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PubMed1991

[The regulation of feed intake and selection with special reference to poultry].

Feed intake is regulated in a dialogue between the animal and the feed, which is influenced by numerous factors. The hypothalamus has a central integrative function. Furthermore, caudal brain areas (medulla oblongata, pons) are of importance because these areas are relays of peripheral signals and gustatory afferents. All peripheral informations are integrated by various neurotransmitters and neurohormones. The function of this neuronal system is not exactly known yet. Sensorial informations, mechano-, chemo- and osmoreceptors of the gastrointestinal tract and gastrointestinal hormones are discussed as influences of the periphery. The physiological satiety function of cholecystokinin is questionable in poultry. Hepatic chemoreceptors, which are activated by various metabolites, influence the amount of feed ingested. The feed choice appears to be regulated by the same mechanisms. Our knowledge about the translation of peripheral signals into choice behaviour by changes of neurotransmitter systems is limited.

Animal Feed↗
PubMed2005

Glucagon-like peptide-1 as a treatment option for type 2 diabetes and its role in restoring beta-cell mass.

The "incretin effect" describes the enhanced insulin response from orally ingested glucose compared with intravenous glucose leading to identical postprandial plasma glucose excursions. It makes up to 60% of the postprandial insulin secretion but is diminished in type 2 diabetes. Gastrointestinal hormones promoting the incretin effect are called incretins. Glucagon-like peptide- 1 (GLP-1) is an important incretin. In vitro and animal data have demonstrated that GLP-1 increases beta-cell mass by stimulating islet cell neogenesis and by inhibiting apoptosis of islets. The improvement of beta-cell function can be indirectly observed from the increased insulin secretory capacity of humans receiving GLP-1 or incretin mimetics that act like GLP-1. Furthermore, GLP-1 inhibits glucagon secretion and rarely causes hypoglycemia. It may represent an attractive therapeutic method for type 2 diabetes because of its multiple effects, including a slowing of gastric emptying and the simulation of satiety by acting as a transmitter in the CNS. Native GLP-1 is degraded rapidly upon intravenous or subcutaneous administration and is therefore not feasable for routine therapy. Long-acting GLP-1 analogs (e.g., Liraglutide [Novo Nordisk, Copenhagen, Denmark]) and exenadin-4 (Exenatide [Eli Lilly, Indianapolis, IN]) that are resistant to degradation, called "incretin mimetics," are being investigated in clinical trials. Dipeptidyl peptidase IV inhibitors (e.g., Vildagliptin [Novartis, Basel, Switzerland]) that inhibit the enzyme responsible for incretin degradation are also under study.

Amino Acid Sequence↗
PubMed1995

Effect of hyperglycemia on gastric acid secretion and gastrin release induced by intravenous amino acids.

Intravenous amino acids (IVAAs) are able to stimulate gastric acid secretion. We investigated the effect of concomitant intravenous infusion of glucose, leading to hyperglycemia, on gastric acid secretion induced by IVAAs. Seven healthy volunteers were studied twice, once during normoglycemia and once during acute hyperglycemia with blood glucose concentrations stabilized at approximately 15 mmol/L. Amino acids were infused intravenously at the rate of 10 g/h for 180 min. Acid output was measured by continuous aspiration using a recovery markers. Serum gastrin and plasma pancreatic polypeptide (PP) concentrations were determined at regular intervals. IVAAs significantly stimulated acid output compared with basal values (2.3 +/- 0.2 and 1.4 +/- 0.4 mmol/15 min, respectively, P < 0.05), release of gastrin, and PP during normoglycemia. Hyperglycemia completely inhibited (P < 0.05) IVAA-induced gastric acid output and significantly inhibited (P < 0.05) release of gastrin and PP. We conclude that IVAAs stimulate gastric acid secretion, and gastrin and PP release; acute hyperglycemia reduces IVAA-stimulated acid output, and gastrin and PP release; and circulating nutrients influence gastric acid and gastrointestinal hormone secretion.

Adult↗
PubMed1999

Effects of age on concentrations of plasma cholecystokinin, glucagon-like peptide 1, and peptide YY and their relation to appetite and pyloric motility.

BACKGROUND: Aging is associated with a decrease in appetite and a slowing of gastric emptying. The gastrointestinal hormones cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), and peptide YY (PYY) may mediate these changes. OBJECTIVE: We investigated whether aging influenced the secretion of CCK, GLP-1, and PYY and their effects on appetite and pyloric motility. DESIGN: Eight healthy older (65-80 y) and 7 younger (20-34 y) men received isoenergetic (12.1 kJ/min) intraduodenal infusions of lipid and glucose for 120 min on separate days. Plasma CCK, GLP-1, and PYY concentrations were measured. RESULTS: Plasma CCK concentrations were higher in older than in younger subjects (P = 0.004) as a result of higher baseline values (4.7+/-0.2 compared with 3.2+/-0.2 pmol/L; P < 0.0001) and a greater rise during lipid infusion (increase from baseline: 7.1+/-0.5 compared with 5.3+/-0.6 pmol/L; P = 0.048). Plasma GLP-1 and PYY concentrations were not significantly different between groups. The decrease in hunger during intraduodenal lipid infusion was inversely related to the increase in CCK, GLP-1, and PYY in younger but not older subjects. During intraduodenal lipid infusion, the increase in isolated pyloric pressure wave (IPPW) frequency was positively related to GLP-1 and PYY and the increase in IPPW amplitude was positively related to CCK in older but not younger subjects, whereas the increase in IPPW amplitude and pyloric tone was negatively related to GLP-1 and PYY in younger subjects. CONCLUSIONS: Human aging is associated with increased CCK concentrations, which may contribute to the slowing of gastric emptying, mediated by increased pyloric motility. The role of increased plasma CCK concentrations in mediating the age-related decrease in appetite remains to be established.

