Biomedical subjects

J C Thompson

Publications and source records attributed to J C Thompson.

At least 127 records · Page 7Linked to original sources

PubMed1993

The effect of endogenous cholecystokinin released by bombesin and trypsin inhibitor on the regeneration of the pancreas.

OBJECTIVE: This study examined the effects of endogenous cholecystokinin (CCK) released by bombesin and FOY-305 (a synthetic inhibitor of trypsin on pancreatic regeneration in rats). SUMMARY BACKGROUND DATA: Trophic gut hormones (CCK and bombesin) stimulate the growth of the normal rat pancreas. However, the influence of endogenous gut hormones on pancreatic regeneration is unclear. METHODS: Male Fisher rats (n = 6 to 8 per group) were fed a protein-free diet and given ethionine (700 mg/kg intraperitoneally daily) for 8 to 9 days to induce degeneration of the pancreas. Regeneration was stimulated by giving the rats a regular chow diet. The effects of bombesin (10 micrograms/kg three times a day for 7 days) or FOY-305 (200 mg/kg daily for 8 days) on the process of regeneration were examined. RESULTS: At the end of the degeneration phase, there was near-total destruction of pancreatic acinar cells. Both bombesin and FOY-305 stimulated pancreatic regeneration. Growth measurements (weight and total content of DNA and protein) were significantly increased (p < 0.05) in the bombesin- and FOY-305-treated rats compared with controls. Histologic examination revealed widespread repopulation of the pancreas with acinar cells in the bombesin- and FOY-305-treated groups. The stimulating effects of both bombesin and FOY-305 on pancreatic regeneration were blocked completely by the CCK-receptor antagonist L-364,718. Growth measurements were not significantly increased in the groups of control rats or rats given L-364,718 alone. CONCLUSIONS: These results show that bombesin and FOY-305 significantly stimulated pancreatic regeneration. Because the stimulating effects of bombesin and FOY-305 on regeneration were blocked by the specific CCK-receptor antagonist L-364,718, it was concluded that this effect was mediated by endogenous CCK.

Animals↗

PubMed1993

Cortivazol increases glucocorticoid receptor expression and inhibits growth of hamster pancreatic cancer (H2T) in vivo.

Glucocorticoids are effective in the treatment of certain leukemias and lymphomas, but their effects on the growth of several solid tumors have not been determined. We report here that cortivazol (CVZ), a potent synthetic glucocorticoid, inhibits the growth of a hamster pancreatic adenocarcinoma, H2T, in vivo. CVZ regulation of glucocorticoid receptor (GR) expression was followed as a specific molecular correlate. H2T cells were injected into cheek pouches of male Syrian golden hamsters, where they formed readily measurable tumors. Two studies were performed. In the first, hamsters were randomized to three groups immediately after injection of tumor cells: control, CVZ (0.1 micrograms/g body wt), or CVZ (0.3 micrograms/g body wt). Injections of either CVZ or its vehicle were administered on a 14-day cycle of 5 treatment days, followed by 9 days off treatment. Tumors were measured and areas calculated weekly. On day 48, the hamsters were killed and the tumors excised, weighed, and analyzed for DNA, RNA, and protein content. In the second study, randomization and treatment schedule were as before, except that on day 33 the hamsters were killed, tumors were excised and weighed, and total RNA from the tumors was isolated. GR mRNA content was determined by filter hybridization with a 32P-labeled GR cDNA probe, and the signal normalized by reprobing for alpha-tubulin as an invariant, independent signal. At either dose, CVZ significantly inhibited H2T tumor area and weight and DNA, RNA, and protein content. Body weights of animals treated with CVZ were not significantly decreased as compared with controls. In addition, GR mRNA in H2T cells was increased approximately twofold by CVZ.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

PubMed1993

Radioimmunoimaging of xenograft pancreatic cancer with 131I-monoclonal antibody P2.

