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Roman Hovorka, Ludovic Chassin, Stephen D. Luzio, Rebecca Playle, David R. Owens, Pancreatic β-Cell Responsiveness during Meal Tolerance Test: Model Assessment in Normal Subjects and Subjects with Newly Diagnosed Noninsulin-Dependent Diabetes Mellitus, The Journal of Clinical Endocrinology & Metabolism, Volume 83, Issue 3, 1 March 1998, Pages 744–750, https://doi.org/10.1210/jcem.83.3.4646
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A model-based method was developed to quantify pancreaticβ -cell responsiveness during a meal tolerance test (MTT). C peptide secretion was related in a linear fashion to glucose concentration, whereas the standard population model was used to derive transfer rate constants of the two compartmental model of C peptide kinetics. Two indexes of pancreatic β-cell responsiveness were defined: 1) postprandial sensitivity MI (ability of postprandial glucose to stimulate β-cell), and 2) basal sensitivity M0 (ability of fasting glucose to stimulate β-cell). The method was evaluated using plasma glucose and C peptide measured over 180 min with a 10- to 30-min sampling interval during a MTT (75 g carbohydrates; 500 Cal) performed in 16 normal subjects (7 men and 9 women; age, 50± 10 yr; body mass index, 29.2 ± 3.6 kg/m2; fasting plasma glucose, 5.1 ± 0.5 mmol/L; mean ± sd) and 16 body mass index-matched subjects with newly diagnosed noninsulin-dependent diabetes mellitus (NIDDM; 15 men and 1 woman; age, 50 ± 9 yr; body mass index, 29.3 ± 3.7 kg/m2; fasting plasma glucose, 12.6 ± 3.2 mmol/L). MI and M0 indexes were estimated with very good precision (coefficient of variation, <15%). Subjects with NIDDM demonstrated lower postprandial sensitivity MI (17.7 ± 11.4 vs. 90.0 ± 43.3 × 10−9/min; NIDDM vs. normal, P < 0.001) and basal sensitivity M0 (5.4 ± 2.2 vs. 10.3 ± 4.9 × 10−9/min; P< 0.005). Deconvolution analysis documented that the relationship between C peptide secretion and glucose concentration is approximately linear during MTT in both normal subjects (plasma glucose range, 5–8 mmol/L) and subjects with NIDDM (12–17 mmol/L). We conclude that pancreatic responsiveness during glucose stimulation (MI) and under basal conditions (M0) can be obtained from this novel method during MTT in healthy and disease states.
