Role of the gut Peptide glucose-induced insulinomimetic Peptide in energy balance.
Role of the gut Peptide glucose-induced insulinomimetic Peptide in energy balance.
复制标题
肠肽葡萄糖诱导的拟胰岛素肽在能量平衡中的作用
DOI：
10.1007/978-3-642-14426-4_15
复制
发表时间：
2010
影响因子：
--
通讯作者：
Isken F
中科院分区：
文献类型：
--
作者：
Pfeiffer AF1;Rudovich N;Weickert MO;Isken F
葡萄糖诱导的拟胰岛素肽（GIP）是由肠粘膜中的肠内分泌K细胞响应于脂肪、葡萄糖和蛋白质而产生的肠道激素。GIP从胰岛β细胞释放胰岛素，因此是一种肠促胰岛素激素。GIP作用于广泛分布于体内的G蛋白偶联受体，包括脂肪组织、胃、脑等。GIP受体（GIPR）的缺失使小鼠对高脂饮食诱导的体重增加具有抵抗力。我们观察到，雌性小鼠中卵巢切除诱导的体重增加通过GIPR缺失而被阻止，GIPR缺失与食物摄入减少和下丘脑中食欲神经递质表达减少有关。此外，给予高血糖指数饮食的老年雄性GIPR−/−小鼠保持了较高的胰岛素敏感性，并且比对照组活跃得多，这在年轻动物中没有观察到。因此，GIP增强了对营养素的反应，从而防止肥胖和胰岛素抵抗。然后，我们研究了人类对GIP治疗的急性反应，GIP的剂量模拟餐后血浆水平约为100 pmol/L。在基础葡萄糖下，GIP不引起胰岛素释放。使用Agilent全人类基因组测定分析在GIP处理4小时之前和之后采集的脂肪活检的转录组学应答。在通路分析中，炎症表达模式有高度显著的上调。
Glucose-induced insulinomimetic peptide (GIP) is a gut hormone produced by enteroendocrine K-cells in the intestinal mucosa in response to fat, glucose, and also protein. GIP releases insulin from the β cells of the pancreatic islets of Langerhans and therefore is an incretin hormone. GIP acts on a G-protein–coupled receptor that is widely distributed in the body including adipose tissue, stomach, brain, and others. Deletion of the GIP receptor (GIPR) renders mice resistant to weight gain induced by a high fat diet.We observed that weight gain induced by ovarectomy in female mice is prevented by GIPR deletion that is linked to reduced food intake and reduced hypothalamic expression of orectic neurotransmitters. Moreover, old male GIPR−/−mice placed on a high glycemic index diet maintained a high insulin sensitivity and were much more active than controls, which was not seen in young animals. Thus, GIP elicits central effects in response to nutrients that protect against obesity and insulin resistance. We then investigated the acute responses of humans to treatment with GIP over 4h in a dose mimicking postprandial plasma levels of about 100pmol/L. At basal glucose, GIP does not elicit insulin release. Fat biopsies taken before and after 4h of GIP treatment were analyzed for transcriptomic responses using Agilent whole human genome assays. There was a highly significant upregulation of an inflammatory expression pattern in a pathway analysis.
慢性阻塞性肺疾病骨骼肌中异常肌浆网 Ca2 隔离特性。
DOI：
--
发表时间：
2008
期刊：
American Journal of Physiology - Cell Physiology
影响因子：
--
作者：
H. Green;M. Burnett;Todd A. Duhamel;C. D’Arsigny;D. E. O'Donnell;K. Webb;Ouyang Jing
通讯作者：
Ouyang Jing
DOI：
10.1152/ajpendo.00515.2009
发表时间：
2010-02-01
影响因子：
5.1
作者：
Isken, F.;Klaus, S.;Weickert, M. O.
通讯作者：
Weickert, M. O.