Separate impact of obesity and glucose tolerance on the incretin effect in normal subjects and type 2 diabetic patients
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Separate impact of obesity and glucose tolerance on the incretin effect in normal subjects and type 2 diabetic patients. / Muscelli, Elza; Mari, Andrea; Casolaro, Arturo; Camastra, Stefania; Seghieri, Giuseppe; Gastaldelli, Amalia; Holst, Jens Juul; Ferrannini, Ele.
In: Diabetes, Vol. 57, No. 5, 05.2008, p. 1340-8.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Separate impact of obesity and glucose tolerance on the incretin effect in normal subjects and type 2 diabetic patients
AU - Muscelli, Elza
AU - Mari, Andrea
AU - Casolaro, Arturo
AU - Camastra, Stefania
AU - Seghieri, Giuseppe
AU - Gastaldelli, Amalia
AU - Holst, Jens Juul
AU - Ferrannini, Ele
PY - 2008/5
Y1 - 2008/5
N2 - OBJECTIVE: To quantitate the separate impact of obesity and hyperglycemia on the incretin effect (i.e., the gain in beta-cell function after oral glucose versus intravenous glucose).RESEARCH DESIGN AND METHODS: Isoglycemic oral (75 g) and intravenous glucose administration was performed in 51 subjects (24 with normal glucose tolerance [NGT], 17 with impaired glucose tolerance [IGT], and 10 with type 2 diabetes) with a wide range of BMI (20-61 kg/m(2)). C-peptide deconvolution was used to reconstruct insulin secretion rates, and beta-cell glucose sensitivity (slope of the insulin secretion/glucose concentration dose-response curve) was determined by mathematical modeling. The incretin effect was defined as the oral-to-intravenous ratio of responses. In 8 subjects with NGT and 10 with diabetes, oral glucose appearance was measured by the double-tracer technique.RESULTS: The incretin effect on total insulin secretion and beta-cell glucose sensitivity and the GLP-1 response to oral glucose were significantly reduced in diabetes compared with NGT or IGT (P CONCLUSIONS: Potentiation of insulin secretion, glucose sensing, glucagon-like peptide-1 release, and glucagon suppression are physiological manifestations of the incretin effect. Glucose tolerance and obesity impair the incretin effect independently of one another.
AB - OBJECTIVE: To quantitate the separate impact of obesity and hyperglycemia on the incretin effect (i.e., the gain in beta-cell function after oral glucose versus intravenous glucose).RESEARCH DESIGN AND METHODS: Isoglycemic oral (75 g) and intravenous glucose administration was performed in 51 subjects (24 with normal glucose tolerance [NGT], 17 with impaired glucose tolerance [IGT], and 10 with type 2 diabetes) with a wide range of BMI (20-61 kg/m(2)). C-peptide deconvolution was used to reconstruct insulin secretion rates, and beta-cell glucose sensitivity (slope of the insulin secretion/glucose concentration dose-response curve) was determined by mathematical modeling. The incretin effect was defined as the oral-to-intravenous ratio of responses. In 8 subjects with NGT and 10 with diabetes, oral glucose appearance was measured by the double-tracer technique.RESULTS: The incretin effect on total insulin secretion and beta-cell glucose sensitivity and the GLP-1 response to oral glucose were significantly reduced in diabetes compared with NGT or IGT (P CONCLUSIONS: Potentiation of insulin secretion, glucose sensing, glucagon-like peptide-1 release, and glucagon suppression are physiological manifestations of the incretin effect. Glucose tolerance and obesity impair the incretin effect independently of one another.
KW - Adult
KW - Blood Glucose
KW - Body Mass Index
KW - Diabetes Mellitus, Type 2
KW - Female
KW - Glucose Tolerance Test
KW - Humans
KW - Hypoglycemic Agents
KW - Insulin
KW - Insulin-Secreting Cells
KW - Male
KW - Middle Aged
KW - Obesity
KW - Reference Values
U2 - 10.2337/db07-1315
DO - 10.2337/db07-1315
M3 - Journal article
C2 - 18162504
VL - 57
SP - 1340
EP - 1348
JO - Diabetes
JF - Diabetes
SN - 0901-3652
IS - 5
ER -
ID: 132049607