TY - JOUR
T1 - Effects of nonglucose nutrients on insulin secretion and action in people with pre-diabetes
AU - Bock, Gerlies
AU - Man, Chiara Dalla
AU - Campioni, Marco
AU - Chittilapilly, Elizabeth
AU - Basu, Rita
AU - Toffolo, Gianna
AU - Cobelli, Claudio
AU - Rizza, Robert
PY - 2007/4
Y1 - 2007/4
N2 - To determine whether nonglucose nutrient-induced insulin secretion is impaired in pre-diabetes, subjects with impaired or normal fasting glucose were studied after ingesting either a mixed meal containing 75 g glucose or 75 g glucose alone. Despite comparable glucose areas above basal, glucose-induced insulin secretion was higher (P < 0.05) and insulin action lower (P < 0.05) during the meal than the oral glucose tolerance test (OGTT) in all subgroups regardless of whether they had abnormal or normal glucose tolerance (NGT). However, the nutrientinduced δ (meal minus OGTT) in insulin secretion and glucagon concentrations did not differ among groups. Furthermore, the decrease in insulin action after meal ingestion was compensated in all groups by an appropriate increase in insulin secretion resulting in disposition indexes during meals that were equal to or greater than those present during the OGTT. In contrast, disposition indexes were reduced (P < 0.01) during the OGTT in the impaired glucose tolerance groups, indicating that reduced glucose induced insulin secretion. We conclude that, whereas glucose-induced insulin secretion is impaired in people with abnormal glucose tolerance, nonglucose nutrient-induced secretion is intact, suggesting that a glucosespecific defect in the insulin secretory pathway is an early event in the evolution of type 2 diabetes.
AB - To determine whether nonglucose nutrient-induced insulin secretion is impaired in pre-diabetes, subjects with impaired or normal fasting glucose were studied after ingesting either a mixed meal containing 75 g glucose or 75 g glucose alone. Despite comparable glucose areas above basal, glucose-induced insulin secretion was higher (P < 0.05) and insulin action lower (P < 0.05) during the meal than the oral glucose tolerance test (OGTT) in all subgroups regardless of whether they had abnormal or normal glucose tolerance (NGT). However, the nutrientinduced δ (meal minus OGTT) in insulin secretion and glucagon concentrations did not differ among groups. Furthermore, the decrease in insulin action after meal ingestion was compensated in all groups by an appropriate increase in insulin secretion resulting in disposition indexes during meals that were equal to or greater than those present during the OGTT. In contrast, disposition indexes were reduced (P < 0.01) during the OGTT in the impaired glucose tolerance groups, indicating that reduced glucose induced insulin secretion. We conclude that, whereas glucose-induced insulin secretion is impaired in people with abnormal glucose tolerance, nonglucose nutrient-induced secretion is intact, suggesting that a glucosespecific defect in the insulin secretory pathway is an early event in the evolution of type 2 diabetes.
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U2 - 10.2337/db06-1272
DO - 10.2337/db06-1272
M3 - Article
C2 - 17395750
AN - SCOPUS:34047190277
SN - 0012-1797
VL - 56
SP - 1113
EP - 1119
JO - Diabetes
JF - Diabetes
IS - 4
ER -