TY - JOUR
T1 - Estimation of prehepatic insulin secretion
T2 - Comparison between standardized C-peptide and insulin kinetic models
AU - Tura, Andrea
AU - Pacini, Giovanni
AU - Kautzky-Willer, Alexandra
AU - Gastaldelli, Amalia
AU - Defronzo, Ralph A.
AU - Ferrannini, Ele
AU - Mari, Andrea
PY - 2012/3
Y1 - 2012/3
N2 - Our aim was to compare traditional C-peptide-based method and insulin-based method with standardized kinetic parameters in the estimation of prehepatic insulin secretion rate (ISR). One-hundred thirty-four subjects with varying degrees of glucose tolerance received an insulin-modified intravenous glucose tolerance test and a standard oral glucose tolerance test with measurement of plasma insulin and C-peptide. From the intravenous glucose tolerance test, we determined insulin kinetics parameters and selected standardized kinetic parameters based on mean values in a selected subgroup. We computed ISR from insulin concentration during the oral glucose tolerance test using these parameters and compared ISR with the standard C-peptide deconvolution approach. We then performed the same comparison in an independent data set (231 subjects). In the first data set, total ISRs from insulin and C-peptide were highly correlated (R 2 = 0.75, P <.0001), although on average different (103 ± 6 vs 108 ± 3 nmol, P <.001). Good correlation was also found in the second data set (R 2 = 0.54, P <.0001). The insulin method somewhat overestimated total ISR (85 ± 5 vs 67 ± 3 nmol, P =.002), in part because of differences in insulin assay. Similar results were obtained for fasting ISR. Despite the modest bias, the insulin and C-peptide methods were consistent in predicting differences between groups (eg, obese vs nonobese) and relationships with other physiological variables (eg, body mass index, insulin resistance). The insulin method estimated first-phase ISR peak similarly to the C-peptide method and better than the simple use of insulin concentration. The insulin-based ISR method compares favorably with the C-peptide approach. The method will be particularly useful in data sets lacking C-peptide to assess β-cell function through models requiring prehepatic secretion.
AB - Our aim was to compare traditional C-peptide-based method and insulin-based method with standardized kinetic parameters in the estimation of prehepatic insulin secretion rate (ISR). One-hundred thirty-four subjects with varying degrees of glucose tolerance received an insulin-modified intravenous glucose tolerance test and a standard oral glucose tolerance test with measurement of plasma insulin and C-peptide. From the intravenous glucose tolerance test, we determined insulin kinetics parameters and selected standardized kinetic parameters based on mean values in a selected subgroup. We computed ISR from insulin concentration during the oral glucose tolerance test using these parameters and compared ISR with the standard C-peptide deconvolution approach. We then performed the same comparison in an independent data set (231 subjects). In the first data set, total ISRs from insulin and C-peptide were highly correlated (R 2 = 0.75, P <.0001), although on average different (103 ± 6 vs 108 ± 3 nmol, P <.001). Good correlation was also found in the second data set (R 2 = 0.54, P <.0001). The insulin method somewhat overestimated total ISR (85 ± 5 vs 67 ± 3 nmol, P =.002), in part because of differences in insulin assay. Similar results were obtained for fasting ISR. Despite the modest bias, the insulin and C-peptide methods were consistent in predicting differences between groups (eg, obese vs nonobese) and relationships with other physiological variables (eg, body mass index, insulin resistance). The insulin method estimated first-phase ISR peak similarly to the C-peptide method and better than the simple use of insulin concentration. The insulin-based ISR method compares favorably with the C-peptide approach. The method will be particularly useful in data sets lacking C-peptide to assess β-cell function through models requiring prehepatic secretion.
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U2 - 10.1016/j.metabol.2011.08.001
DO - 10.1016/j.metabol.2011.08.001
M3 - Article
C2 - 21944265
AN - SCOPUS:84857503964
SN - 0026-0495
VL - 61
SP - 434
EP - 443
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 3
ER -