Details

Autor(en) / Beteiligte

• Ma, J.
• Pilichiewicz, A. N.
• Feinle-Bisset, C.
• Wishart, J. M.
• Jones, K. L.
• Horowitz, M.
• Rayner, C. K.

Titel

Effects of variations in duodenal glucose load on glycaemic, insulin, and incretin responses in type 2 diabetes

Ist Teil von

• Diabetic medicine, 2012-05, Vol.29 (5), p.604-608

Ort / Verlag

Oxford, UK: Blackwell Publishing Ltd

Erscheinungsjahr

2012

Quelle

MEDLINE

Beschreibungen/Notizen

• Diabet. Med. 29, 604–608 (2012) Aims  Postprandial glucagon‐like peptide‐1 (GLP‐1) secretion and the ‘incretin effect’ have been reported to be deficient in Type 2 diabetes, but most studies have not controlled for variations in the rate of gastric emptying. We evaluated blood glucose, and plasma insulin, GLP‐1 and glucose‐dependent insulinotropic polypeptide (GIP) responses to intraduodenal glucose in Type 2 diabetes, and compared these with data from healthy controls. Methods  Eight males with well‐controlled Type 2 diabetes, managed by diet alone, were studied on four occasions in single‐blind, randomized order. Blood glucose, and plasma insulin, GLP‐1, and GIP were measured during 120‐min intraduodenal glucose infusions at 1 kcal/min (G1), 2 kcal/min (G2) and 4 kcal/min (G4) or saline control. Results  Type 2 patients had higher basal (P < 0.0005) and incremental (P < 0.0005) blood glucose responses to G2 and G4, when compared with healthy controls. In both groups, the stimulation of insulin and GLP‐1 by increasing glucose loads was not linear; responses to G1 and G2 were minimal, whereas responses to G4 were much greater (P < 0.005 for each) (incremental area under the GLP‐1 curve 224 ± 65, 756 ± 331 and 2807 ± 473 pmol/l.min, respectively, in Type 2 patients and 373 ± 231, 505 ± 161 and 1742 ± 456 pmol/l.min, respectively, in healthy controls). The GLP‐1 responses appeared comparable in the two groups. In both groups there was a load‐dependent increase in plasma GIP with no difference between them. Conclusions  In patients with well‐controlled Type 2 diabetes, blood glucose, insulin and GLP‐1 responses are critically dependent on the small intestinal glucose load, and GLP‐1 responses are not deficient.