PMID: 1959705Oct 1, 1991

Risk for developing type 1 (insulin-dependent) diabetes mellitus and the presence of islet 64K antibodies

H BärmeierA Lernmark


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...Continue Reading


Sep 1, 1994·Diabetologia·A Lernmark
Jan 1, 1997·Endocrine Pathology·Gunter Kloppel, Andreas Clemens
Feb 1, 1995·Diabetes Research and Clinical Practice·A GottsäterW A Hagopian
Apr 1, 1996·Diabetes Research and Clinical Practice·E KawasakiS Nagataki
Oct 1, 1996·Diabetes Research and Clinical Practice·M Serrano-RíosP Zimmet
Jul 28, 2001·Diabetes Technology & Therapeutics·W HaoA Lernmark
Oct 1, 1993·Journal of Internal Medicine·A LernmarkC Sanjeevi
Nov 23, 2005·Pediatric Clinics of North America·Anna CasuM Pietropaolo
Dec 25, 2003·Primary Care·Irl B Hirsch
Jan 3, 2001·The Journal of Clinical Endocrinology and Metabolism·C TörnJ Ostman
Dec 1, 1993·Journal of Endocrinological Investigation·R CalafioreP Brunetti


Dec 11, 1976·Lancet·R LendrumD R Gamble
Aug 24, 1978·The New England Journal of Medicine·A LernmarkH S Traisman
Jun 26, 1976·British Medical Journal·R LendrumD R Gamble
Feb 1, 1990·Journal of Neurochemistry·S L Erdö, J R Wolff
Dec 1, 1989·Clinical Immunology and Immunopathology·R Wassmuth, A Lernmark
Apr 16, 1988·Lancet·A TarnE A Gale
Jan 21, 1988·Journal of Immunological Methods·E BonifacioR L Dawkins
Jan 1, 1988·Advances in Experimental Medicine and Biology·D A Pyke
Jan 1, 1988·Advances in Experimental Medicine and Biology·D KumarT M Mack
Mar 1, 1987·The Journal of Clinical Investigation·S BaekkeskovF Lindgren
Sep 20, 1985·JAMA : the Journal of the American Medical Association·F Ginsberg-FellnerA L Notkins
Jan 1, 1984·Virchows Archiv. A, Pathological Anatomy and Histopathology·Gunter KloppelP U Heitz
Feb 1, 1981·Diabetologia·A H BarnettD A Pyke

Related Concepts

Insulin Sensitivity
Glutamate Decarboxylase
HLA Antigens
Islet cell surface antibodies
Disease Susceptibility
Islet Cell
Family Investigation, NOS

Related Feeds

Autoimmune Diabetes & Tolerance

Patients with type I diabetes lack insulin-producing beta cells due to the loss of immunological tolerance and autoimmune disease. Discover the latest research on targeting tolerance to prevent diabetes.