Risk for developing Type 1 (insulin-dependent) diabetes mellitus and the presence of islet 64K antibodies
Bärmeier, H. ; McCulloch, D. K. ; Neifing, J. L. ; Warnock, G. ; Rajotte, R. V. ; Palmer, J. P. and Lernmark, Å LU
(1991)
In Diabetologia
34(10).
p.727-733
- Abstract
First-degree relatives of Type 1 (insulin-dependent) diabetic patients are at increased risk for developing clinical diabetes. The presence of islet cell or insulin autoantibodies further identifies relatives at greater risk, but not all immunologic-marker-positive relatives progress to disease. Beta-cell dysfunction, however, seems to be more prevalent than clinical Type 1 diabetes, since stable subclinical pancreatic Beta-cell dysfunction may occur. Antibodies against a Mr 64,000 (64K) islet Beta-cell protein, identified as glutamic acid decarboxylase, have been reported both at and several years prior to the clinical onset of Type 1 diabetes. We measured 64K antibodies in first-degree relatives with varying degrees of... (More)
First-degree relatives of Type 1 (insulin-dependent) diabetic patients are at increased risk for developing clinical diabetes. The presence of islet cell or insulin autoantibodies further identifies relatives at greater risk, but not all immunologic-marker-positive relatives progress to disease. Beta-cell dysfunction, however, seems to be more prevalent than clinical Type 1 diabetes, since stable subclinical pancreatic Beta-cell dysfunction may occur. Antibodies against a Mr 64,000 (64K) islet Beta-cell protein, identified as glutamic acid decarboxylase, have been reported both at and several years prior to the clinical onset of Type 1 diabetes. We measured 64K antibodies in first-degree relatives with varying degrees of Beta-cell dysfunction and risk for subsequent Type 1 diabetes to determine whether 64K antibodies improve the predictive power of islet cell antibodies and/or insulin autoantibodies. In the Seattle Family Study first-degree relatives of Type 1 diabetic patients are followed prospectively using detailed Beta-cell function tests, insulin sensitivity, quantitative evaluation of islet cell antibodies and fluid phase assay insulin autoantibodies. 64K antibodies were measured using dog islets. Relatives were selected, based on Beta-cell function to represent individuals at high (n=6) and low (n=30) risk for subsequent Type 1 diabetes. The 30 low-risk individuals followed-up for 78 months, had stable Beta-cell function, and six (20%) were negative for all autoantibodies, ten (33%) were positive for insulin autoantibodies, 16 (53%) were islet cell antibody positive while six (20%) were positive for 64K antibodies. In contrast, of the six subjects with progressively declining Beta-cell function who are therefore at high risk, two of whom have already developed Type 1 diabetes, two (33%) were positive for insulin autoantibodies, four (67%) were islet cell antibody positive, while all six (100%) were positive for 64K antibodies. We conclude that antibodies to the Mr 64,000 islet protein correlate with progressive Beta-cell dysfunction more closely than either islet cell antibodies or insulin autoantibodies, but can sometimes be present in individuals whose Beta-cell function remains stable over several years.
(Less)
- author
- Bärmeier, H.
; McCulloch, D. K.
; Neifing, J. L.
; Warnock, G.
; Rajotte, R. V.
; Palmer, J. P.
and Lernmark, Å
LU
- publishing date
- 1991-10-01
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- glutamic acid decarboxylase antibodies, insulin autoantibodies, intravenous glucose tolerance test, islet cell antibodies, prediabetes, Type 1 (insulin-dependent) diabetes mellitus
- in
- Diabetologia
- volume
- 34
- issue
- 10
- pages
- 727 - 733
- publisher
- Springer
- external identifiers
-
- pmid:1959705
- scopus:0025940439
- ISSN
- 0012-186X
- DOI
- 10.1007/BF00401518
- language
- English
- LU publication?
- no
- id
- 01949b61-6f0c-4230-bd61-24d492ecff80
- date added to LUP
- 2019-09-11 09:37:51
- date last changed
- 2024-03-13 08:01:18
@article{01949b61-6f0c-4230-bd61-24d492ecff80,
abstract = {{<p>First-degree relatives of Type 1 (insulin-dependent) diabetic patients are at increased risk for developing clinical diabetes. The presence of islet cell or insulin autoantibodies further identifies relatives at greater risk, but not all immunologic-marker-positive relatives progress to disease. Beta-cell dysfunction, however, seems to be more prevalent than clinical Type 1 diabetes, since stable subclinical pancreatic Beta-cell dysfunction may occur. Antibodies against a M<sub>r</sub> 64,000 (64K) islet Beta-cell protein, identified as glutamic acid decarboxylase, have been reported both at and several years prior to the clinical onset of Type 1 diabetes. We measured 64K antibodies in first-degree relatives with varying degrees of Beta-cell dysfunction and risk for subsequent Type 1 diabetes to determine whether 64K antibodies improve the predictive power of islet cell antibodies and/or insulin autoantibodies. In the Seattle Family Study first-degree relatives of Type 1 diabetic patients are followed prospectively using detailed Beta-cell function tests, insulin sensitivity, quantitative evaluation of islet cell antibodies and fluid phase assay insulin autoantibodies. 64K antibodies were measured using dog islets. Relatives were selected, based on Beta-cell function to represent individuals at high (n=6) and low (n=30) risk for subsequent Type 1 diabetes. The 30 low-risk individuals followed-up for 78 months, had stable Beta-cell function, and six (20%) were negative for all autoantibodies, ten (33%) were positive for insulin autoantibodies, 16 (53%) were islet cell antibody positive while six (20%) were positive for 64K antibodies. In contrast, of the six subjects with progressively declining Beta-cell function who are therefore at high risk, two of whom have already developed Type 1 diabetes, two (33%) were positive for insulin autoantibodies, four (67%) were islet cell antibody positive, while all six (100%) were positive for 64K antibodies. We conclude that antibodies to the M<sub>r</sub> 64,000 islet protein correlate with progressive Beta-cell dysfunction more closely than either islet cell antibodies or insulin autoantibodies, but can sometimes be present in individuals whose Beta-cell function remains stable over several years.</p>}},
author = {{Bärmeier, H. and McCulloch, D. K. and Neifing, J. L. and Warnock, G. and Rajotte, R. V. and Palmer, J. P. and Lernmark, Å}},
issn = {{0012-186X}},
keywords = {{glutamic acid decarboxylase antibodies; insulin autoantibodies; intravenous glucose tolerance test; islet cell antibodies; prediabetes; Type 1 (insulin-dependent) diabetes mellitus}},
language = {{eng}},
month = {{10}},
number = {{10}},
pages = {{727--733}},
publisher = {{Springer}},
series = {{Diabetologia}},
title = {{Risk for developing Type 1 (insulin-dependent) diabetes mellitus and the presence of islet 64K antibodies}},
url = {{http://dx.doi.org/10.1007/BF00401518}},
doi = {{10.1007/BF00401518}},
volume = {{34}},
year = {{1991}},
}