Human C-peptide in normal and diabetic subjects

Abstract

Concentrations of human C-peptide, IRI (immunoreactive insulin) and glucose were determined during oral glucose tolerance test (1.75 g glucose/kg ideal body weight) in 14 normal persons (N), 9 maturity-onset diabetics (DI) and 10 insulin-requiring diabetics (DII) never treated with insulin and in 3 formerly insulin treated diabetics. The mean fasting levels of C-peptide and IRI in the first three groups were: N: 0.37 +/- 0.02 nM and 0.048 +/- 0.009 nM, DI: 0.86 +/- 0.17 nM and 0.11 +/- 0.029 nM, DH: 0.37 +/- 0.04 nM and 0.063 +/- 0.009 nM. One hour after oral glucose ingestion, the respective values increased to: N: 2.53 +/- 0.20 nM and 0.52 +/- 0.077 nM, DI: 2.49 +/- 0.31 nM and 0.49 +/- 0.11 nM, DH: 0.49 +/- 0.05 nM and 0.11 +/- 0.014 nM. Although secreted from the pancreas in equimolar concentrations, the molar ratio of C-peptide to insulin in peripheral blood was about 7 in the fasting state, falling to about 5 in the glucose stimulated condition. Maturity-onset diabetics had higher fasting levels of C-peptide than normal subjects, in agreement with the IRI levels. Three patients previously treated with insulin and having insulin antibodies showed C-peptide responses significantly below the normal range. In one of these patients, the test was repeated 9 months later when the insulin antibodies had disappeared, and the C-peptide response observed at that time was much higher. It is suggested that insulin antibodies cause an impaired IRI - and consequently C-peptide response - by constantly removing insulin from the granules in the B-cell. In normal humans the peripheral C-peptide responses to the oral glucose load showed less relative variation than do the insulin responses. Therefore, a radioimmunoassay for C-peptide in addition to the assay for insulin will provide supplementary information on insulinsecretion.

Low O2-induced ATP release from erythrocytes of humans with type 2 diabetes is restored by physiological ratios of C-peptide and insulin

“…retain modest beta-cell activity, allowing for the production of low levels of C-peptide (9,10,20). In a study analyzing patient tertiles based on C-peptide levels, the incidence of retinopathy, nephropathy, and neuropathy decreased from the first (Cpeptide Յ 0.47 nM) to the third tertile (C-peptide Ն 0.80 nM) (7).…”

Residual β-Cell Function and Islet Cell Antibodies in Diabetic Children

“…Fasting serum concentrations may be within the normal nondiabetic range (5) at the time of diagnosis of diabetes (4,12), but decline subsequently (12,13). ~ntibodies directed against pancreatic islet cells (ICA) have been detected in the serum of more than one-half of newly diagnosed insulin-dependent diabetics (8, 1 l).…”

C-peptide, insulin and proinsulinlike components in diabetic and nondiabetic human pancreas.

“…Recently the immunoassay system of human C-peptide of insulin has been developed by Melani et al (1970a), and Kaneko et al (1974), and many clinical results on the plasma or urine C-peptide immunoreactivity (CPR) have been reported in various diseases, especially in patients with [insulinoma or in insulin-treated diabetic subjects (Block et al, 1972(Block et al, , 1973Horwitz et al, 1975;Heding and Rasmussen, 1975;Kuzuya et al, 1977;Jaspan et al, 1977). The PLC contents of pancreas from diabetic and nondiabetic subjects were already studied (Rastogi et al, 1973;Hayashi et al, 1977), but the amount of C-peptide in human pancreas has not been reported.…”