Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state?
Research output: Contribution to journal › Journal article › Research › peer-review
Standard
Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state? / Knop, Filip K; Vilsbøll, Tina; Højberg, Patricia V; Larsen, Steen; Madsbad, Sten; Vølund, Aage; Holst, Jens J; Krarup, Thure.
In: Diabetes, Vol. 56, No. 8, 2007, p. 1951-9.Research output: Contribution to journal › Journal article › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state?
AU - Knop, Filip K
AU - Vilsbøll, Tina
AU - Højberg, Patricia V
AU - Larsen, Steen
AU - Madsbad, Sten
AU - Vølund, Aage
AU - Holst, Jens J
AU - Krarup, Thure
N1 - Keywords: Adult; Aged; Blood Glucose; C-Peptide; Diabetes Mellitus, Type 2; Female; Gastric Inhibitory Polypeptide; Glucagon; Glucagon-Like Peptide 1; Glutaminase; Homeostasis; Humans; Insulin; Intracellular Signaling Peptides and Proteins; Male; Middle Aged; Models, Biological
PY - 2007
Y1 - 2007
N2 - We aimed to investigate whether the reduced incretin effect observed in patients with type 2 diabetes is a primary event in the pathogenesis of type 2 diabetes or a consequence of the diabetic state. Eight patients with chronic pancreatitis and secondary diabetes (A1C mean [range] of 6.9% [6.2-8.0]), eight patients with chronic pancreatitis and normal glucose tolerance (NGT; 5.3 [4.9-5.7]), eight patients with type 2 diabetes (6.9 [6.2-8.0]); and eight healthy subjects (5.5 [5.1-5.8]) were studied. Blood was sampled over 4 h on 2 separate days after a 50-g oral glucose load and an isoglycemic intravenous glucose infusion, respectively. The incretin effect (100% x [beta-cell secretory response to oral glucose tolerance test - intravenous beta-cell secretory response]/beta-cell secretory response to oral glucose tolerance test) was significantly (P <0.05) reduced (means +/- SE) in patients with chronic pancreatitis and secondary diabetes (31 +/- 4%) compared with patients with chronic pancreatitis and NGT (68 +/- 3) and healthy subjects (60 +/- 4), respectively. In the type 2 diabetes group, the incretin effect amounted to 36 +/- 6%, significantly (P <0.05) lower than in chronic pancreatitis patients with NGT and in healthy subjects, respectively. These results suggest that the reduced incretin effect is not a primary event in the development of type 2 diabetes, but rather a consequence of the diabetic state.
AB - We aimed to investigate whether the reduced incretin effect observed in patients with type 2 diabetes is a primary event in the pathogenesis of type 2 diabetes or a consequence of the diabetic state. Eight patients with chronic pancreatitis and secondary diabetes (A1C mean [range] of 6.9% [6.2-8.0]), eight patients with chronic pancreatitis and normal glucose tolerance (NGT; 5.3 [4.9-5.7]), eight patients with type 2 diabetes (6.9 [6.2-8.0]); and eight healthy subjects (5.5 [5.1-5.8]) were studied. Blood was sampled over 4 h on 2 separate days after a 50-g oral glucose load and an isoglycemic intravenous glucose infusion, respectively. The incretin effect (100% x [beta-cell secretory response to oral glucose tolerance test - intravenous beta-cell secretory response]/beta-cell secretory response to oral glucose tolerance test) was significantly (P <0.05) reduced (means +/- SE) in patients with chronic pancreatitis and secondary diabetes (31 +/- 4%) compared with patients with chronic pancreatitis and NGT (68 +/- 3) and healthy subjects (60 +/- 4), respectively. In the type 2 diabetes group, the incretin effect amounted to 36 +/- 6%, significantly (P <0.05) lower than in chronic pancreatitis patients with NGT and in healthy subjects, respectively. These results suggest that the reduced incretin effect is not a primary event in the development of type 2 diabetes, but rather a consequence of the diabetic state.
U2 - 10.2337/db07-0100
DO - 10.2337/db07-0100
M3 - Journal article
C2 - 17513701
VL - 56
SP - 1951
EP - 1959
JO - Diabetes
JF - Diabetes
SN - 0012-1797
IS - 8
ER -
ID: 8465380