Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GASTROINTESTINAL HORMONES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,027 records · Page 57Linked to original sources
PubMed2001

Diurnal metabolic profiles after 14 d of an ad libitum high-starch, high-sucrose, or high-fat diet in normal-weight never-obese and postobese women.

BACKGROUND: The influence of the amount and type of carbohydrates in the diet on risk factors for obesity, diabetes, and cardiovascular disease remains unclear. OBJECTIVE: We investigated the effects of 2 low-fat diets (high-sucrose and high-starch) and a high-fat diet on glycemia, lipidemia, and hormonal responses in never-obese and postobese women. DESIGN: Eighteen normal-weight women (8 postobese and 10 never-obese) consumed 3 ad libitum diets (high-fat, high-starch, and high-sucrose) for 14 d each. On day 15, we measured fasting and postprandial glucose, lactate, insulin, triacylglycerol, nonesterified fatty acids (NEFA), glycerol, glucagon, glucose-dependent insulinotropic polypeptide, and glucagon-like peptide 1. RESULTS: The high-sucrose diet induced significantly lower total areas under the curve (AUCs) for glucose and NEFA and a significantly higher lactate AUC than did the high-fat and high-starch diets; there were no significant differences in the insulin AUCs. The triacylglycerol AUC was greater with the high-fat and high-sucrose diets than with the high-starch diet. Gastrointestinal hormone concentrations differed between diets, but not between the 2 subject groups. Comparisons between subject groups for all diets combined showed lower relative insulin resistance and lower AUCs for glucose, insulin, and triacylglycerol in the postobese group. CONCLUSIONS: High-starch and high-sucrose diets had no adverse effects on postprandial glycemia, insulinemia, or lipidemia compared with a high-fat diet. A sucrose-rich diet may improve glucose metabolism, but may have an adverse effect on lipidemia, compared with a starch-rich diet. Postobese women seemed to be more insulin-sensitive and more efficient at storing triacylglycerol than were never-obese women, regardless of dietary composition.

Adult↗
PubMed2004

The protective and hormonal effects of proanthocyanidin against gastric mucosal injury in Wistar rats.

BACKGROUND: Proanthocyanidin, a grape-seed polyphenol, has been reported to have protective properties against vascular injury and ulcers, preventive effects against atherosclerosis and cancer, and antioxidative effects, such as improving lipid metabolism and slowing aging. However, little has been reported on its antiulcer effects. We aimed to elucidate the antiulcer mechanism of proanthocyanidin. METHODS: Gravinol, containing 89.3% proanthocyanidin, was used. Proanthocyanidin solution, in distilled water, at 0.002%, 0.02%, 0.2%, or 1%, was given to rats ad libitum for 2 weeks. Distilled water was given to control rats. The effect of proanthocyanidin on gastric mucosal injury was investigated with the water-immersion restraint stress model. The ratios of areas of hemorrhagic erosion were compared as the lesion index. Myeloperoxidase activities were also examined, as an index of tissue injury. Superoxide dismutase activity was measured to examine its antioxidative effect. Furthermore, serum gastrin, somatostatin, histamine, and prostaglandin E(2) levels were measured in this rat model. RESULTS: Proanthocyanidin administration significantly suppressed gastric mucosal injury, induced by water-immersion restraint stress, in a dose-dependent manner. Myeloperoxidase activities were also significantly inhibited, whereas superoxide dismutase activities were significantly stimulated. As to gastrointestinal hormones, the secretion of gastrin, somatostatin, and histamine was significantly inhibited, while prostaglandin E(2) secretion was significantly stimulated. CONCLUSIONS: Proanthocyanidin was shown to have a protective effect on the gastric mucosa. The mechanisms underlying the effect of proanthocyanidin were considered to be the following: anti-gastrin and anti-histamine effects to prevent attacks by water-immersion restraint stress, and mucoprotective properties, bestowed by increased prostaglandin and increased superoxide dismutase activities in the gastric mucosa.

Animals↗
PubMed1977

The effects of glucagon, secretin, pancreozymin and pentagastrin on the hepatic arterial vascular bed of the dog.

