Determination of Free and Total Insulin and C-Peptide in Insulin-treated Diabetics

Kuzuya, Hideshi; Blix, Petra M.; Horwitz, David L.; Steiner, Donald F.; Rubenstein, Arthur H.

doi:10.2337/diab.26.1.22

Cited by 499 publications

(158 citation statements)

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“…The present data indicate that insulin antibodies may theoretically contribute to the insulin resistance shown by some patients thus confirming previous hypotheses [15,16]. Kahn's results, however suggest that anti-insulin antibodies might also potentially enhance insulin action [25].…”

Section: Discussionsupporting

confidence: 92%

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Insulin antibodies prevent insulin-receptor interactions

et al. 1980

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Summary. The study was carried out to investigate whether insulin bound to antibody is able to bind the insulin receptor of target tissues. Three specific rabbit anti-insulin sera as well as sera from eight diabetic patients with insulin antibodies were incubated, free of insulin, with labelled insulin for 48 h at 4 ~ following incubation labelled insulin was employed in binding experiments on monocytes, erythrocytes and placenta membranes. Using rabbit sera, receptor binding was absent when insulin was totally combined with antibody, and appeared in increasing amounts as the percentage of free insulin increased to reach a maximum when no insulin was combined with antibody. The same experiment using sera from diabetic patients showed a close negative relationship (r = 0.95) between the amount of insulin bound to the antibody and the amount bound to receptors. The influence of the insulin-antibody complex on the insulin receptor interaction was evaluated by exposing the insulin-antibody complex to the receptor in pH, temperature and competition-inhibition curve experiments. The complex had no effect on receptor affinity or on the pH and temperature relationship influence with insulin-receptor interaction. The findings suggest that insulin resistance in the presence of insulin antibodies is due only to an alteration occurring before the interaction of insulin with its receptor, and demonstrate that the insulin-antibody complex does not influence the insulin receptor interaction.

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Section: Discussionsupporting

confidence: 92%

“…Insulin resistance due to insulin antibodies may thus be considered a pre-receptor phenomenon [15,16] with insulin bound to antibody being unavailable for receptor binding [15,16].…”

mentioning

confidence: 99%

Insulin antibodies prevent insulin-receptor interactions

et al. 1980

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“…C-peptide concentrations were measured by methods published previously [13]. Fasting and 2-h stimulated C-peptide levels (after 240 ml Sustacal, Mead Johnson, Evansville, Indiana, USA) were obtained before the studies began.…”

Section: -mentioning

confidence: 99%

Immunogenicity of recombinant DNA human insulin

et al. 1983

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“…Serum C-peptide was measured according to Heding [19] using antiserum M 1230 (Novo Research Institute, Copenhagen, Denmark). Antibody-bound proinsulin was separated from the C-peptide by polyethylene glycol before assay [20]. The sensitivity of the assay was 0.02 nmol/1 and the interassay coefficient of variation 10%.…”

Section: Subjectsmentioning

confidence: 99%

Evidence of delayed ?-cell destruction in Type 1 (insulin-dependent) diabetic patients with persisting complement-fixing cytoplasmic islet cell antibodies

et al. 1984

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Summary. Forty-four children with Type 1 (insulin-dependent) diabetes (aged 0.7-16.7 years) were observed from diagnosis for cytoplasmic islet cell antibodies and serum C-peptide concentrations. Islet cell antibodies were analysed by indirect immunofluorescence for both conventional IgG and complement-fixing antibodies. Thirty-seven children (84%) were found to be positive for conventional islet cell antibodies at diagnosis, and 21 (48%) remained positive over the observation period. Twenty-six patients (59%) were positive for complement-fixing antibodies at diagnosis and eight remained so during the follow-up period. The serum C-peptide concentrations increased significantly during the first 3 months after diagnosis, after which there was a gradual decrease in the levels. Those children who remained positive for complement-fixing antibodies over the observation period had significantly higher serum C-peptide concentrations on several occasions during the second year and had also a higher integrated serum C-peptide concentration over the initial 2 years than those who became negative for complement-fixing antibodies. These observations suggest that the continuous production of complement-fixing islet cell antibodies in those patients who are positive for these antibodies at diagnosis presupposes the preservation of a sufficient amount of functioning/~ cells for antigenic stimulation. These results support the view that the complement-fixing islet cell antibodies reflect ongoing destructive processes in the/3 cells.

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Determination of Free and Total Insulin and C-Peptide in Insulin-treated Diabetics

Cited by 499 publications

References 0 publications

Insulin antibodies prevent insulin-receptor interactions

Insulin antibodies prevent insulin-receptor interactions

Immunogenicity of recombinant DNA human insulin

Evidence of delayed ?-cell destruction in Type 1 (insulin-dependent) diabetic patients with persisting complement-fixing cytoplasmic islet cell antibodies

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