Functional state of the β cell affects expression of both forms of glutamic acid decarboxylase
Hao, Wei ; Li, Linsong ; Mehta, Vivek ; Lernmark, Åke LU
and Palmer, Jerry P.
(1994)
In Pancreas
9(5).
p.558-562
- Abstract
Glutamic acid decarboxylase (GAD) is a candidate target autoantigen involved in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). The functional state of the B cells has been suggested to play a pathogenic role in IDDM by altering β-cell autoantigen expression. In this study, we investigated expression of GAD-65 and GAD-67 in isolated Sprague-Dawley rat islets cultured at different glucose concentrations. Using GAD isoform-specific antibodies in an immunoblot assay, we found that expression of both GAD-65 and GAD-67 in cultured islets was glucose dependent and that increased expression of both forms of GAD correlated with increased functional state of the β cell. Our data indicate that the functional state of the β cell... (More)
Glutamic acid decarboxylase (GAD) is a candidate target autoantigen involved in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). The functional state of the B cells has been suggested to play a pathogenic role in IDDM by altering β-cell autoantigen expression. In this study, we investigated expression of GAD-65 and GAD-67 in isolated Sprague-Dawley rat islets cultured at different glucose concentrations. Using GAD isoform-specific antibodies in an immunoblot assay, we found that expression of both GAD-65 and GAD-67 in cultured islets was glucose dependent and that increased expression of both forms of GAD correlated with increased functional state of the β cell. Our data indicate that the functional state of the β cell influences islet cell expression of GAD. Thus, decreasing islet cell expression of GAD by suppressing β cells activity may have a potential role in blunting the autoimmune destruction of pancreatic islet B cells.
(Less)
- author
- Hao, Wei
; Li, Linsong
; Mehta, Vivek
; Lernmark, Åke
LU
and Palmer, Jerry P.
- publishing date
- 1994-01-01
- type
- Contribution to journal
- publication status
- published
- keywords
- Glutamic acid decarboxylase, Insulin-dependent diabetes mellitus, β cell function
- in
- Pancreas
- volume
- 9
- issue
- 5
- pages
- 558 - 562
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- scopus:0028070978
- pmid:7809009
- ISSN
- 0885-3177
- DOI
- 10.1097/00006676-199409000-00003
- language
- English
- LU publication?
- no
- id
- 04e99312-0a9a-4072-b395-9757614cfe2b
- date added to LUP
- 2019-09-11 09:07:36
- date last changed
- 2024-03-13 08:08:25
@article{04e99312-0a9a-4072-b395-9757614cfe2b,
abstract = {{<p>Glutamic acid decarboxylase (GAD) is a candidate target autoantigen involved in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). The functional state of the B cells has been suggested to play a pathogenic role in IDDM by altering β-cell autoantigen expression. In this study, we investigated expression of GAD-65 and GAD-67 in isolated Sprague-Dawley rat islets cultured at different glucose concentrations. Using GAD isoform-specific antibodies in an immunoblot assay, we found that expression of both GAD-65 and GAD-67 in cultured islets was glucose dependent and that increased expression of both forms of GAD correlated with increased functional state of the β cell. Our data indicate that the functional state of the β cell influences islet cell expression of GAD. Thus, decreasing islet cell expression of GAD by suppressing β cells activity may have a potential role in blunting the autoimmune destruction of pancreatic islet B cells.</p>}},
author = {{Hao, Wei and Li, Linsong and Mehta, Vivek and Lernmark, Åke and Palmer, Jerry P.}},
issn = {{0885-3177}},
keywords = {{Glutamic acid decarboxylase; Insulin-dependent diabetes mellitus; β cell function}},
language = {{eng}},
month = {{01}},
number = {{5}},
pages = {{558--562}},
publisher = {{Lippincott Williams & Wilkins}},
series = {{Pancreas}},
title = {{Functional state of the β cell affects expression of both forms of glutamic acid decarboxylase}},
url = {{http://dx.doi.org/10.1097/00006676-199409000-00003}},
doi = {{10.1097/00006676-199409000-00003}},
volume = {{9}},
year = {{1994}},
}