Glycation May Cause Slower Insulin Releases than C-Peptides: A Theoretical Approach.

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Title:	Glycation May Cause Slower Insulin Releases than C-Peptides: A Theoretical Approach.
Authors:	(Chiu-Lan, Hsieh);(Chiung- Huei Peng);(Charng-Cherng Chayu);(Li-Yun Lin);彭瓊琦(Chiung-Chi Peng);(Kuan-Chou Chen);(Wen-Ta Chiu);(Robert Y. Peng);(Chien-Ning Huang)*
Contributors:	健康照護學院復健科學研究所
Keywords:	Glycation;Theoretical Approach;Peptide Fragments;Insulin Secretion;Report
Date:	2007
Issue Date:	2010-09-23 19:56:29 (UTC+8)
Abstract:	Based on Farah report, insulin can be glycated as monoglycation or diglycation product. Central sites for insulin glycation are B 1-13 and B 22-30 peptide fragment. Since glycation can alter the mobility of insulin molecule, we speculate that slower release of insulin than C-peptides may accordingly occur during insulin secretion by exocytosis of the vesicles. Here we theoretically propose some possibility combinations that insulin secretion can be dependent on many factors: Glycation status of insulin and cargo proteins; ageing process; deficiency of zinc ions; deficiency of calcium ions; the polymeric forms of insulin in vesicles; the ageing related stress with ROS production; the chronic psychological stress; the effect of environmental hormones; and finally the retrograde impairment of insulin release by insulin resistance.
Relation:	International Journal of Molecular Medicine and Advanced Sciences 3(3):108-117
Appears in Collections:	[Department of Physical Therapy, Graduate Institute of Rehabilitation Science] Journal articles

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