Monoclonal antibodies (McAbs) to pancreatic cancer were developed by fusing SP2/0 cells and splenocytes from Balb/c mice immunized with CH-2 cells. The specific binding rates of McAb P1 and P2 were 40.1 and 43.8%, respectively, shown by binding radioreactivity assay in vitro, which were in sharp contrast with those of control groups (p < 0.05). The biodistribution of radioiodinated McAb P2 was studied by measuring parameters of tumor-specific radioreactivity in nude mice bearing CH-2 tumors. The ratios of tumors to nontumors were all > 2 at 48 h. The localization index of cancer and the ratio of tumor to pancreas were 4.05 and 4.16, respectively, at 72 h. Therefore, 131I-McAbs may be useful for radioimmunoimaging (RII) of pancreatic cancer. After intraperitoneal injection of 131I-McAb P2 into tumor-bearing nude mice, imaging of xenograft pancreatic cancer became increasingly distinct with the nonspecific background fading, especially in the period of 72-96 h. Examination of pancreatic cancer tissues by immunohistochemical methods revealed that McAb P2 was strongly positive (86%) in comparison with other tumors and normal tissues. The results demonstrated that clinical RII of pancreatic cancer was feasible with McAb P2.

Animals↗

PubMed1993

Successful intracerebroventricular allotransplantation of parathyroid tissue in rats without immunosuppression.

The lateral ventricle of the brain may be an immunoprivileged site for viable allografts. Allotransplanted parathyroid tissue from histoincompatible ACI rats survived and remained functional for more than 3 months in the cerebroventricles of recipient F344 rats. Microscopic examination proved that the allotransplanted parathyroid tissues retained normal histological features. In sharp contrast, when the parathyroid was placed beneath the renal capsule the allografted parathyroid tissue uniformly lost its capacity to liberate parathyroid hormone within one month, and only residual scar tissue remained at the transplantation site. After allotransplantation of parathyroid tissue into the cerebroventricle, the serum concentrations of both Ca++ and parathyroid hormone were maintained at levels similar to those before parathyroidectomy, until the time of sacrifice. During the 3-month period of post-transplantation observation, no neurological symptoms were noted in any of the F344 rats.

Animals↗

PubMed1993

Effects of FK506 and cyclosporine on dynamic insulin secretion from isolated dog pancreatic islets.

Pancreatic islet transplantation may be the most ideal treatment for patients with insulin-dependent diabetes mellitus. However, immunosuppressive agents such as cyclosporine A(CsA) and FK506, used for these transplanted patients have been reported to cause glucose intolerance. In the present study, we have compared the effects of CsA and FK506 on glucose-stimulated insulin release from the isolated dog pancreatic islets, which have been maintained in culture for 3 days after isolation. The isolated dog pancreatic islets, pretreated for 24 hr with either CsA or FK506 (1, 10, and 100 nM), were perifused with 16.7 mM glucose. Pretreatment with both drugs suppressed glucose-stimulated insulin secretion in a dose-dependent fashion. CsA (100 nM), which is a therapeutically relevant concentration, significantly suppressed both the first and second phases of glucose-stimulated insulin release compared with 100 nM FK506. These findings suggest that, with a therapeutically relevant concentration, FK506 may be less toxic than CsA against pancreatic islets in patients with organ or cell transplantation.

Animals↗

PubMed1993

Pituitary adenylate cyclase activating polypeptide stimulates release of peptide YY.

The purpose of these experiments was to examine the effects of the recently discovered gastrointestinal peptide, pituitary adenylate cyclase activating polypeptide (PACAP), and two structurally related peptides, vasoactive intestinal polypeptide and secretin, on release of peptide YY (PYY) in conscious dogs. Intravenous administration of PACAP-27 or -38 stimulated a dose-related release of PYY; PACAP-27 was more potent than PACAP-38. PACAP-stimulated release of PYY was inhibited significantly by atropine, whereas ganglionic or beta-adrenergic blockade with hexamethonium and propranolol treatment, respectively, did not affect PACAP-induced release of PYY significantly (P > 0.05). These results indicate that PACAP-induced release of PYY is cholinergic dependent and that beta-adrenergic tone and ganglionic transmission do not participate in PACAP-induced release of PYY. PACAP may play a role in the neural regulation of PYY release.

Animals↗

PubMed1993

Age-related changes in gallbladder contractility and cytoplasmic Ca2+ concentration in the guinea pig.

