دانلود رایگان مقاله لاتین لیپید و مولکول مصنوعی از سایت الزویر
عنوان فارسی مقاله:
سیگنالینگ مغرضانه لیپیدها و اقدامات آلوستریک مولکول های مصنوعی برای GPR119
عنوان انگلیسی مقاله:
Biased signaling of lipids and allosteric actions of synthetic molecules for GPR119
سال انتشار : 2016
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مقدمه انگلیسی مقاله:
1. Introduction
The number of people suffering from type 2 diabetes mellitus (T2DM) has escalated worldwide as a consequence of unhealthy lifestyle and obesity [1]. T2DM is characterized by insulinresistance, decreased insulin secretion from the pancreatic b-cells and loss of intestinal glucagon-like-peptide (GLP)-1 release in response to diet; deficits that are even more pronounced in obese individuals [2]. The G protein-coupled receptor (GPR) 119 acts as a lipid-sensor in the gut, where it induces the release of incretin hormones, GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) from the intestinal L and K-cells, respectively, in response to dietary lipids [3–6]. Besides its expression in intestinal enteroendocrine cells (EEC), GPR119 is also expressed in pancreatic b-cells,where it leads to insulin secretion in a glucose-dependent manner [7–9]. GPR119 in pancreas may possibly be stimulated by 2-monoacylglycerol (MAG) generated by lipoprotein lipase [10]. GPR119 couples to Gas with high constitutive activity and in response to lipid-based agonists like lysophosphatidylcholines (LPCs), oleic-acid containing N-acyl-amino compounds like N-oleoyldopamine (OLDA) and N-acylethanolamines (NAEs) [3,8,9,11–14]. Of these, the oleic-acid containing OEA is the most potent lipid-based GPR119 agonist [3]. It stimulates cAMP accumulation in GPR119 transfected cells with high potency (EC50 of 0.2–2.9 lM) [3,12] and releases GLP-1 in vitro from GLUTag-cells, an EEC cell-line with endogenous GPR119 expression, and in vivo after intraluminal injection in mice [15]. Monoacylglycerols (MAGs) such as 2-oleoyl glycerol (2-OG), which is generated in high amounts during digestion of the diet, also activate GPR119 as shown in recent in vivo studies in humans, where ingested 2-OG stimulated GLP-1 release [3,4]. Similar experiments in wild type and GPR119-deficient mice proved that the GLP-1 secretion induced by 2-OG (and the more stable ether analog of 2-OG) indeed is mediated via GPR119 activation [5]
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کلمات کلیدی:
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