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Glutamate decarboxylase antibody levels predict rate of β-cell decline in adult-onset diabetes

Gottsäter, A. LU ; Landin-Olsson, M. LU ; Lernmark, Å LU orcid ; Fernlund, P. LU ; Sundkvist, G. LU and Hagopian, W. A. (1995) In Diabetes Research and Clinical Practice 27(2). p.133-140
Abstract

Glutamate decarboxylase autoantibodies (GAD65Ab) and β-cell function were evaluated at and 3 years after diabetes onset in consecutive subjects over 15 years of age. At onset, 21 32 (66%) insulin-treated patients (mean age 43, range 16-79 years) had GAD65Ab; all GAD65Ab persisted 3 years later. At onset, 20 82 (24%) non-insulin-treated patients (mean age 56, range 20-79 years) had GAD65Ab. Of those with persistent GAD65Ab, 8 non-insulin-treated and 11 insulin-treated patients consented to follow-up glucose and glucagon stimulation tests. For non-insulin-treated patients, quantitative GAD65Ab index at onset correlated inversely with 1+3 min C-peptide response to glucose (r = -0.68, P < 0.05) and to glucagon (r = -0.79, P < 0.05) 3... (More)

Glutamate decarboxylase autoantibodies (GAD65Ab) and β-cell function were evaluated at and 3 years after diabetes onset in consecutive subjects over 15 years of age. At onset, 21 32 (66%) insulin-treated patients (mean age 43, range 16-79 years) had GAD65Ab; all GAD65Ab persisted 3 years later. At onset, 20 82 (24%) non-insulin-treated patients (mean age 56, range 20-79 years) had GAD65Ab. Of those with persistent GAD65Ab, 8 non-insulin-treated and 11 insulin-treated patients consented to follow-up glucose and glucagon stimulation tests. For non-insulin-treated patients, quantitative GAD65Ab index at onset correlated inversely with 1+3 min C-peptide response to glucose (r = -0.68, P < 0.05) and to glucagon (r = -0.79, P < 0.05) 3 years later. Those with high (> 0.50) initial GAD65Ab index had lower C-peptide (fasting, 1+3 min after glucose and after glucagon) 3 years later, versus those with low (<0.50) initial GAD65Ab index (P < 0.05). In conclusion, not only did GAD65Ab presence predict future insulin dependence, but higher GAD65Ab levels may mark more rapid decline in β-cell function in apparent non-insulin-dependent diabetes.

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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Autoantigen, Autoimmunity, Glutamate decarboxylase (GAD), β-Cell function
in
Diabetes Research and Clinical Practice
volume
27
issue
2
pages
133 - 140
publisher
Elsevier
external identifiers
  • scopus:0028958719
  • pmid:7607051
ISSN
0168-8227
DOI
10.1016/0168-8227(95)01026-A
language
English
LU publication?
yes
id
15af2242-858c-4261-8559-623b020b8c8a
date added to LUP
2019-09-11 08:54:20
date last changed
2024-03-13 08:08:35
@article{15af2242-858c-4261-8559-623b020b8c8a,
  abstract     = {{<p>Glutamate decarboxylase autoantibodies (GAD65Ab) and β-cell function were evaluated at and 3 years after diabetes onset in consecutive subjects over 15 years of age. At onset, 21 32 (66%) insulin-treated patients (mean age 43, range 16-79 years) had GAD65Ab; all GAD65Ab persisted 3 years later. At onset, 20 82 (24%) non-insulin-treated patients (mean age 56, range 20-79 years) had GAD65Ab. Of those with persistent GAD65Ab, 8 non-insulin-treated and 11 insulin-treated patients consented to follow-up glucose and glucagon stimulation tests. For non-insulin-treated patients, quantitative GAD65Ab index at onset correlated inversely with 1+3 min C-peptide response to glucose (r = -0.68, P &lt; 0.05) and to glucagon (r = -0.79, P &lt; 0.05) 3 years later. Those with high (&gt; 0.50) initial GAD65Ab index had lower C-peptide (fasting, 1+3 min after glucose and after glucagon) 3 years later, versus those with low (&lt;0.50) initial GAD65Ab index (P &lt; 0.05). In conclusion, not only did GAD65Ab presence predict future insulin dependence, but higher GAD65Ab levels may mark more rapid decline in β-cell function in apparent non-insulin-dependent diabetes.</p>}},
  author       = {{Gottsäter, A. and Landin-Olsson, M. and Lernmark, Å and Fernlund, P. and Sundkvist, G. and Hagopian, W. A.}},
  issn         = {{0168-8227}},
  keywords     = {{Autoantigen; Autoimmunity; Glutamate decarboxylase (GAD); β-Cell function}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{2}},
  pages        = {{133--140}},
  publisher    = {{Elsevier}},
  series       = {{Diabetes Research and Clinical Practice}},
  title        = {{Glutamate decarboxylase antibody levels predict rate of β-cell decline in adult-onset diabetes}},
  url          = {{http://dx.doi.org/10.1016/0168-8227(95)01026-A}},
  doi          = {{10.1016/0168-8227(95)01026-A}},
  volume       = {{27}},
  year         = {{1995}},
}