Gallbladder (GB) motility diminishes with aging. This study was performed to characterize mechanisms that are involved in changes in GB contractility that occur during aging. Cytoplasmic Ca2+ concentrations ([Ca2+]i) and the contractile force of guinea pig GB muscle strips were simultaneously measured using fura-2 and force-displacement transducers. The binding ability of the Ca2+ channel antagonist and GB muscle compliance were also examined. The COOH-terminal octapeptide of cholecystokinin (CCK-8) evoked a dose-dependent increase in force and [Ca2+]i. Changes of [Ca2+]i and contractile force of muscle strips in response to CCK-8 were significantly greater in young (2 mo old) compared with mature and aged (12 and 24 mo old) guinea pigs (changes in [Ca2+]i, ED50: 46.1 nM at 2 mo, 6.1 microM at 12 mo, and 2.8 mM at 24 mo; changes of contractile force, ED50: 24.8 microM at 2 mo, 2.1 mM at 12 mo, and 357 mM at 24 mo). However, the magnitude of the contraction at each percent change in [Ca2+]i was actually similar in young and aged guinea pigs. In a Ca(2+)-free buffer, the responses of [Ca2+]i and force to CCK-8 in both young and aged GB muscles decreased, but those were still dose and age dependent. Binding ability of the Ca2+ channel antagonist did not differ in the young and aged groups, but the compliance of the GB muscle strip decreased with aging. These results suggest that both a reduced mobilization of intracellular Ca2+ and a decreased muscle compliance are responsible, at least in part, for age-related reduced contraction of guinea pig GB in response to CCK.

Aging↗

PubMed1993

Differential expression of the neurotensin gene in the developing rat and human gastrointestinal tract.

Neurotensin (NT) is an important hormone regulating gut motility, secretion, and growth. The purpose of this study was to determine the developmental expression of the NT/neuromedin N gene (NT/N) in the gut and pancreas of rats and humans. We found that NT/N expression, initially low in the fetal rat jejunum and ileum, is increased by postnatal day 3. This increase is independent of contact with luminal nutrients as demonstrated by elevated NT/N expression in rat jejunoileal grafts implanted in nude mice. NT/N expression reaches maximal levels in the small bowel by postnatal day 14. After postnatal day 28, NT/N mRNA levels remain constant in the ileum but decrease in the jejunum. Transient NT/N expression is found in the colon of fetal and postnatal rats. Similar to the rat, NT/N expression is low in the human fetal ileum but increases in the adult. In the human colon, NT/N is transiently expressed in the fetus at midgestation but disappears by birth and, similarly, is not apparent in the adult. We conclude the following. 1) The NT/N gene demonstrates a complex pattern of tissue-specific expression; the jejunum and ileum show a similar pattern of expression until the end of the fourth postnatal week, when NT/N levels decrease in the jejunum to assume the distinctive adult topographical distribution with NT/N increasing along the jejunoileal axis. 2) NT/N is transiently expressed in the colon of rats and humans during a developmental stage characterized by morphological and functional similarities to the small bowel; therefore, NT/N may provide a useful endocrine marker to further define the complex differentiation pathway leading to small bowel and colonic phenotypes.

Adult↗

PubMed1993

The extracellular matrix components laminin, fibronectin, and collagen IV are present among the epithelial cells forming Rathke's pouch.

Cell-matrix interactions probably play a cooperative role with cell-hormone interactions to ensure normal differentiation of the adenohypophysis. The extracellular matrix (ECM) surrounding adult adenohypophysial cells contains laminin but its embryonic development has not been described. This study was carried out to test the hypothesis that adenohypophysial cells are associated with components in the ECM prior to cellular differentiation in the adenohypophysis. Fetuses were removed from Golden Syrian hamsters every 12 h from embryonic days 8.5-14. Coronal and sagittal 5-microns-thick sections of paraplast-embedded embryos were stained for fibronectin, laminin, or collagen IV using avidin-biotin immunoperoxidase staining. The adenohypophysial anlage was observed initially as a group of epithelial cells (Rathke's pouch) in the roof of the stomatodeum in contact with a basement membrane. The basement membrane stained positively for laminin, collagen IV and fibronectin. Lighter staining for laminin, fibronectin and collagen IV was observed between the developing adenohypophysial cells in Rathke's pouch. Proliferative activity was apparent in the antero-inferior region of Rathke's pouch and resulted in the formation of the bulk of the adenohypophysis. Mesenchyme infiltrates the region between the base of Rathke's pouch and the oral epithelium, thus separating the two. The basement membrane surrounding the pouch appears to become discontinuous in the regions of high proliferative activity. These results show that ECM components appear early during the development of adenohypophysial cells prior to their cellular differentiation into hormone-containing cells. This association between ECM components and developing adenohypophysial cells provides the anatomical basis for cell-ECM interactions to influence adenohypophysial development and differentiation.