1 The sympathetically-innervated arterial vascular bed of the dog's liver was perfused from a femoral artery. Arterial blood flow and perfusion pressure were monitored continuously and the hepatic arterial vascular resistance (HAVR) calculated from these measurements. 2 Commercial preparations of secretin, pancroezymin, glucagon and pentagastrin were administered by intra-arterial (i.a.) injection and infusion. 3 Secretin and pancreozymin by injection caused dose-dependent hepatic arterial vasodilatation, and on a molar basis were both more potent than glucagon or pentagastrin. 4 Intra-arterial infusions of secretin and pancreozymin caused hepatic arterial vasodilatation at calculated blood concentrations close to those measured under physiological conditions by other investigators. The vasodilatation was of the same duration as that of the hormone infusions. 5 Pentagastrin by i.a. injection caused dose-dependent hepatic arterial vasodilatation; by i.a. infusion, vasodilatation occurred but there was marked 'escape' from the effects during the continued infusion. 6 As reported previously, glucagon by injection caused dose-dependent hepatic arterial vasodilatation of long duration; by infusion, glucagon caused vasodilatation that persisted after the cessation of the infusion. 7 Glucagon infused i.a. inhibited the vasoconstricter effects of i.a. noradrenaline, over the same range of infusions that caused hepatic arterial vasodilatation. 8 Secretin or pancreozymin did not antagonize the effects of noradrenaline on the hepatic arterial vascular bed at any doses used. 9 Pentagastrin did not antagonize the vasoconstrictor effect of noradrenaline whether hepatic arterial vasodilatation resulted from the pentagastrin infusion, or not. 10 These results are discussed with respect to the possible control of the hepatic arterial vascular bed by gastrointestinal hormones.

Animals↗
PubMed2001

Upregulation of Ghrelin expression in the stomach upon fasting, insulin-induced hypoglycemia, and leptin administration.

Ghrelin is a novel gut-brain peptide that binds to the growth hormone secretagogue receptor (GHS-R), thereby functioning in the regulation of growth hormone (GH) release and food intake. Ghrelin-producing cells are most abundant in the oxyntic glands of the stomach. The regulatory mechanism that governs the biosynthesis and secretion of ghrelin has not been clarified. We report that ghrelin mRNA expression in the gastric fundus was increased, but that ghrelin peptide content decreased after a 48-h fast. Both values returned to control levels after refeeding. The ghrelin plasma concentration in the gastric vein and systemic venous blood increased after 24- and 48-h fasts. Furthermore, des-octanoylated ghrelin and n-octanoylated ghrelin were found in rat stomach, with the ratio of des-octanoylated ghrelin to n-octanoylated ghrelin markedly increased after fasting. The ghrelin mRNA level in the stomach also increased after administration of insulin and leptin. Conversely, db/db mice, which are deficient in the leptin receptor, had lower ghrelin mRNA levels than control mice. These findings suggest that this novel gastrointestinal hormone plays a role in the regulation of energy balance.

Animals↗
PubMed1991

[Relations between gastrointestinal interdigestive motility and secretion].

The motility of the upper gastrointestinal tract in the interdigestive state shows a cycling pattern called Migrating Motor Complex (MMC) and is composed by phases I, II and III. Gastric, biliary and pancreatic secretion show cyclical fluctuations during fasting closely associated with the motor activity. The motor and secretory interdigestive activity is regulated by a complex interplay of nerval and humoral mechanisms. Among them, motilin, a gastrointestinal hormone mainly secreted from the duodenum, is supposed to play a central role in the initiation of phase III. Gastric acid secretion, directly or by means of motilin release, may modulate the duration of the MMC and the propagation of phase III in the small intestine. Pancreatic secretion does not initiate phase III but may exert a control on gastric interdigestive motility probably by means of pancreatic polypeptide release. Biliary interdigestive secretion seems to play a little or no role in the control of these phenomena. The coordination of motor and secretory events is likely to be under control of the duodenum.

Animals↗
PubMed1981

Sorbin, a peptide contained in porcine upper small intestine which induces the absorption of water and sodium in the rat duodenum.

