Ghrelin与肥胖和胰岛素抵抗的关系

Ghrelin是一种新型的脑-肠肽,具有促进生长激素分泌,增进食欲,参与调节能量平衡,引起肥胖的作用.它主要通过促进食欲、加快胃排空、降低机体基础代谢率、增加呼吸商等途径引起正能量平衡,导致肥胖.此外,ghrelin水平在餐前上升,餐后下降,这种对进食起始和结束的潜在作用与胰岛素的分泌节律恰好相反.空腹ghrelin水平和口服葡萄糖耐量试验中ghrelin的抑制均受胰岛素敏感性的调节.Ghrelin与胰岛素抵抗两者的确切关系尚有待进一步研究.     

ghrelin影响机体肥胖和能量平衡的作用及其调节机制

ghrelin是生长激素促分泌素受体的内源性天然配基。ghrelin不仅是生长激素的强烈的促分泌剂,而且与机体的能量摄取、葡萄糖、胰岛素、胰岛素抵抗之间存在联系;ghrelin还对甾体生成及性腺功能有调控作用。进一步探讨ghrelin的作用对研究人体的热量摄取、肥胖、胰岛素抵抗及其与生长激素的联系有指导意义。     

小于胎龄儿新生儿期ghrelin水平与生长轴关系的研究

目的通过比较小于胎龄儿（SGA）与适于胎龄儿（AGA）新生儿早期血ghrelin水平和代谢促生长轴各因素的差别和相关性,探索ghrelin在SGA发病机制中的作用。方法通过配对对17例SGA和17例AGA的血清ghrelin、IGF-1、生长激素、胰岛素、血糖浓度进行比较并分析其差异的意义。结果与AGA组相比,SGA组血ghrelin水平显著升高（P〈0．05）,血IGF-1、胰岛素水平显著下降（P〈0．05）,血生长激素和血糖水平差异无统计学意义。结论与AGA相比,SGA新生儿有高ghrelin血症。SGA新生儿的高血ghrenlin水平伴随其低下的出生体重、身长、血IGF-1、胰岛素水平,在一定程度上反映了其宫内营养不良状况。ghrelin作为胰岛素的反调节激素,SGA的ghrelin高分泌可能是宫内能量负平衡所致低胰岛素、低IGF-1状态反馈和／或重整性调控的结果。     

Ghrelin与肥胖

肥胖已成为当今社会普遍存在的严重医学问题.Ghrelin是新发现的一种脑肠肽,是生长激素促分泌素受体的内源性配体,具有强烈的刺激生长激素分泌、刺激摄食、维持能量正平衡、减少脂肪利用、促进胃酸分泌等作用, ghrelin的这些作用与肥胖的发生和发展密切相关.该文主要讨论ghrelin在肥胖发生中的作用机制.     

肥胖儿童糖负荷时ghrelin的动态变化

为进一步了解脑肠肽——ghrelin在肥胖儿童胰岛素抵抗发病机制中的作用和意义,2005年7—9月,我们测定了肥胖儿童口服糖耐量试验后ghrelin的变化,对肥胖儿童和正常对照儿童空腹ghrelin进行了比较,并分析了糖耐量试验中血糖、胰岛素和ghrelin之间的相关性。     

resistin与胰岛素抵抗的研究进展

肥胖可引起胰岛素抵抗和2型糖尿病,但其确切机制尚不清楚。新近发现小鼠白色脂肪组织可特异分泌一种富含半胱氨酸的蛋白质,被认为是小鼠肥胖与胰岛素抵抗的重要中间环节,称为胰岛素抵抗因子（resistin）。小鼠resistin的基因定位于第8对染色体上,resistin仅在小鼠的白色脂肪组织中有高度表达,属于富含半胱氨酸的分泌型蛋白RELMs（resistin-like molecules）家族,其水平在由3T3-L1细胞向成熟脂肪细胞转化的过程中显著增高,并与胰岛素抵抗有紧密的联系。地塞米松能促进resistin基因表达,而异丙肾上腺素与肿瘤坏死因子α则能抑制其表达。在人类脂肪细胞表达的resistin同源物,基因定位在第19对染色体,其组织分布与作用尚有待进一步研究。本文介绍了胰岛素抵抗因resistin的发现过程、其家族特点、与胰岛素抵抗及其调节因子的关系等。     

resistin与胰岛素抵抗的研究进展

肥胖可引起胰岛素抵抗和2型糖尿病，但其确切机制尚不清楚。新近发现小鼠白色脂肪组织可特异分泌一种富含半胱氨酸的蛋白质，被认为是小鼠肥胖与胰岛素抵抗的重要中间五，称为胰岛素抵抗因子（resistin)。小鼠resistin的基因定位于第8对染色体上，resistin仅在小鼠的白色脂肪组织中有高度表达，属于富含半胱氨酸的分泌型蛋白RELMs(resistin-like molecules)家族，其水平在由3T3－L1细胞向成熟脂肪细胞转化的过程中显著增高，并与胰岛素抵抗有紧密的联系。地塞米松能促进resistin基因表达，而异丙肾上腺素与肿瘤坏死因子α则能抑制其表达。在人类脂肪细胞表达的resistin同源物，基因定位在第19对染色体，其组织分布与作用尚有待进一步研究。本文介绍了胰岛素抵抗因resistin的发现过程、其家族特点、与胰岛素抵抗及其调节因子的关系等。     

