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Delaying colostrum intake by one day has important effects on metabolic traits and on gastrointestinal and metabolic hormones in neonatal calves.

Effects on metabolic and endocrine traits of feeding colostrum on d 1 and 2, then mature milk up to d 7, or glucose or water on d 1, colostrum on d 2 and 3 and then mature milk up to d 7 were studied in calves. Calves fed colostrum within the first 24 h after birth had significantly higher rectal temperatures, heart rates and respiratory frequencies than calves provided only water or glucose. Significantly elevated plasma nonesterified fatty acid and bilirubin concentrations on d 1 and 2 of life in calves fed only water on d 1 compared with calves of the other groups mirrored reduced energy intake. Fecal consistency was significantly higher during wk 1 of life, and gastrin and glucose-dependent insulinotropic polypeptide increased only on d 1 and/or 2 of life in calves already fed colostrum on d 1, expressing improved functioning of the gastrointestinal tract. Significantly higher plasma globulin levels up to d 7 in calves fed colostrum on d 1 than in those starting colostrum intake only on d 2 demonstrated significantly enhanced efficiency of gamma-globulin absorption. Furthermore, significantly higher circulating glucose, albumin, insulin, insulin-like growth factor-I concentrations and significantly lower urea levels in calves fed colostrum on d 1 compared with those fed colostrum starting on d 2 of life indicated stimulation of anabolic processes. In conclusion, colostrum intake by calves within the first 24 h of life is needed not only for an adequate immune status, but also to produce the additional important and favorable effects on metabolic and endocrine traits and on vitality.

Animal Nutritional Physiological Phenomena↗

Gastrointestinal growth factors and neoplasia.

Gastrointestinal (GI) hormones are chemical messengers that have been recognized for over a century as regulatory factors for normal physiologic functions in the GI tract and pancreas, including absorption, secretion, motility, and digestion. These hormones traditionally act in a true endocrine fashion with release from a distant site to regulate physiologic functions of specific target organs. In general, GI hormones bind to their G-protein-coupled receptors (GPCRs) to produce their endocrine effects. In addition to effects on physiologic functions of the GI tract and pancreas, selected GI hormones can act in an endocrine, paracrine, and/or autocrine fashion to stimulate the proliferation of normal and neoplastic GI tissues as well as non-GI tissues. This review will focus on effects of GI hormones on neoplastic tissues concentrating on the hormones that have been best characterized for these effects.

Biomarkers, Tumor↗

Effect of jejunal infusion of nutrients on gastrointestinal transit and hormonal response in man.

The effects of jejunal infusion of nutrients on gastric emptying and secretion, intestinal transit and hormone release were studied in human volunteers. Two caloric loads, 1.3 and 3.3 kcal/min, of a nutrient solution consisting of 18 percent protein, 27 percent lipids, and 55 percent carbohydrates were tested. These were first used in random order in 6 subjects to assess the effects on intestinal transit. For the study of gastric emptying, jejunal infusion was started 1 h after intragastric instillation of a 490 kcal, 400 ml, homogenized meal. Intestinal transit time and gastric emptying half-time increased with the rate of nutrient infusion into the jejunum. Postprandial gastric secretion was reduced. The two caloric loads induced significant rises of plasma cholecystokinin and gastric inhibitory polypeptide concentrations. Plasma motilin decreased in relation to the jejunal caloric load. The other peptides were essentially not affected by jejunal nutrient infusion in fasting subjects. We conclude that in man, gastric emptying rate, gastric secretion, and intestinal transit are regulated by the presence of nutrients in the jejunum.

Adult↗

Gastric myoelectrical activity and gut hormone secretion in myotonic dystrophy.