Animals↗

PubMed1993

Characterization of peptide-YY release in response to intracolonic infusion of amino acids.

Peptide-YY-(1-36) [PYY-(1-36)] is an endocrine peptide that is found primarily in the mucosal layer of the colon. We reported previously that a direct intracolonic (IC) infusion of amino acids in dogs resulted in a robust release of PYY compared to other nutrients (fat, glucose, and protein). The objective of this study was to investigate the possible mechanisms underlying the release of PYY in response to IC infusion of amino acids. Intracolonic infusion of a mixture of tryptophan and phenylalanine (Trp+Phe; 100 mM; 200 ml/h) resulted in a significant release of PYY [integrated PYY release, 74.5 +/- 14.0 ng (0-120 min)/ml], which was not affected by iv atropine, hexamethonium, or propranolol treatment. Intravenous infusion of Trp+Phe failed to release PYY [integrated PYY release, -0.6 +/- 0.9 ng (0-120 min)/ml]. Intracolonic infusion of aromatic amino acids (Trp+Phe) was more potent in releasing PYY than aliphatic (leucine and glycine) and charged (arginine) amino acids. PYY release in response to IC infusion of the deamino and decarboxylated forms of Phe was significantly (P < 0.05) decreased [integrated PYY release, 17.5 +/- 2.6 and 12.1 +/- 2.8 ng (0-120 min)/ml, respectively] compared to that in response to intact Phe [integrated PYY release, 39.4 +/- 4.3 ng (0-120 min)/ml]. These results suggest that 1) PYY release in response to IC administered amino acids is independent of ganglionic, cholinergic, and beta-adrenergic transmission; 2) PYY release in response to IC amino acids is due to a direct contact of amino acids with the luminal pole of PYY cells in the colon and is not the result of a stimulatory action of amino acids via the general circulation; and 3) the amino and carboxylic groups of an amino acid as well as the ring structures of aromatic amino acids are structural requirements for PYY release.

Animals↗

PubMed1993

Studies of growth regulation in a neuroendocrine cell line.

Studies of growth-regulation of neuroendocrine cells have been hampered by a lack of suitable in vitro models. We established and have maintained a functioning human pancreatic carcinoid cell (BON) line. BON cells synthesize and secrete several growth factors. Among those, we have found that serotonin stimulates growth of BON cells through specific receptors linked to cyclic AMP pathway. In this study, effects of other growth factors on growth and serotonin release, and the effects of serotonin and TGF-beta 1 on the polyamine biosynthetic pathway, were examined. TGF-beta 1 inhibited both growth and serotonin release in a dose-dependent fashion. Basic FGF stimulated growth, but failed to affect serotonin release. Other peptide growth factors had no effect on either growth or serotonin release. Serotonin stimulated ODC enzyme activity, but TGF-beta 1 failed to affect ODC enzyme activity. These findings suggest that growth of neuroendocrine cells can be delicately regulated by their own products in an autocrine fashion.

Adult↗

PubMed1993

Persistence of the circadian variation and altered response to hepatectomy of hepatic ornithine decarboxylase activity with malignant tumor burden.

We measured the effect of MC-26 mouse colon cancers (of different sizes) on the circadian rhythm of hepatic ornithine decarboxylase (ODC) activity and hepatic ODC activity during the 24 hr after 60% hepatectomy. Tumor-free control mice showed a normal circadian rhythm of ODC activity with the highest levels at 1100 hr and the lowest levels at 2300 hr. The amplitude of the rhythm was diminished significantly in mice with a large tumor burden (3% of their body weight), and hepatic ODC activity was significantly less than in the tumor-free mice at every point during the 24 hr of the study. In mice with "early" tumors (0.3% of body weight), basal activity of ODC was normal and there was no reactive increase in activity following hepatectomy. In contrast, mice with "late" (3% of body weight) tumors had significantly lower basal ODC activities and the increase in ODC activity following hepatectomy was prolonged and exaggerated. We concluded that tumor burden is associated with abnormal ODC activity and that these differences are exaggerated after hepatectomy. Furthermore, although average ODC concentrations in tumor-bearing mice fell precipitously, the circadian rhythm in hepatic ODC persisted. This finding indicates early recognition by the host of tumor presence, which has a profound negative regulatory effect on hepatic ODC. Apparently, this effect does not impinge on circadian control mechanisms, indicating that these signals act independently.

