Hyperglycaemia stimulates pyloric motility in normal subjects.
The motor correlates of the delay in gastric emptying produced by hyperglycaemia were investigated in 11 healthy volunteers. Fasting gastroduodenal motility was measured during euglycaemia (blood glucose concentration 3-5 mmol/l) and during hyperglycaemia induced by intravenous dextrose (blood glucose concentration 12-16 mmol/l). Antral, pyloric, and proximal duodenal pressures were recorded by a sleeve/sidehole manometric assembly positioned across the pylorus, with the aid of measurements of transmucosal potential difference. During hyperglycaemia there was stimulation of isolated pyloric pressure waves when compared with the euglycaemia period (p less than 0.05). This was associated with inhibition of antral pressure waves (p less than 0.05). In nine of the 11 subjects an episode of duodenal 'phase III like' activity occurred within 15 minutes of the onset of hyperglycaemia. It is proposed that the stimulation of localised pyloric contractions and inhibition of antral contractions contribute to the delayed gastric emptying induced by hyperglycaemia. Abnormal gastric motility in patients with diabetes mellitus may be the result of hyperglycaemia itself, rather than irreversible autonomic neuropathy.
Fraser
R
R
Gastroenterology Unit, Royal Adelaide Hospital, South Australia.
Horowitz
M
M
Dent
J
J
D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000502:physiology; D005260:Female; D005746:Gastric Emptying / Q000502:physiology*; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology*; D007262:Infusions, Intravenous; D008297:Male; D008365:Manometry; D008564:Membrane Potentials / Q000502:physiology; D011706:Pyloric Antrum / Q000502:physiology; D011708:Pylorus / Q000502:physiology; D013997:Time Factors
D001786:Blood Glucose; D005947:Glucose