Es. Bjornsson et al., EFFECTS OF INSULIN AND BETA-ADRENERGIC-BLOCKADE ON THE MIGRATING MOTOR COMPLEX IN HUMANS, Scandinavian journal of gastroenterology, 30(3), 1995, pp. 219-224
Background: Interdigestive small-intestinal motility is suppressed by
hyperglycemia and also by hyperinsulinemia per se. Since hyperinsuline
mia may increase sympathetic activity, the present study was undertake
n to ascertain to what extent insulin affects phase III of the migrati
ng motor complex (MMC) and MMC-related duodenal retroperistalsis and w
hether beta-adrenergic receptors may mediate the effects of insulin. M
ethods: Fasting motility was studied in eight healthy volunteers on th
ree occasions with an eight-lumen perfused pressure catheter, with clo
sely spaced recording points in the proximal duodenum. On the control
day 5-h antroduodenojejunal manometry was performed. On another study
day euglycemic hyperinsulinemic clamping was performed for 2 h after a
n initial basal recording. On a 3rd day motility was recorded during p
ropranolol infusion, combined with a period of euglycemic hyperinsulin
emia. Results: During hyperinsulinemia complete absence of phase III o
f the MMC in the gastric antrum was observed, whereas 55% of the MMC h
ad a gastric phase-III component on the control day. The duration of p
hase III in the proximal duodenum was decreased during hyperinsulinemi
a compared with the control period (p < 0.05). This inhibitory effect
of insulin on the activity front was not prevented by beta blockade. U
nder control conditions the proportion of retroperistaltic pressure wa
ves in the proximal duodenum was 13 +/- 8% in early phase III, increas
ing in late phase III to 79 +/- 15% (p < 0.01). Duodenal phase III dur
ing hyperinsulinemia showed a similar increase in retroperistalsis, fr
om 4 +/- 4% in early phase III to 67 +/- 21% in late phase III (p < 0.
01). The corresponding proportions during beta blockade were 16 +/- 10
% and 86 +/- 14%, respectively. Conclusions: Hyperinsulinemia per se a
bolishes antral phase III and makes the duodenal phase III shorter but
does not interrupt the distinct pattern of retroperistalsis in late p
hase III. Beta-adrenergic receptors seem not to be important for these
effects of insulin or for the retroperistalsis in duodenal phase III.