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Graves' disease of the beta cell: glucose dysregulation due to islet-cell stimulating antibodies.

Abstract
The immunoglobulin fractions of serum from patients with spontaneous hyperinsulinaemic hypoglycaemia and others with type 1 diabetes stimulated insulin release both in islet-cell cultures and in vivo in rats. Serum from patients with type 2 diabetes, which is not an autoimmune disease, did not stimulate insulin release. The discovery of islet-cell-stimulating antibodies (ICSTA) completes for the islet the triad of autoantibodies (anticytoplasmic, antiproduct, and antireceptor) previously described in autoimmune thyroid disease. ICSTA may be important modulators of islet-cell secretion in man.
AuthorsT J Wilkin, P Hammonds, I Mirza, A J Bone, K Webster
JournalLancet (London, England) (Lancet) Vol. 2 Issue 8621 Pg. 1155-8 (Nov 19 1988) ISSN: 0140-6736 [Print] England
PMID2903375 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Autoantibodies
  • Blood Glucose
  • Insulin
  • Insulin Antibodies
  • islet cell antibody
  • islet-cell-stimulating antibodies
Topics
  • Adolescent
  • Adult
  • Aged
  • Animals
  • Autoantibodies (immunology)
  • Blood Glucose (analysis)
  • Cell Line
  • Child
  • Child, Preschool
  • Cricetinae
  • Diabetes Mellitus, Type 1 (immunology)
  • Female
  • Graves Disease (immunology)
  • Humans
  • Hyperinsulinism (immunology)
  • Hypoglycemia (immunology)
  • Insulin (blood, metabolism)
  • Insulin Antibodies (immunology)
  • Insulin Secretion
  • Islets of Langerhans (immunology)
  • Male
  • Middle Aged
  • Rats
  • Rats, Inbred Strains

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