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Results for “Intestinal Absorption”

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PubMed1978

Effects of early wound healing and wound treatment with zinc tape on intestinal absorption and distribution of zinc in rats.

In rats operated with large excisional skin wounds which were not treated with zinc tape, the serum zinc concentration was decreased at every observation time during the first post-operative day and the absorption of zinc from the intestine was increased. Slight decreases in the zinc concentration were seen in some tissues while liver zinc was very high. In rats with wounds treated with zinc tape, serum zinc was markedly increased at 6 hours, lower but above control levels at 7 and 12 hours and markedly increased again at 24 hours. The absorption of zinc from the intestine was low. Zinc concentration were elevated in most tissues sampled; they were high in testis and kidney and very high in liver. The results strongly indicate that the operative trauma and/or acute inflammatory conditions in the wounds in animals not treated with zinc tape initiate a movement of zinc from serum, some tissues and the content of the intestine to the liver. In the zinc tape treated group the increase in liver zinc was supplied mostly by the zinc tape. It is assumed that these large increases in zinc concentration in the liver are the result of the incorporation of zinc into certain zinc containing proteins which are produced in response to the inflammatory process in the wound. An increase was also found in the copper concentration in the liver of zinc tape treated animals and a decrease in the iron concentration in the liver of both groups of operated animals compared to controls.

Absorption↗
PubMed2003

Involvement of mast cells in basal and neurotensin-induced intestinal absorption of taurocholate in rats.

Neurotensin (NT), a hormone released from intestine by ingested fat, facilitates lipid digestion by stimulating pancreatic secretion and slowing the movement of chyme. In addition, NT can contract the gall bladder and enhance the enterohepatic circulation (EHC) of bile acids to promote micelle formation. Our recent finding that NT enhanced and an NT antagonist inhibited [(3)H]taurocholate ([(3)H]TC) absorption from proximal rat small intestine indicated a role for endogenous NT in the regulation of EHC. Here, we postulate the involvement of intestinal mast cells in the TC uptake process and in the stimulatory effect of NT. In anesthetized rats with the bile duct cannulated for bile collection, infusion of NT (10 pmol.kg(-1).min(-1)) enhanced the [(3)H]TC recovery rate from duodenojejunum by 2.2-fold. This response was abolished by pretreatment with mast cell stabilizers (cromoglycate, doxantrazole) and inhibitors of mast cell mediators (diphenhydramine, metergoline, zileuton). In contrast, mast cell degranulators (compound 48/80, substance P) and mast cell mediators (histamine, leukotriene C(4)) reproduced the effect of NT. N(G)-nitro-l-arginine methyl ester enhanced and l-arginine inhibited basal and NT-induced TC uptake, consistent with the known inhibitory effect of nitric oxide (NO) on mast cell reactivity. These results argue that basal and NT-stimulated TC uptake in rat jejunum are similarly dependent on mast cells, are largely mediated by release of mast cell mediators, and are subject to regulation by NO.

Animals↗