GASTRIC-EMPTYING AND RELEASE OF INCRETIN HORMONES AFTER GLUCOSE-INGESTION IN HUMANS

Citation
J. Schirra et al., GASTRIC-EMPTYING AND RELEASE OF INCRETIN HORMONES AFTER GLUCOSE-INGESTION IN HUMANS, The Journal of clinical investigation, 97(1), 1996, pp. 92-103
Citations number
53
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
00219738
Volume
97
Issue
1
Year of publication
1996
Pages
92 - 103
Database
ISI
SICI code
0021-9738(1996)97:1<92:GAROIH>2.0.ZU;2-B
Abstract
This study investigated in eight healthy male volunteers (a) the gastr ic emptying pattern of 50 and 100 grams of glucose; (b) its relation t o the phase of interdigestive motility (phase I or II) existing when g lucose was ingested; and (c) the interplay between gastric emptying or duodenal perfusion of glucose (1.1 and 2.2 kcal/min; identical total glucose loads as orally given) and release of glucose-dependent insuli notropic peptide (GIP), glucagon-like peptide-1(7-36)amide (GLP-1), C- peptide, insulin, and plasma glucose, The phase of interdigestive moti lity existing at the time of glucose ingestion did not affect gastric emptying or any metabolic parameter, Gastric emptying of glucose displ ayed a power exponential pattern with a short initial lag period. Duod enal delivery of glucose was not constant but exponentially declined o ver time. Increasing the glucose load reduced the rate of gastric empt ying by 27.5% (P < 0.05) but increased the fractional duodenal deliver y of glucose, Both glucose loads induced a fed motor pattern which was terminated by an antral phase III when similar to 95% Of the meal had emptied. Plasma GLP-1 rose from basal levels of similar to 1 pmol/lit er to peaks of 3.2 +/- 0.6 mol/liter with 50 grams of glucose and of 7 .2 +/- 1.6 pmoll/liter with 100 grams of glucose. These peaks occurred 20 min after glucose intake irrespective of the load. A duodenal deli very of glucose exceeding 1.4 kcal/min was required to maintain GLP-1 release in contrast to ongoing GIP release with negligibly low emptyin g of glucose. Oral administration of glucose yielded higher GLP-1 and insulin releases but an equal GIP release compared with the isocaloric duodenal perfusion. We conclude that (a) gastric emptying of glucose displays a power exponential pattern with duodenal delivery exponentia lly declining over time and (b) a threshold rate of gastric emptying o f glucose must be exceeded to release GLP-1, whereas GIP release is no t controlled by gastric emptying.