کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10771967 1050846 2005 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Lysophosphatidylcholine enhances glucose-dependent insulin secretion via an orphan G-protein-coupled receptor
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Lysophosphatidylcholine enhances glucose-dependent insulin secretion via an orphan G-protein-coupled receptor
چکیده انگلیسی
A lysophospholipid series, such as lysophosphatidic acid, lysophosphatidylserine, and lysophosphatidylcholine (LPC), is a bioactive lipid mediator with diverse physiological and pathological functions. LPC has been reported to induce insulin secretion from pancreatic β-cells, however, the precise mechanism has remained elusive to date. Here we show that an orphan G-protein-coupled receptor GPR119 plays a pivotal role in this event. LPC potently enhances insulin secretion in response to high concentrations of glucose in the perfused rat pancreas via stimulation of adenylate cyclase, and dose-dependently induces intracellular cAMP accumulation and insulin secretion in a mouse pancreatic β-cell line, NIT-1 cells. The Gs-protein-coupled receptor for LPC was identified as GPR119, which is predominantly expressed in the pancreas. GPR119-specific siRNA significantly blocked LPC-induced insulin secretion from NIT-1 cells. Our findings suggest that GPR119, which is a novel endogenous receptor for LPC, is involved in insulin secretion from β-cells, and is a potential target for anti-diabetic drug development.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 326, Issue 4, 28 January 2005, Pages 744-751
نویسندگان
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