A fraction increasing water and sodium absorption in rat duodenum was detected in the material obtained at an early stage of purification of the hitherto isolated duodenal hormones. In Wistar rats, duodenal loops were made in situ and filled with a solution containing 0.138 mM NaCl, with 14C PEG and 22Na as markers; the final content was collected after 1 h and the movements of water and Na measured. In contrast to secretin, cholecystokinin, and somatostatin, which induced duodenal secretion, and with pentagastrin, which induced duodenal absorption and stimulated acid secretion, this fraction induced duodenal absorption f Na and water without stimulating acid secretion. The fraction was obtained by chromatography of a concentrate of intestinal peptides in 0.2 M acetic acid on Sephadex G25 (fine), and its active component was found to be methanol-soluble at pH4 and insoluble at pH7.5. It was eluted from carboxymethylcellulose 22 with 0.04 M ammonium bicarbonate and gel filtration of Sephadex G50 *fine), resulting in a tenfold increase in activity. Incubation with chymotrypsin suppressed the biological activity, indicating a peptidic nature. The substance displayed biological and radioimmunological properties distinct from those of the gastrointestinal hormones. Particularly, no cross-reactivity was found with gastrin, prolactin, and angiotensin, which are known to increase intestinal absorption. It therefore seems possible that the activity described is due to a peptide that has as yet not been isolated. The name 'sorbin' is proposed for this active principle.

Animals↗
PubMed1993

Physiology of motor function of the sphincter of Oddi.

Human and experimental studies of the sphincter of Oddi have established that the sphincter is not a simple and passive smooth muscle portion of the biliary system; rather, it plays an active role in modulating bile flow into the duodenum in both the fasted and the postprandial states. The sphincter of Oddi in the opossum, and likely in man, demonstrates spontaneous phasic and perhaps peristaltic activity that affects bile flow into the duodenum. The sphincter appears to be under the control of a smooth muscle pacemaking-like region in the proximal sphincter that controls the frequency and direction of propagation of the phasic contractions. Immunohistochemical studies have documented the presence of dense concentrations of neuropeptide-containing myenteric nerves in the sphincter of Oddi. Physiologic studies have confirmed that these peptides, in combination with the classic gastrointestinal hormones, exert significant effects on biliary motility. Experimental studies of the motor physiology of the sphincter of Oddi have advanced our understanding of human biliary motility and dysmotility. A subset of patients experiences biliary-like pain after cholecystectomy. This pain may be attributable to either mechanical stenosis of the papilla or dysfunction of the sphincter of Oddi. No definitive test currently exists to establish the diagnosis with adequate sensitivity or specificity. It is hoped that further development of ultrasonographic, scintigraphic, manometric, or electromyographic techniques will allow a clearer definition of patients who truly have sphincter dysfunction and who might benefit from medical, endoscopic, or surgical therapy.

Animals↗
PubMed1986

Effect of methionine-enkephalin analog (FK 33-824) on plasma motilin.

In an attempt to elucidate the effect of opioid peptide on the secretion of various gastrointestinal hormones, the methionine-enkephalin analog, FK 33-824 (FK) was injected intramuscularly in healthy male adults. The plasma levels of motilin, gastrin and cholecystokinin were assessed by specific radioimmunoassay. After the injection of FK, the plasma level of motilin markedly decreased from the baseline value of 456 +/- 70.2 pg/ml to 264 +/- 44.7 pg/ml at 120 min. On the other hand, the plasma levels of cholecystokinin and gastrin remained unchanged. These data indicate that endogenous methionine-enkephalin may have an direct inhibitory effect on the secretion of motilin.

Adult↗
PubMed1995

Studies in transgenic mice reveal potential relationships between secretin-producing cells and other endocrine cell types.

We have produced transgenic mice expressing fusion genes consisting of 1.6 kilobase pairs of the secretin gene 5' flanking region to direct the expression of human growth hormone (hGH) or simian virus 40 large T antigen to secretin-producing cells. Analysis of different mouse tissues for hGH transcripts revealed expression in each of the major secretin-producing tissues, namely the intestine and endocrine pancrease. Multiple label immunohistochemistry demonstrated that the transgene was correctly directed to secretin cells in the intestinal tract, including a previously unrecognized population of secretin cells in the colon of adult and developing mice. In the small intestine, subpopulations of hGH-containing cells frequently coexpressed substance P, serotonin, and cholecystokinin, whereas in the colon, cells expressing hGH frequently coexpressed glucagon, peptide YY, or neurotensin. Transgenic mice expressing large T antigen in secretin cells developed poorly differentiated neuroendocrine tumors of the small intestine, well differentiated colonic tumors containing glucagon-expressing cells, and insulin-producing tumors in pancreas. These studies indicate that the major cis-regulatory sequences necessary for secretin expression in enteroendocrine cells and fetal islets are localized with 1.6 kilobase pairs of the transcriptional start site. Coexpression of reporter transgenes with several gastrointestinal hormones suggests a potential relationships between secretin cells and other enteroendocrine cell types, as well as pancreatic beta cells.