Animals↗

PubMed1993

Glutamine is essential for epidermal growth factor-stimulated intestinal cell proliferation.

BACKGROUND: Glutamine stimulates growth of intestinal mucosa in vivo, but the mechanisms involved are unknown. The purpose of this study was to determine whether glutamine is essential for proliferation of enterocytes stimulated by epidermal growth factor (EGF). In addition, we determined which specific mitogenic actions of EGF require glutamine. METHODS: A nontransformed rat intestinal mucosal cell line (IEC-6) was stimulated with EGF (20 ng/ml) without and with glutamine (0.1 to 10 mmol/L). DNA, RNA, and protein synthesis were quantitated by determining incorporation of tritiated thymidine, tritiated uridine, and 14C-leucine, respectively. Cell numbers and messenger RNA levels of early growth response genes (zif268, jun-B, c-myc) were also determined. RESULTS: Glutamine was required for EGF stimulation of DNA, RNA, and protein synthesis and cell replication; however, EGF-stimulated expression of zif268, jun-B, and c-myc occurred in the absence of glutamine. CONCLUSIONS: This study showed that glutamine is essential for EGF-stimulated intestinal mucosal cell proliferation. The mitogenic effects of EGF can be divided into the glutamine-independent, such as the signal transduction pathway leading to the induction of early growth response genes, and the glutamine-dependent, including DNA, RNA, and protein synthesis.

Animals↗

PubMed1993

New experimental model of proximal and distal colon transposition in rats.

The proximal and distal portions of the colon have different morphologic and histochemical features. To ascertain whether these features are genetically or environmentally determined, we attempted to develop a transposition model of the proximal and distal portions of the colon in rats. Four-month-old male Fisher 344 rats were used. Four centimeters of the proximal colon segment circulated by the right colonic artery and 4 cm of the distal colon segment circulated by the middle colic artery were interchanged isoperistaltically. In the control group, the colon was transected and reanastomosed. All rats tolerated the surgery and maintained good condition for 4 weeks, when they were euthanized. No differences in body weight and food intake were observed between the transposition and control groups. Macroscopic appearance of the stomach and small intestine was normal in both the transposition and control groups, but the cecum was dilated and the new proximal portion of the colon was slightly dilated in the transposition group. This new experimental model will be helpful in examining the mechanism by which different features of the proximal and distal portions of the colon are derived. It will also assist in the research of carcinogenesis in the colon, in determining why the distal portion of the colon is more susceptible to carcinogens, compared with the proximal portion of the colon.

Animals↗

PubMed1992

Unexpected growth-stimulatory effect of somatostatin analogue on cultured human pancreatic carcinoid cells.

Therapeutic efficacy of a synthetic somatostatin analogue for the treatment of carcinoid tumors is still controversial. In vivo studies performed in our laboratory showed that a somatostatin analogue, SMS 201-995, significantly inhibited growth of human pancreatic carcinoid (BON) tumors xenotransplanted into athymic nude mice. In the present study, however, SMS 201-995 did not inhibit in vitro growth of BON cells, but rather SMS 201-995 stimulated growth in a dose-dependent fashion. The growth-stimulatory effect was likely mediated through the reduction of cyclic AMP production. Unsuccessful treatment of certain types of carcinoid tumor with SMS 201-995 may be partly due to the direct growth-stimulatory effect of SMS 201-995 on carcinoid cells.

Carcinoid Tumor↗

PubMed1992

Receptor-mediated autocrine growth-stimulatory effect of 5-hydroxytryptamine on cultured human pancreatic carcinoid cells.

