Postprandial serum C-peptide to plasma glucose concentration ratio correlates with oral glucose tolerance test- and glucose clamp-based disposition indexes
“…C-peptide can also be measured across a 75 g oral glucose tolerance test (OGTT) [21]. C-peptide sampling as part of the OGTT has been found to significantly correlate with insulin secretion in type 2 diabetes mellitus (T2DM), when samples are taken at 0, 30, 60, 90, and 120 min (with the possibility of extending this to include sampling at 150, 180, 240, and 300 min) [22]. Adding c-peptide determination to the protocol of an OGTT may therefore be a practical means of estimating beta cell function when the test is already being performed for diagnostic reasons, if further interval sampling is taken between 0 and 120 min.Fig.…”
Section: Methods Of Collection Of C-peptidementioning
C-peptide is a widely used measure of pancreatic beta cell function. It is produced in equimolar amounts to endogenous insulin but is excreted at a more constant rate over a longer time. Methods of estimation include urinary and unstimulated and stimulated serum sampling. Modern assays detect levels of c-peptide which can be used to guide diabetes diagnosis and management. We explore the evidence behind the various tests available. We recommend the glucagon stimulation c-peptide testing owing to its balance of sensitivity and practicality. C-peptide levels are associated with diabetes type and duration of disease. Specifically a c-peptide level of less than 0.2 nmol/l is associated with a diagnosis of type 1 diabetes mellitus (T1DM). C-peptide level may correlate with microvascular and macrovascular complications and future use of insulin therapy, as well as likely response to other individual therapies. We explore the potential uses of c-peptide measurement in clinical practice.
“…C-peptide can also be measured across a 75 g oral glucose tolerance test (OGTT) [21]. C-peptide sampling as part of the OGTT has been found to significantly correlate with insulin secretion in type 2 diabetes mellitus (T2DM), when samples are taken at 0, 30, 60, 90, and 120 min (with the possibility of extending this to include sampling at 150, 180, 240, and 300 min) [22]. Adding c-peptide determination to the protocol of an OGTT may therefore be a practical means of estimating beta cell function when the test is already being performed for diagnostic reasons, if further interval sampling is taken between 0 and 120 min.Fig.…”
Section: Methods Of Collection Of C-peptidementioning
C-peptide is a widely used measure of pancreatic beta cell function. It is produced in equimolar amounts to endogenous insulin but is excreted at a more constant rate over a longer time. Methods of estimation include urinary and unstimulated and stimulated serum sampling. Modern assays detect levels of c-peptide which can be used to guide diabetes diagnosis and management. We explore the evidence behind the various tests available. We recommend the glucagon stimulation c-peptide testing owing to its balance of sensitivity and practicality. C-peptide levels are associated with diabetes type and duration of disease. Specifically a c-peptide level of less than 0.2 nmol/l is associated with a diagnosis of type 1 diabetes mellitus (T1DM). C-peptide level may correlate with microvascular and macrovascular complications and future use of insulin therapy, as well as likely response to other individual therapies. We explore the potential uses of c-peptide measurement in clinical practice.
“…The results are shown as National Glycohemoglobin Standardization Program values as recommended by the Japan Diabetes Society. The CPI, which is closely correlated with other indices of β‐cell function, such as homeostatic model assessment of β‐cell function and insulinogenic index, and has been widely used as a practical index to estimate β‐cell function in clinical settings, was calculated as follows: 100 × fasting CPR / fasting plasma glucose. The patients continued pre‐existing insulin therapy up until the night before the measurement of fasting serum CPR in the morning to avoid hyperglycemia.…”
Aims/IntroductionThe glucose‐lowering effects of the glucagon‐like peptide‐1 receptor agonist, liraglutide, have been shown to rely on remaining β‐cell function. However, the possible associations of remaining β‐cell function with the glucose‐lowering effects of liraglutide in combination with basal insulin remain unknown and warrant investigation.Materials and MethodsThis was a single‐center, retrospective, observational study carried out in a private hospital in Osaka, Japan. Type 2 diabetes patients who received a prescription change from insulin therapy, both multiple‐dose insulin and basal insulin‐supported oral therapy, to liraglutide and basal insulin combination and continued the therapy for 54 weeks without additional oral antidiabetic drugs or bolus insulin were retrospectively analyzed.ResultsAmong the 72 participants who received a prescription change from multiple‐dose insulin and basal insulin‐supported oral therapy to liraglutide and basal insulin combination, 57 continued the therapy for 54 weeks. Of those who continued the therapy without receiving additional oral antidiabetic drugs or bolus insulin, seven participants achieved glycated hemoglobin < 7.0% at 54 weeks, but 30 participants did not. The participants who achieved glycated hemoglobin < 7.0% at 54 weeks had a significantly higher C‐peptide immunoreactivity index, a β‐cell function‐related index frequently used in Japanese clinical settings. The receiver operating curve analysis showed that the C‐peptide immunoreactivity index cut‐off value for the achievement of glycated hemoglobin <7.0% at 54 weeks is 1.103.ConclusionsThe current findings show that the glucose‐lowering effects of liraglutide rely on remaining β‐cell function, even when used with basal insulin; and suggest that liraglutide and basal insulin combination might require additional bolus insulin to fully compensate insulin insufficiency in individuals with reduced β‐cell function.
“…Meier et al3 reported a good correlation of FCP:FPG ratio with human pancreatic β-cell mass in a small group of patients who underwent pancreatic surgery. Okuno et al4 showed in a much bigger population of patients with type 2 diabetes, that FCP:FPG ratio strongly correlates with accepted measures as the HOMA-β (r = 0.79) and hyperglycaemic clamp (increase in Area Under the Curve insulin/glucose 90 minutes, r = 0.721).…”
In this trial, 390 insulin-treated patients with type 2 diabetes were randomized to either placebo or metformin. Fasting levels of glucose, insulin and C peptide were determined at baseline, after 4 months and yearly thereafter for 4 years to assess fasting estimates of beta cell function. The primary endpoint was the fasting C peptide-to-glucose ratio (FCPGR) and secondary measures were the disposition index (DI) and the fasting C peptide (FCP). We analysed the results with a general linear mixed model. Baseline FCPGR was 5.27 (95% CI, 4.83 - 5.71). Compared to placebo, FCPGR increased in the metformin group with 1.48 (95% CI, 1.09 - 1.87, P < 0.001). The DI showed comparable results with a treatment effect of 1.50 (95% CI, 1.17 - 1.83; P < 0.001). FCP also increased in the metformin group but did not reach statistical significance vs placebo (0.034 nmol, 95% CI, -0.005 - 0.072; P = 0.085). Treatment with metformin vs placebo, added to insulin in patients with type 2 diabetes, improves long-term estimates of beta cell function in the fasting state.
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