Animals↗
PubMedDate not supplied

On the mechanism of hormone recognition and binding by the CCK-B/gastrin receptor.

Lipidation with long-chain di-fattyacyl-glycerol moieties was used to anchor gastrin in CCK peptides irreversibly to lipid bilayers lipopeptide transfer to model phospholipid bilayers is fast and quantitative, leading to a different mode of insertion of lipo-gastrin and lipo-CCK in lipid layers. Lipo-gastrin remains exposed to the bulk solvent in a predominantly random coil structure as a consequence of electrostatic repulsion, whereas lipo-CCK exhibits a pronounced tendency to form peptide domains with insertion of its C-terminus into more hydrophobic compartments of the bilayers. Thereby Ca2+ at physiological concentrations favours this aggregational phenomenon. Since both lipo-peptides were found to retain almost full receptor affinity despite their irreversible anchorage to the bilayer, a membrane-bound pathway in the receptor recognition and binding process is indeed possible. According to the data collected in this study, CCK might possibly use this pathway, whereas accumulation of gastrin on the cell membrane with prefolding of the ligand at the water/lipid interface is hardly conceivable. Nevertheless the observed receptor interaction of the deliberately membrane-anchored gastrin offers interesting constraints for computational docking experiments on a modelled CCK-B/gastrin receptor by additionally taking into account information derived from mutagenesis studies. Despite the limitations of such modelling experiments, the resulting picture of the gastrin/receptor complex allowed the visualization and rationalization of the experimental results of the extensive structure-function studies performed previously on this family of gastrointestinal hormones.

Animals↗
PubMed1995

Pathogenesis of feline diabetes mellitus.

Cats are one of the few species that develop a form of diabetes mellitus that is clinically and histologically analogous to human type 2 diabetes mellitus. Figure 9 summarizes the etiologic factors thought to be involved in the development of feline and human type 2 diabetes. The main metabolic characteristics of type 2 diabetes mellitus are impaired insulin secretion and resistance to the action of insulin in its target tissues. Impaired beta cell function occurs before histologic changes become evident. The characteristic histologic finding in cats with type 2 diabetes is deposition of amyloid in pancreatic islets. Amyloid deposition occurs before the onset of clinical signs, but does not seem to be the primary defect. Pancreatic amyloid is derived form the recently discovered pancreatic hormone amylin. Amylin is synthesized in pancreatic beta cells, and is co-stored and co-secreted with insulin. Amylin has been postulated to be involved in the pathogenesis of feline diabetes mellitus both through its metabolic effects, which include inhibition of insulin secretion and induction of insulin resistance, and via progressive amyloid deposition and beta cell degeneration. Increased amylin concentration has been documented intracellularly in cats with impaired glucose tolerance and in the plasma of diabetic cats, and supports the hypothesis that amylin is involved in the pathogenesis of type 2 diabetes. Obesity is a common finding in diabetic felines and is a contributing factor to the insulin resistance present in type 2 diabetes. Clinical signs of diabetes develop once total insulin secretion decreases to 20% to 25% of normal levels. Many diabetic cats have been treated successfully with oral hypoglycemics, but 50% to 70% of diabetic cats are insulin dependent. Based on histologic evidence, this is the result of extensive amyloid deposition and subsequent beta cell degeneration, rather than autoimmune destruction of pancreatic beta cells associated with type 1 diabetes. Alternative ways of treating type 2 diabetes currently are being investigated. Amylin antagonists recently have been proposed as a novel treatment to reverse the deleterious effects of excessive amylin concentrations. The gastrointestinal hormone glucagon-like peptide-1 may also prove useful in treating diabetic cats, because of its stimulatory effect on insulin secretion and synthesis, and the absence of significant hypoglycemic effect.

Amyloid↗
PubMed1991

Effects of somatostatin analog SMS 201-995 on enterotoxigenic diarrhea.