BACKGROUND: Myotonic dystrophy (MD) is a systemic disease affecting striated, cardiac and smooth muscles, as well as nerve structures and endocrine glands. Patients with MD may suffer from slow gastric emptying. OBJECTIVE: To study electrogastrograms (EGG) and postprandial gut hormone profiles in MD in order to evaluate whether disturbances in these regulatory mechanisms could explain, or contribute to, the delayed gastric emptying. SUBJECTS: Ten patients with MD complaining of symptoms consistent with slow gastric emptying, and ten healthy matched controls. METHODS: After an overnight fast, the patients and the control subjects were examined with standard EGG using surface electrodes before and during intake of a standard meal. Blood tests were drawn at regular time intervals for hormone analyses. RESULTS: The EGG in MD showed a reduced amount of normal three cycles per minute activity compared with controls (P < 0.04). The dominant frequency in MD was less stable than in controls (P < 0.03), and the power of the signal showed less increase after a meal. The postprandial increase in plasma motilin (P < 0.05) and glucagon-like peptide-1 (GLP-1) (P < 0.001) was significantly less pronounced in MD compared with controls, whereas the plasma concentrations of cholecystokinin (CCK), neurotensin (NT), peptide YY (PYY) and somatostatin (SOM) did not differ significantly. CONCLUSION: Disturbed electrophysiological control of the stomach and impaired secretion of gastrointestinal peptide hormones could contribute to slow gastric emptying in MD. Combined impairment of gastric pacing and gastrointestinal hormone responses was found in patients with the most prominent retardation of gastric emptying.

Adult↗

Pharmacology of the esophageal motor funciton.

In the striated muscle of the upper esophageal sphincter, tonic maintenance of closure is probably mediated via tonic central excitation of the extrinsic motor innervation; relaxation represents central inhibition of this mechanism. The motor nerves are probably cholinergic and act through nicotinic receptors like those of somatic striated muscle. In the striated muscle of the esophageal body, swallowing-induced contraction is also probably a cholinergic and nicotinic response. In the smooth muscle of the esophageal body, the control of contractions is cholinergic and muscarinic in part, but there is evidence for a nonadrenergic and noncholinergic component as well. The muscarinic component may arise from the cholinergic innervation of the longitudinal muscle layer. The other component may lie in the cryptic innervation of the circular muscular layer. In the smooth-muscled lower esophageal sphincter, resting closure tension appears to reflect a variety of possible control mechanisms. No single control system predominates. The evidence for muscarinic excitation is equivocal. An excitatory adrenergic alpha mechanism and inhibitory adrenergic beta receptors may contribute. A role for the polypeptide hormones from the gastrointestinal tract seems unlikely. Relaxation of the lower sphincter with swallowing seems not to involve any of these mechanisms, but is apparently accomplished by nonadrenergic noncholinergic inhibitory nerves like those present elsewhere in the gut (87). The possibility that the transmitter of these nerves is an adenine nucleotide has been raised from studies of other parts of the gut, but that hypothesis has not yet been examined critically in the lower esophageal sphincter.

Adrenergic alpha-Agonists↗

Secretin as a neuropeptide.

The role of secretin as a classical hormone in the gastrointestinal system is well-established. The recent debate on the use of secretin as a potential therapeutic treatment for autistic patients urges a better understanding of the neuroactive functions of secretin. Indeed, there is an increasing body of evidence pointing to the direction that, in addition to other peptides in the secretin/glucagon superfamily, secretin is also a neuropeptide. The purpose of this review is to discuss the recent data for supporting the neurocrine roles of secretin in rodents. By in situ hybridization and immunostaining, secretin was found to be expressed in distinct neuronal populations within the cerebellum and cerebral cortex, whereas the receptor transcript was found throughout the brain. In the rat cerebellum, secretin functions as a retrograde messenger to facilitate GABA transmission, indicating that it can modulate motor and other functions. In summary, the recent data support strongly the neuropeptide role of secretin, although the secretin-autism link remains to be clarified in the future.

Amino Acid Sequence↗

[Effects of induced hyperglycemia on the activity of pancreatic and gastrointestinal secretion of hormones in oncologic patients].

