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Diabetes 56:1951-1959, 2007
DOI: 10.2337/db07-0100
© 2007 by the American Diabetes Association
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Reduced Incretin Effect in Type 2 Diabetes
Cause or Consequence of the Diabetic State?
1 Department of Internal Medicine F, Gentofte Hospital, Hellerup, Denmark
2 Department of Medical Physiology, The Panum Institute, University of Copenhagen, Copenhagen, Denmark
3 Department of Internal Medicine M, Glostrup Hospital, Hellerup, Denmark
4 Department of Endocrinology, Hvidovre Hospital, Hvidovre, Denmark
5 Department of Biostatistics, Novo Nordisk, Copenhagen, Denmark
Address correspondence and reprint requests to Filip Krag Knop, MD, Department of Internal Medicine, Gentofte Hospital, University of Copenhagen, Niels Andersens Vej 65, DK-2900 Hellerup, Denmark. E-mail: filipknop{at}dadlnet.dk
Abbreviations:
AUC, area under the curve; FPG, fasting plasma glucose; GIP, glucose-dependent insulinotropic polypeptide; GLP, glucagon-like peptide; HOMA, homeostasis model assessment; HOMA-IR, HOMA for insulin resistance; ICA, islet cell autoantibody; ISR, insulin secretion rate; NGT, normal glucose tolerance; OGTT; oral glucose tolerance test; PG, plasma glucose
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 [ß-cell secretory response to oral glucose tolerance test – intravenous ß-cell secretory response]/ß-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.
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S. P. Choukem and J.-F. Gautier Comment on: Knop et al. (2007) Reduced Incretin Effect in Type 2 Diabetes: Cause or Consequence of the Diabetic State? Diabetes 56:1951 1959 Diabetes, January 1, 2008; 57(1): e1 - e1. [Full Text] [PDF]
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F. K. Knop, T. Vilsboll, S. Madsbad, T. Krarup, and J. J. Holst Response to Comment on: Knop et al. (2007) Reduced Incretin Effect in Type 2 Diabetes: Cause or Consequence of the Diabetic State? Diabetes 56:1951 1959 Diabetes, January 1, 2008; 57(1): e2 - e3. [Full Text] [PDF]
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