Somatostatin analog SMS 201-995 causes a dose-related suppression of the release and/or action of several gastrointestinal hormones and impairs several anterior pituitary functions. Some patients with illness involving abnormal hormonal activity have responded to treatment with SMS 201-995, including resolution of severe secretory diarrhea. This study examined SMS 201-995 inhibition of Escherichia coli heat-stable enterotoxin STa (STa) effects and effects of the analog in the rabbit RITARD model with enterotoxigenic Escherichia coli. SMS 201-995 did not alter STa binding to its receptor on piglet brush border membranes. The analog, at concentrations of 0.1 micrograms/ml (0.1 microM) and 1 microgram/ml (1 microM) did not significantly alter STa activation of intestinal epithelial cell particulate guanylate cyclase. At maximal dosing the analog significantly reduced intestinal fluid secretion in suckling mice that was induced by either 8-bromo cyclic GMP or STa. In piglets, the analog reduced by 37-44% the amount of diarrhea induced by STa. However, even with maximal dosing, the piglets still had significant diarrhea, although of a lesser amount. In the rabbit RITARD model the drug failed to alter the severe diarrheal response seen when dosing the animals with enterotoxigenic Escherichia coli. Overall, SMS 201-995 had a significant but incomplete effect in reducing the STa effects seen in the various assays. Additionally, in the RITARD model the analog did not alter the clinical responses to various enterotoxigenic bacteria. SMS 201-995 should be useful as a probe into the mechanisms involved in intestinal fluid secretion, but a clinical role in enterotoxigenic gastrointestinal disease was not supported by this study.

Animals↗
PubMed1989

Culture of human neoplastic gastrointestinal smooth muscle cells.

Due to limited growth potential of primary cultures and the absence of continuous lines of healthy enteric smooth muscle, we have studied the culture behavior of neoplastic gastrointestinal smooth muscle cells. Forty-six human enteric smooth muscle neoplasms (leiomyomas and leiomyosarcomas) were studied while fresh and/or after culture in vitro and growth in vivo in athymic nude mice, with assessments made of morphology, growth characteristics, and biochemical markers of differentiation. The state of differentiation of the tumors varied, with well-differentiated tumors tending to express binding sites for the gastrointestinal hormone cholecystokinin, whereas less well-differentiated tumors did not. Poorly differentiated tumors were the easiest to establish in culture in vitro and to grow in vivo in nude mice. When the cells placed directly into culture proliferated to confluent density, they underwent morphologic differentiation from a spread, fibroblastlike shape to a slender spindle morphology, with these cells possessing fewer biosynthetic organelles and arranging themselves in characteristic "hill and valley" arrays. However, the highly differentiated characteristics of expression of desmin or cholecystokinin-binding sites were not observed in cultured cells. In contrast, cells that had been passaged in nude mice before culture displayed a proliferative phenotype and failed to undergo morphologic differentiation on reaching confluent density. Four human enteric smooth muscle cell lines (documented by chromosomal analysis) originating in stomach, jejunum, ileum, and rectum were established using this strategy.

Cholecystokinin↗
PubMed1994

Peptidergic nerves in Hirschsprung's disease and its allied disorders.

To clarify the significance of peptidergic nerves in Hirschsprung's disease (aganglionosis), hypoganglionosis, and neuronal intestinal dysplasia (NID), we investigated enteric nerve responses in colonic tissues obtained from patients with these diseases. Colonic tissue specimens were obtained from 12 patients with aganglionosis, 8 patients with hypoganglionosis, and 6 patients with NID. Colon specimens from 20 patients without constipation were used as controls. A mechanograph was used to evaluate in vitro colonic responses to electrical field stimulation (EFS) of the adrenergic and cholinergic nerve blockers and gastrointestinal hormones. The following results were obtained: (1) Non-adrenergic inhibitory nerves were found to act on the normal human colon and to a lesser extent in colons with hypoganglionosis or NID, but had no effect on the enteric nerves in colons with aganglionosis. (2) Peptidergic neurotransmitters such as VIP, substance P, and neurotensin apparently act in the normal human colon, and to a lesser extent in the colons with hypoganglionosis or NID, but their effect was almost absent in aganglionosis. (3) VIP acts via neural mechanisms, while substance P and neurotensin may act both via nerves and also directly on the bowel smooth muscle. The diminution of action of non-adrenergic inhibitory nerves and peptidergic nerves may be largely related to the impaired motility observed in hypoganglionosis, NID and aganglionosis.

Adolescent↗
PubMed2003

Phenotypic identification of rat rostroventrolateral medullary presympathetic vasomotor neurons inhibited by exogenous cholecystokinin.