Artificial hyperglycemia (AHG) used in the cancer treatment considerably increases the insulin and S-peptide content in blood, decreases the glucagon concentration and tissue glucose tolerance. The changes are reversible, have a functional character, that indicates the absence of a disbalance in hormonal mechanisms of carbohydrate metabolism control as well as marked disorders of the pancreas function. In order to achieve a wider range of indications for using AHG in complex schemes of the cancer treatment, it is necessary to take measures on optimization of the carbohydrate metabolism state which should be controlled by the suggested complex of laboratory tests.

Antineoplastic Agents↗

Stereospecific opiate receptors in the actions of thyrotropin releasing hormone and morphine on gastrointestinal transit.

Studies in these laboratories have shown that morphine and thyrotropin releasing hormone (TRH) inhibit gastrointestinal transit in the mouse. Administration of morphine sulfate (5 mg/kg, s.c.) or TRH (10 microgram i.c.v.) to mice inhibited gastrointestinal transit as measured by the charcoal meal test. In order to determine whether the effects of TRH and morphine were mediated via stereospecific opiate receptors, the effects of two stereoisomers of an antagonist, (-) alpha -5,9-diethyl-2'-hydroxy-2-(3-furylmethyl)6,7-benzomorphan (MR2266), the active isomer and (+) alpha-5,9-diethyl-2'-hydroxy-2-(3-furylmethyl)6,7-benzomorphan (MR 2267), the inactive isomer, on morphine and TRH induced changes in gastrointestinal transit were determined. Morphine and THR induced inhibition of gastrointestinal transit was antagonized by MR 2266 (1 and 3 mg/kg, s.c.) but was unaffected by MR 2267. These studies provide evidence for the involvement of opiate receptors in the actions of morphine and TRH on gastrointestinal transit, and further suggest that the receptors are stereospecific in nature.

Animals↗

Improved cumulated nitrogen balance after administration of recombinant human growth hormone in patients undergoing gastrointestinal surgery.

OBJECTIVE: To examine the effect of recombinant human growth hormone (rhGH) on the catabolic state following major gastrointestinal surgery. DESIGN: The study was designed as a prospective controlled randomized clinical trial. SETTING: Intensive care unit and the surgical ward of the Department of Surgery, Städtische Kliniken Dortmund, FRG. PATIENTS: 39 patients were studied postoperatively following gastrectomy or resection of the rectum. The patients were 40-75 years old. INTERVENTION: 0.075 (n = 11), 0.15 (n = 9) or 0.30 IU rhGH/kg/day (n = 9) or placebo (n = 10) were given subcutaneously at 8:00 a.m. during 5 postoperative days. Resting energy expenditure (REE) on the 1st postoperative day was 2,042 +/- 82 kcal/24 h (REE/BEE 1.44 +/- 0.04). Isocaloric, isonitrogenous total parenteral nutrition provided the energy requirements (4 g carbohydrates/kg, 0.9 g fat/kg, 1.25 g amino acids/kg). RESULTS: After 5 days of treatment, cumulated nitrogen balance (CNB) was improved dose-relatedly. In controls, net nitrogen losses (-20.47 +/- 3.86 g) were significantly higher than after 0.15 (-12.14 +/- 3.5 g) and 0.30 IU rhGH/kg (-10.0 +/- 2.61 g). 0.075 IU rhGH/kg showed no significant effect on CNB (-18.07 +/- 5.73 g). The modulation of protein metabolism by GH may be mediated by insulin-like growth factor-I (IGF-I). Postoperatively serum (S)-IGF-I was decreased in all groups. rhGH caused a significant dose-related increase in S-IGF-I levels on day 6, whereas in controls it remained unchanged during the study period. Besides significant elevations in serum glucose in some cases of both larger dosage groups no side effects were detected. CONCLUSIONS: The protein-sparing effect of rhGH after major gastrointestinal surgery is dose related but not linear. A threshold value for a significant improvement in the CNB seems to be at least at 0.15 IU rhGH/kg/day.

Adult↗