proteinaceous royal jelly that is produced by the hive bees. Hive bees use the jelly to feed larvae, queen, workers, and drones. This finding suggests that the evolution of a brood-rearing worker class and a specialized forager class in an advanced eusocial insect society has been directed by an alternative utilization of yolk protein.     

Purification of testicular anti-Müllerian hormone allowing direct visualization of the pure glycoprotein and determination of yield and purification factor

An improved method is described for the purification of anti-Müllerian hormone from incubation medium of bovine fetal testes, using RIA to optimize the yield at different steps. Proteins present in incubation medium are precipitated by ammonium sulphate at 30–45% saturation and subjected to ion-exchange chromatography on DEAE-Sepharose. The bulk of the hormone is eluted from the ion-exchanger by a 0.12 M concentration of NaCl. Purification is achieved by immunochromatography on a monoclonal antibody: usually, addition of extraneous protein to the eluting buffer is required, but can be dispensed with if a second, cumulative, immunochromatography is performed by pooling the eluates from the first procedure. AMH obtained by this procedure has been studied using Coomassie blue and immunoblotting, and compared with fucose-labelled AMH, which is recognized by the same monoclonal antibodies as the carrier of the anti-Müllerian biological activity. In the absence of reducing conditions, several multimers, from 145 000 to 235 000 in molecular weight, are present. Reduction of disulphide bond linkages results in the disappearance of the multimeric forms, and the appearance of a 72000 monomer. Equivalence between RIA and weight units has been established in one experiment: one AMH unit corresponds to 15 μg of protein. Pure AMH isolated by this procedure is highly bioactive at a concentration of 200 mU/ml.     

Cholestasis of pregnancy

Cholestasis of pregnancy is the commonest liver disease unique to pregnancy and is characterized by pruritus in the mother in late pregnancy, without any skin rashes. This is accompanied by an elevation of the serum bile acids. Liver function test abnormalities may occur. Abdominal pain is not a feature and liver failure does not occur. The diagnosis is made by a suggestive history and exclusion of other causes by the history, serology and an upper abdominal ultrasound. All symptoms and signs should disappear within 4 weeks post-partum; prolonged post-partum courses should prompt a search for other causes, such as primary biliary cirrhosis. The syndrome is associated with a five-fold increased incidence of stillbirth, intra-partum foetal distress and pre-term labour. The reason is not clear and not predictable. The accepted management is induction or delivery at 38 weeks, which has led to a reduction in poor foetal outcome. Preliminary studies using ursodeoxycholic acid show symptomatic and biochemical improvement in most women treated. There is also a suggestion of an improved foetal outcome and treatment should be considered in women who present with the condition earlier in pregnancy.