Systemic administration of the gastrointestinal hormone cholecystokinin (CCK) selectively inhibits splanchnic sympathetic vasomotor discharge and differentially affects presympathetic vasomotor neurons of the rostroventrolateral medulla (RVLM). Stimulation of the sympathoexcitatory region of the periaqueductal grey (PAG) produces profound mesenteric vasoconstriction. In this study, our aim was to identify phenotypically different populations of RVLM presympathetic vasomotor neurons using juxtacellular neuronal labelling and immunohistochemical detection of the adrenergic neuronal marker phenylethanolamine-N-methyl transferase (PNMT) and to determine whether the PAG provides functional excitatory input to these neurons. Fifty-eight percent (36/62) of RVLM presympathetic neurons were inhibited by systemic administration of CCK. These cells had conduction velocities (3.6 +/- 0.2 m/sec) in the non-C-fiber range consistent with neurons possessing lightly myelinated spinal axons. Of these, 79% (22/28) were excited by PAG stimulation, and 59% (10/17) were not immunoreactive for PNMT. Conversely, 42% (26/62) of RVLM presympathetic neurons were either unaffected or activated by CCK administration and had slower conduction velocities (1.4 +/- 0.3 m/sec) than cells inhibited by CCK. Fifty percent (11/22) of these cells were driven by PAG stimulation, and most (11/14 or 79%) were PNMT-positive. These results suggest that cardiovascular responses elicited by PAG stimulation occur via activation of non-C1 and C1 RVLM presympathetic neurons. RVLM neurons inhibited by CCK were more likely to be driven by PAG stimulation and may be a subset of neurons responsible for driving gastrointestinal sympathetic vasomotor tone. CCK-induced inhibition of a subpopulation of RVLM presympathetic neurons may be implicated in postprandial hyperemia and postprandial hypotension.

Animals↗
PubMed1989

Presence of membrane binding sites for [D-TRP6]-luteinizing hormone-releasing hormone in experimental pancreatic cancer.

Characteristics of binding sites (dissociation constant: Kd and maximal binding capacity: Bmax) for [D-Trp6]-luteinizing hormone-releasing hormone [( D-Trp6]-LH-RH]), somatostatin (SS-14) and epidermal growth factor (EGF) were evaluated in membrane fractions of N-Nitrosobis (2-oxopropyl) amine (BOP)-induced pancreatic adenocarcinoma of hamsters. Intact, normal hamster pancreata did not show any binding sites for [D-Trp6]-LH-RH, but specific [D-Trp6]-LH-RH binding sites with low affinity and high capacity were found after pancreatic cancer was induced with BOP. Membrane binding sites for SS-14 and EGF, with high affinity and low capacity were present, both in normal and cancerous pancreata. Normal hamster pancreatic tissue had significantly higher levels of SS-14 binding sites and lower concentration of EGF binding sites as compared to pancreatic carcinoma. In vivo treatment of hamsters bearing pancreatic cancers with microcapsules of agonist [D-Trp6]-LH-RH and the somatostatin analog RC-160 alone, or in combination, caused histopathological regression of tumors and concomitantly decreased the Kd and Bmax of [D-Trp6]-LH-RH, and increased the Bmax of the SS-14 binding sites. These findings represent the first demonstration of binding sites for [D-Trp6]-LH-RH in pancreatic cancers. Our results also suggest that tumor inhibitory effects of [D-Trp6]-LH-RH and RC-160 in pancreatic cancer could be mediated not only indirectly through suppression of sex-steroids, gastrointestinal hormones and growth factors, but also directly by an action on specific binding sites located on the tumor membranes.

Animals↗
PubMed1998

Protein in infant formulas. Future aspects of development.

Cow's milk protein intolerant infants (CMPI), shifted to a cow's milk protein hydrolysate based formula, often experience an improvement in signs of malabsorption; on the other hand, they also present a pattern of watery stools. In an attempt to find high levels of some gastrointestinal hormones that might induce hypermotility, motilin and neurotensin levels were studied in infants on starting formula and in cow's milk protein intolerant infants, on a cow's milk protein hydrolysate based formula. In 12 infants on unmodified cow's milk based formula (starting formula), motilin levels were: mean 71.66 pmol/L (s: 17); neurotensin 26.53 (s: 10.9). In 19 cow's milk protein intolerant infants on a cow's milk protein hydrolysate based formula, motilin levels were: mean 163.65 pmol/L (s: 70.06) (p<0.05); neurotensin: 31.76 pmol/L (s: 15.03) (p>0.05). Motilin (but not neurotensin) is higher in cow's milk protein intolerant infants on a cow's milk protein hydrolysate based formula. We conclude that high motilin levels can induce a different pattern of motility, and can be a pathogenetic factor in the persistence of loose and watery stools in infants with CMPI on a protein hydrolysate based formula.

Body Height↗