Authors: Jonatan I Bagger Filip K Knop Asger Lund Jens J Holst Tina Vilsbøll
Publish Date: 2014/05/31
Volume: 57, Issue: 8, Pages: 1720-1725
Abstract
Type 2 diabetes is associated with hypersecretion of glucagon during an OGTT whereas iv glucose suppresses glucagon levels This suggests that type 2 diabetic hyperglucagonaemia may result from glucose stimulation of the gastrointestinal tract We evaluated glucagon responses to increasing amounts of glucose given orally and corresponding isoglycaemic iv glucose infusions IIGIs in patients with type 2 diabetes and in healthy controlsPlasma glucagon responses were measured during three 4 h OGTTs with increasing loads of glucose 25 g 75 g and 125 g and three corresponding IIGIs in eight patients with type 2 diabetes age mean ± SEM 57 ± 4 years BMI 295 ± 10 kg/m2 HbA1c 70 ± 03 53 ± 2 mmol/mol and eight healthy individuals age 57 ± 4 years BMI 289 ± 07 kg/m2 HbA1c 54 ± 01 36 ± 1 mmol/molIn healthy controls no difference in glucagon suppression during the first 45 min of the 25 g OGTT and the corresponding IIGI −153 ± 35 vs −133 ± 24 min × pmol/l p = NS was observed whereas patients with type 2 diabetes only exhibited significant glucagon suppression following IIGI 29 ± 27 vs −144 ± 20 min × pmol/l p = 0005 At higher oral glucose loads this difference increased and also became evident in healthy controlsIn patients with type 2 diabetes increasing amounts of oral glucose elicit hypersecretion of glucagon whereas corresponding IIGIs result in significant glucagon suppression a phenomenon that is also observed in healthy individuals when larger glucose loads are ingested orally This suggests that the hyperglucagonaemic response to oral glucose in type 2 diabetes may represent a pathological version of a gutderived physiological phenomenon
Keywords: