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Glutamate decarboxylase 67 contributes to compensatory insulin secretion in aged pancreatic islets

Title
Glutamate decarboxylase 67 contributes to compensatory insulin secretion in aged pancreatic islets
Authors
Cho, Jung HoonLee, Kyeong-MinLee, Yun-IlNam, Hong GilJeon, Won Bae
DGIST Authors
Lee, Kyeong-MinLee, Yun-IlNam, Hong GilJeon, Won Bae
Issue Date
2019-03
Citation
Islets, 11(2), 33-43
Type
Article
Article Type
Article
Author Keywords
AgingGAD67insulin secretionpancreatic islets
Keywords
GAMMA-AMINOBUTYRIC-ACIDBETA-CELLS3-MERCAPTOPROPIONIC ACIDGENE-EXPRESSIONGLUCOSEGABARATTRANSCRIPTIONGADMICROVESICLES
ISSN
1938-2014
Abstract
Pancreatic islets play an essential role in regulating blood glucose levels. Age-dependent development of glucose intolerance and insulin resistance results in hyperglycemia, which in turn stimulates insulin synthesis and secretion from aged islets, to fulfill the increased demand for insulin. However, the mechanism underlying enhanced insulin secretion remains unknown. Glutamic acid decarboxylase 67 (GAD67) catalyzes the conversion of glutamate into γ-aminobutyric acid (GABA) and CO 2 . Both glutamate and GABA can affect islet function. Here, we investigated the role of GAD67 in insulin secretion in young (3 month old) and aged (24 month old) C57BL/6J male mice. Unlike young mice, aged mice displayed glucose-intolerance and insulin-resistance. However, aged mice secreted more insulin and showed lower fed blood glucose levels than young mice. GAD67 levels in primary islets increased with aging and in response to high glucose levels. Inhibition of GAD67 activity using a potent inhibitor of GAD, 3-mercaptopropionic acid, abrogated glucose-stimulated insulin secretion from a pancreatic β-cell line and from young and aged islets. Collectively, our results suggest that blood glucose levels regulate GAD67 expression, which contributes to β-cell responses to impaired glucose homeostasis caused by advanced aging. © 2019, © 2019 The Author(s). Published with license by Taylor & Francis Group, LLC.
URI
http://hdl.handle.net/20.500.11750/10055
DOI
10.1080/19382014.2019.1599708
Publisher
Taylor and Francis Inc.
Related Researcher
Files:
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Collection:
Department of New BiologyCBRG(Complex Biology Research Group)1. Journal Articles
Division of Biotechnology1. Journal Articles


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