Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state?

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

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.

I: Diabetes, Bind 56, Nr. 8, 2007, s. 1951-9.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Knop, FK, Vilsbøll, T, Højberg, PV, Larsen, S, Madsbad, S, Vølund, A, Holst, JJ & Krarup, T 2007, 'Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state?', Diabetes, bind 56, nr. 8, s. 1951-9. https://doi.org/10.2337/db07-0100

APA

Knop, F. K., Vilsbøll, T., Højberg, P. V., Larsen, S., Madsbad, S., Vølund, A., Holst, J. J., & Krarup, T. (2007). Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state? Diabetes, 56(8), 1951-9. https://doi.org/10.2337/db07-0100

Vancouver

Knop FK, Vilsbøll T, Højberg PV, Larsen S, Madsbad S, Vølund A o.a. Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state? Diabetes. 2007;56(8):1951-9. https://doi.org/10.2337/db07-0100

Author

Knop, Filip K ; Vilsbøll, Tina ; Højberg, Patricia V ; Larsen, Steen ; Madsbad, Sten ; Vølund, Aage ; Holst, Jens J ; Krarup, Thure. / Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state?. I: Diabetes. 2007 ; Bind 56, Nr. 8. s. 1951-9.

Bibtex

@article{1fe48d30acd011ddb538000ea68e967b,

title = "Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state?",

abstract = "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.",

author = "Knop, {Filip K} and Tina Vilsb{\o}ll and H{\o}jberg, {Patricia V} and Steen Larsen and Sten Madsbad and Aage V{\o}lund and Holst, {Jens J} and Thure Krarup",

note = "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",

year = "2007",

doi = "10.2337/db07-0100",

language = "English",

volume = "56",

pages = "1951--9",

journal = "Diabetes",

issn = "0012-1797",

publisher = "American Diabetes Association",

number = "8",