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PubMed1985

Can gastrointestinal hormones enhance intestinal absorption?

Recent studies have suggested that certain gastrointestinal peptides exert a trophic effect on the small intestine. We chose to evaluate the effect of glucagon and cholecystokinin-octapeptide (CCK-OP) on absorption of substrates in both developing and mature small intestine. Developing small intestine was evaluated in a rat fetal intestine transplant model, and mature rat small intestine was studied in in situ but isolated 10 cm segments of jejunum and ileum. Glucagon, 10 micrograms/kg/day, and CCK-OP, 45 micrograms/kg/day, were delivered continuously for 14 days through a subcutaneous osmotic pump. Intestinal absorption was determined with labeled substrates (14C-galactose and 14C-glycine) by a recirculation perfusion technique. Absorption results were expressed as percentage increase over control. The fetal intestine response to glucagon infusion was a 13% rise in galactose absorption and a 27% rise in glycine absorption. After CCK-OP infusion, fetal galactose absorption was 11% and glycine absorption rose 17%. Mature jejunal galactose absorption rose 53% and glycine absorption rose 55% after glucagon infusion. The ileal response to glucagon was a 271% rise in galactose absorption (p less than 0.05) and a 21% increase in glycine absorption. Infusion of CCK-OP decreased jejunal galactose absorption 3% but increased glycine absorption 41%. The ileal response was a 224% increase in galactose absorption (p less than 0.05) and a 19% increase in glycine absorption. Our data suggest that chronic administration of glucagon and CCK-OP can increase substrate absorption in developing and mature rat small intestine. Perhaps manipulation of the gastrointestinal hormone environment may result in increased absorption in man.

Animals↗
PubMed1991

An in vitro evaluation of metabolism and poor membrane permeation impeding intestinal absorption of leucine enkephalin, and methods to increase absorption.

The goals of this study were to evaluate how metabolism and poor membrane permeability act as barriers to absorption of a model peptide, leucine enkephalin (YGGFL), and how those barriers can be overcome. The in vitro everted rat intestine method was used. YGGFL was rapidly metabolized when exposed to the mucosa of the jejunum, and destyrosyl leucine enkephalin was formed. Metabolism was slower for ileal intestinal segments, however, and was almost absent when colonic segments were used. The aminopeptidase inhibitor boroleucine, an aminoboronic acid derivative, reduced the YGGFL metabolism rate 2-fold at 1/100th the concentration of substrate when the intestine was simultaneously exposed to substrate and inhibitor. Pretreatment of the intestine with boroleucine further reduced the metabolism rate. Thiorphan, an inhibitor of endopeptidase 24.11, had additive inhibitory effects with boroleucine. Inhibition of metabolism alone did not enable YGGFL to permeate the membrane. The permeability enhancer, sodium glycocholate, also did not alone enable membrane permeation. Substantial YGGFL permeated the membrane only when metabolism was inhibited and permeability was enhanced. EDTA had both these effects.

Animals↗
PubMed1978

[Jejunal mucosa in infants with the syndrome of disorders of intestinal absorption (ultrastructure and morphometry)].

Ultrastructural studies and counts of interepithelial lymphocytes and the density of cellular infiltration of the lamina propria were carried out on 10 biopsies of the small intestine from infants of 4 months to 2 years with the syndrome of disturbed intestinal absorption. The greatest disorders were found to occur in celiac disease and intolerance to cow milk protein and to be manifested in subtotal atrophy of villi and destructive lesions of enterocytes. The authors believe that the marked infiltration of the epithelial layer with lymphocytes and the lamina propria of the mucous membrane with plasma cells represent manifestations of the local immunological response.

Animals↗