Graves' Disease of the Β Cell: Glucose Dysregulation Due to Islet-Cell Stimulating Antibodies

Tj, Wilkin; Mirza, Intisar; Hammonds, Peter; Bone, A J; Webster, K. A.

doi:10.1016/s0140-6736(88)90232-2

Cited by 27 publications

(11 citation statements)

References 12 publications

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“…In a previous study, Wilkin et al (1988) used an animal-derived -cell line (HIT-T15) and demonstrated that insulin secretion was stimulated by incubation of cells for 1 h with 33% (v/v) sera (four of Figure 2 Anti-GAD concentrations in serum from newly diagnosed patients with IDDM and from normal human individuals. Anti-GAD autoantibodies were quantified in IDDM patient sera and normal human sera samples by indirect ELISA using recombinant human GAD as primary coating antigen, as described in Methods.…”

Section: Discussionmentioning

confidence: 99%

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Evidence for complement-dependent and -independent inhibition of insulin secretion from clonal beta-cells incubated in the presence of sera of newly diagnosed IDDM patients

Conroy¹,

Abdel-Wahab²,

Caraher³

et al. 2000

Journal of Endocrinology

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There are conflicting reports on the effect of serum from patients with insulin-dependent diabetes mellitus (IDDM) or normal human serum on -cell function and insulin secretion. Here, we report that the sera of newly diagnosed IDDM patients potently suppresses insulin secretion from a clonal rat pancreatic -cell line (BRIN-BD11), but do not alter cell viability. Indeed, the viability of the -cells was not significantly different between cells cultured in 10% (v/v) IDDM sera, normal human sera, or fetal calf serum after 24, 48 and 72 h. Alanine-stimulated insulin secretion from cells cultured for 24 h in (10% v/v) IDDM patient sera was reduced to 48% of that secreted from cells cultured in (10% v/v) normal human sera. After depletion of the complement components C1q and C3, the inhibition of insulin secretion induced by IDDM patient sera was significantly reversed (no significant difference was observed between cells cultured in complementdepleted IDDM patient sera and cells cultured in normal human sera or complement-depleted normal human sera).The concentration of glutamic acid decarboxylase (GAD) autoantibodies was markedly increased in the sera of six out of nine newly diagnosed IDDM patients in this study, whereas insulin auto-antibodies (IAA) were detected in the sera of three of the nine patients and islet-cell antibodies (ICA) in the sera of five of them. In addition, the concentration of soluble terminal complement complexes (SC5b-9) was greater in some of the -cell culture media samples after 24 h incubation when the incubation medium was supplemented with IDDM patient sera than when supplementation was with normal human sera.We propose that the mechanism of sera-induced inhibition of insulin secretion from clonal -cells may involve complement-and cytokine-stimulated intracellular events that attenuate the metabolite-induced secretory process.

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Section: Discussionmentioning

confidence: 99%

“…One study reported acute (60-90 min) stimulation of insulin secretion from the HIT-T15 cell line or human islets by IDDM patient sera (Wilkin et al 1988). In addition, release of insulin from mouse islets was stimulated by normal human sera over approximately 1 h of perfusion (Idahl et al 1980).…”

Section: Introductionmentioning

confidence: 99%

Evidence for complement-dependent and -independent inhibition of insulin secretion from clonal beta-cells incubated in the presence of sera of newly diagnosed IDDM patients

Conroy¹,

Abdel-Wahab²,

Caraher³

et al. 2000

Journal of Endocrinology

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show abstract

“…The hyperplasia might reflect increased demand placed upon the islets by the more rapid clearance from the circulation of antibodybound insulin, or conceivably antibody stimulation of the islets corresponding to that seen in Graves' disease of the thyroid. Experiments in vivo, and in vitro with hamster, rat, and human islets, have indeed demonstrated the presence of Igs in sera from patients with the IAS which stimulate the islets to produce insulin (104). Islet cell stimulating antibodies were also demonstrated in sera from patients with newly diagnosed and longstanding type I (but not type II) diabetes.…”

Section: The Biological Implications Of Iaamentioning

confidence: 91%

Insulin Autoantibodies as Markers for Type I Diabetes

Wilkin

1990

Endocrine Reviews

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“…sulinbildung, was zusammen mit dem im Assay mitbestimmten antikörpergebundenen Insulin zu erhöhten Insulin-und C-Peptidspiegeln führte. Beim autoimmunem Insulinsyndrom ist auch eine direkte Stimulation der Insulinsekretion aus β-Zellen durch die Immunglobulinfraktion beschrieben (12 …”

Section: Therapie Und Verlaufunclassified

Hypoglykämien und transienter Diabetes mellitus bei einem Autoimmun-Insulinsyndrom

Reisch

Zwermann²,

Reincke³

2004

Dtsch med Wochenschr

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Graves' Disease of the Β Cell: Glucose Dysregulation Due to Islet-Cell Stimulating Antibodies

Cited by 27 publications

References 12 publications

Evidence for complement-dependent and -independent inhibition of insulin secretion from clonal beta-cells incubated in the presence of sera of newly diagnosed IDDM patients

Evidence for complement-dependent and -independent inhibition of insulin secretion from clonal beta-cells incubated in the presence of sera of newly diagnosed IDDM patients

Insulin Autoantibodies as Markers for Type I Diabetes

Hypoglykämien und transienter Diabetes mellitus bei einem Autoimmun-Insulinsyndrom

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