Ghrelin对3T3-L1前脂肪细胞增殖和分化的影响及相关机制探讨

目的：探讨ghrelin对3T3-L1前脂肪细胞增殖和分化的影响及作用机制。方法：体外培养3T3-L1前脂肪细胞,MTT法检测不同浓度ghrelin对其增殖活力的影响,半定量RT-PCR检测ghrelin对c-myc和胸苷激酶mRNA表达水平的影响;同时在利用胰岛素或ghrelin诱导分化的不同时段,通过油红O染色测定细胞分化程度,半定量RT-PCR检测过氧化物体增殖剂活化受体γ（PPARγ）、CAAT/增强子结合蛋白α（C/EBPα）mRNA的表达。结果：10-7~10-15 mol/L ghrelin作用24 h明显促进前脂肪细胞增殖,ghrelin组c-myc和胸苷激酶mRNA表达水平明显升高,与对照组相比差异均有显著性意义（P<0.05）。Ghrelin干预后,可诱导前脂肪细胞向成熟脂肪细胞的形态转变,但诱导分化率仍少于胰岛素;同时其PPARγ和C/EBPα mRNA表达水平较对照组明显升高（P<0.05）,ghrelin组和胰岛素组PPARγ和C/EBPα mRNA表达量随着分化时间的延长而增加,分化8 d与2 d相比,差异均有显著性意义（P<0.01）。结论：Ghrelin明显促进3T3-L1前脂肪细胞增殖与分化。Ghrelin可能通过增加c-myc的含量,进而引起胸苷激酶的活化,从而导致细胞周期的激活,促进细胞增殖;同时ghrelin可能通过增加PPAR-γ、C/EBP-α mRNA的表达,促进细胞分化,从而提高脂肪细胞对胰岛素的敏感性。［中国当代儿科杂志,2009,11（1）：69-73］     

抵抗素的研究进展

肥胖可以引起胰岛素抵抗 ,然而 ,其确切机制还不清楚。几年前 ,有研究发现 :脂肪细胞分泌一种独特的信号分子———抵抗素 ,它有拮抗胰岛素的作用。所以 ,当时认为抵抗素可能是肥胖引起胰岛素抵抗的关键所在。但是 ,随着研究的深入 ,越来越多的实验对此提出异议 ,认为抵抗素并不是肥胖引起胰岛素抵抗的一种主要激素。关于抵抗素的研究正进一步的展开     

抵抗素的研究进展

肥胖可以引起胰岛素抵抗，然而，其确切机制还不清楚。几年前，有研究发现：脂肪细胞分泌一种独特的信号分子——抵抗素，它有拮抗胰岛素的作用。所以，当时认为抵抗素可能是肥胖引起胰岛素抵抗的关键所在。但是，随着研究的深入，越来越多的实验对此提出异议，认为抵抗素并不是肥胖引起胰岛素抵抗的一种主要激素。关于抵抗素的研究正进一步的展开。     

Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene

OBJECTIVES: Polychlorinated biphenyls (PCBs) and dichlorodiphenyl dichloroethene (DDE) are ubiquitous toxic environmental contaminants. Prenatal and early life exposures affect pubertal events in experimental animals. We studied whether prenatal or lactational exposures to background levels of PCBs or DDE were associated with altered pubertal growth and development in humans.Study design: Follow-up of 594 children from an existing North Carolina cohort whose prenatal and lactational exposures had previously been measured. Height, weight, and stage of pubertal development were assessed through annual mail questionnaires. RESULTS: Height of boys at puberty increased with transplacental exposure to DDE, as did weight adjusted for height; adjusted means for those with the highest exposures (maternal concentration 4+ ppm fat) were 6.3 cm taller and 6.9 kg larger than those with the lowest (0 to 1 ppm). There was no effect on the ages at which pubertal stages were attained. Lactational exposures to DDE had no apparent effects; neither did transplacental or lactational exposure to PCBs. Girls with the highest transplacental PCB exposures were heavier for their heights than other girls by 5.4 kg, but differences were significant only if the analysis was restricted to white girls. CONCLUSIONS: Prenatal exposures at background levels may affect body size at puberty.     

Prevention and treatment of overweight and obesity in children and adolescents

Increasing numbers of obese children and adolescents all over the world demand an investment in the primary and secondary prevention of obesity and overweight in this age group. The goal of preventive measures in children is to avoid the negative short- and long-term health problems associated with obesity. Primary prevention aims at establishing a healthy, active lifestyle and keeping children and adolescents within a range of body weight which is considered to be healthy. Constant availability and affordability of palatable and energy-dense food in the affluent society of the western world demands preventive strategies. Universal or public health prevention seems to be the most suitable form because several other cofactors of morbidity and mortality of affluent societies can also be prevented. However, in most European countries there is a lack of awareness of the necessity of prevention programmes, not only among the general population but also among the medical society. More awareness and consciousness to the problem of obesity must be generated in order to lead to effective therapeutic programmes. For those children and adolescents who are already obese, secondary prevention is mandatory. Therapeutic intervention programmes for the obese aim at long-term weight maintenance and normalisation of body weight and body fat. They have to modify eating and exercise behaviour of the obese child and establish new, healthier behaviour and lifestyle. Treatments programmes must include behavioural components in order to permanently change nutrition and physical exercise of the obese children and adolescents. However, long-term results of treatment programmes in European countries are scarce and the reported results, even of multidisciplinary regimens, are not impressive. Conclusion In most European countries there is an urgent need not only for a growing awareness of the problem of obesity in children and adolescents but also for development of new comprehensive approaches in treating this group.     

Hypokalemia and Hyperkalemia in Infants and Children: Pathophysiology and Treatment

Potassium is the second most abundant cation in the body. About 98% of potassium is intracellular and that is particularly in the skeletal muscle. Electrical disturbances associated with disorders of potassium homeostasis are a function of both the extracellular and intracellular potassium concentrations. Clinical disorders of potassium homeostasis occur with some regularity, especially in hospitalized patients receiving many medications. This article will review the pathophysiology of potassium homeostasis, symptoms, causes, and treatment of hypo- and hyperkalemia.