5-hydroxytryptamine (5-HT) is a mitogen for fibroblasts, vascular smooth muscle cells, renal mesangial cells, and jejunal crypt cells. The human carcinoid cell line (termed BON) that we established in our laboratory from a pancreatic carcinoid tumor produces and secretes 5-HT. In this study, therefore, we examined the effect of 5-HT on growth of BON cells. Furthermore, by use of selective 5-HT receptor antagonists, we examined receptor and post-receptor mechanisms by which 5-HT-induced responses were produced. 5-HT stimulated growth of BON cells. 5-HT stimulated phosphatidylinositol (PI) hydrolysis in a dose-dependent fashion and inhibited cyclic AMP production in a dose-dependent fashion. The 5-HT1A/1B receptor antagonist, SDZ 21-009, prevented the reduction of cyclic AMP production evoked by 5-HT and inhibited the mitogenic action of 5-HT. The 5-HT1C/2 receptor antagonist, mesulergine, competitively inhibited PI hydrolysis, but did not affect the mitogenic action of 5-HT. The mitogenic action of 5-HT and the reduction of cyclic AMP production evoked by 5-HT were also inhibited by pertussis toxin. These results suggest that 5-HT is an autocrine growth factor for BON cells and that mitogenic mechanism of 5-HT involves receptor-mediated inhibition of the production of cyclic AMP which may be linked to pertussis toxin-sensitive GTP binding protein. 8-bromo-cyclic AMP inhibited growth of BON cells whereas 8-bromo-cyclic GMP had no effect on cell growth. Involvement of protein kinase A in BON cell growth regulation was confirmed by the observation that a cAMP-dependent protein kinase antagonist (Rp-cAMPS) could stimulate BON cell growth.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1992

Early stages of gallstone formation in guinea pig are associated with decreased biliary sensitivity to cholecystokinin.

The purpose of this study was to measure differences in gallbladder sensitivity to cholecystokinin (CCK) in vivo during the early stages of gallstone formation and to correlate these findings to gallbladder CCK receptors. Guinea pigs were placed on either a normal diet or a two-week cholelithogenic diet, after which gallbladder emptying pressure to exogenously administered CCK was measured in vivo, according to the presence or absence of gallstones. At all doses of CCK tested (except 10(-10) mol/kg), the gallbladder response to CCK of guinea pigs that did not develop gallstones (on the cholelithogenic diet) was more sensitive than that of guinea pigs that did develop gallstones. Neither group was different from guinea pigs on a normal diet. In a second experiment, CCK receptors were measured on gallbladder muscularis from guinea pigs after two weeks on the same diet as in the first experiment. Those guinea pigs that did not develop gallstones had greater concentrations of CCK receptors (149 +/- 9 fmol/mg protein) than those that did develop gallstones (70 +/- 23 fmol/mg protein). Neither group was different from normal diet guinea pigs (119 +/- 57 fmol/mg protein). At the time point measured, there were no differences in the lipid chemistry or protein concentrations of gallbladder bile between the guinea pigs on the cholelithogenic diet that did or did not develop gallstones, or those on normal guinea pig chow. We conclude that the early stages of gallstone formation in guinea pigs are associated with decreased gallbladder sensitivity to CCK and that this change may be due to a lower concentration of CCK receptors on the gallbladder smooth muscle.

Animals↗

PubMed1992

Neurotensin prevents intestinal mucosal hypoplasia in rats fed an elemental diet.

Liquid elemental diets are associated with mucosal hypoplasia of both the small intestine and colon. Neurotensin, a tridecapeptide widely distributed in the gut, is trophic for the small intestine of rats fed a normal chow diet. The purpose of this study was to determine whether neurotensin could reverse the hypoplasia of intestinal mucosa that is associated with feeding a liquid elemental diet. Forty male Sprague-Dawley rats were randomized into five groups. Four groups were fed (for seven days) a glutamine-free liquid elemental diet. Subcutaneous injection of saline (control) or neurotensin (33, 100 or 300 micrograms/kg) were given to the groups of rats every 8 hr for seven days. Group five (Chow) received rat chow ad libitum for seven days. Rats were killed on day 8, and the proximal jejunum, distal ileum, and proximal colon removed. Mucosal weight, DNA, RNA, and protein contents were determined. Neurotensin (300 micrograms/kg) increased the cellularity of the small intestinal mucosa and reversed mucosal hypoplasia due to an elemental diet; a more pronounced effect was noted in the jejunum compared to the ileum. Neurotensin (33 and 100 micrograms/kg) increased mucosal DNA content in the jejunum but was not effective in reversing the hypoplasia. Neurotensin had no effect on growth of colonic mucosa. These results suggest that neurotensin may be an important trophic hormone for the small intestine. Administration of neurotensin may alleviate hypoplasia of the small bowel mucosa and maintain functional integrity of the gut during prolonged feeding of an elemental diet.

Animals↗