Adult↗
PubMed1981

Circadian variations of liver free amino acid content in mixed-fed and protein-meal-fed rats.

Hepatic amino acid contents were determined at time-points regularly spaced over a light-dark cycle in rats fed either a 12% casein diet or a single daily meal given 2 hours after the onset of the light phase with a protein-free diet and libitum. In mixed-fed rats, non-essential amino acid hepatic content remained stable over 24 hours while that of essential amino acids rose during the early part of the night in connection with the onset of prandial activity, but long before portal levels increased. The possibility of factors related to food intake (insulin, glucagon, gastrointestinal hormones) or to its chronology (corticoids) stimulating active transport is discussed. In separately-fed rats, amino acid pools increased in the 30 minutes following protein administration in connection with rising portal levels. During the rest of the light phase, a general depletion of non-essential amino acids occurred. It was most rapid for glutamine, alanine and aspartic acid and was followed by accumulation during the night phase, a pattern fitting well with gluconeogenesis and ureogenesis stimulation following protein ingestion. Essential amino acid decrease was linear and spanned over both the light and dark phases in correlation with decreasing portal levels.

Amino Acids↗
PubMed1988

High and low inhibitor soybean meals affect human duodenal proteinase activity differently: in vivo comparison with bovine serum albumin.

The objective of this study was to investigate the effects of high and low inhibitor soybean meals on the duodenal enzyme activities and on the possible regulatory role of gastrointestinal hormones in the pancreatic response. After an overnight fast, 11 healthy volunteers received an intraduodenal infusion of saline for 60 min. This was followed by infusion of either of three test meals: extract of raw soybeans (RS), a low inhibitor soy protein isolate (SPI) or bovine serum albumin (BSA), 10 g/h for 60 min. Then saline was again given intraduodenally for 30 min. Gastric juice was collected continuously and duodenal juice and peripheral blood samples were collected every 10 min. Duodenal chymotryptic activity was severely inhibited by RS, whereas SPI and BSA increased the chymotryptic activity. Tryptic activity showed a transient reduction (55%) during RS infusion, whereas BSA and in particular SPI increased the tryptic activity. No change was seen in amylase activity. The lack of total inhibition of tryptic activity has been studied further and is the subject of the accompanying paper. The peripheral plasma levels of cholecystokinin (CCK) increased significantly during BSA but not during SPI or RS infusions. Thus, CCK levels were not increased by the inhibition of the proteolytic activity by RS in duodenal juice.

Adult↗
PubMed1994

Regulation of cholecystokinin synthesis and secretion in rat intestine.

Cholecystokinin is a classical gastrointestinal hormone that is produced by discrete endocrine cells of the upper small intestine. Cholecystokinin is produced in various molecular forms that result from differences in posttranslation processing of a single gene product. Cholecystokinin is secreted from the intestine in response to the ingestion of food. We observed that specific dietary substances increase the rate of transcription of the cholecystokinin gene and stimulate cholecystokinin release in rats. In contrast the paracrine transmitter, somatostatin, inhibits dietary-stimulated cholecystokinin secretion and lowers intestinal mRNA levels. Evidence that cholecystokinin gene expression is not necessarily linked to hormone secretion is supported by the observation that the neuropeptide, bombesin, stimulates cholecystokinin release but does not modify intestinal cholecystokinin mRNA levels. To examine the intracellular messengers that might regulate the cholecystokinin cell directly, we developed an in vitro method for studying cholecystokinin release from isolated intestinal mucosal cells. In this perifusion system, cholecystokinin release was stimulated by membrane depolarizing concentrations of KCl (50 mmol/L), the calcium ionophore A23187 (1 mumol/L), and the cAMP analogue dibutyryl cAMP (1 mumol/L). Biologically active cholecystokinin was also released in a dose-dependent manner by the peptide transmitters, bombesin and monitor peptide. These findings indicate that neurotransmitters and hormones may directly regulate the cholecystokinin cell and suggest that the phosphoinositide and adenylate cyclase cascades mediate stimulated-cholecystokinin secretion.

Animals↗
PubMed2002

Energy metabolism and turnover are increased in mice lacking the cholecystokinin-B receptor.

Cholecystokinin (CCK) is an important gastrointestinal hormone as well as a neurotransmitter. Two types of CCK receptors, types A and B, have been identified. The CCK-A receptor is involved in satiety, food intake and behavior, whereas the B receptor is involved in anxiety. We recently produced CCK-A, -B and AB receptor knockout mice to study the role of these receptors in energy metabolism. Daily energy intake and expenditure were significantly greater in CCK-BR(-/-) and CCK-AR(-/-)BR(-/-) mice than CCK-AR(-/-) and wild-type [CCK-AR(+/+)BR(+/+)] mice. Relative liver and kidney weights (g/kg body) were significantly greater in CCK-AR(-/-)BR(-/-) mice than in wild-type mice. Energy metabolism and energy turnover were increased in mice with a disruption of the CCK-BR gene, although the underlying mechanism is unknown.

Animals↗
PubMed1985

Complete nucleotide sequence of mRNA for caerulein precursor from Xenopus skin: the mRNA contains an unusual repetitive structure.

The complete nucleotide sequence of mRNA for caerulein precursor in the skin of Xenopus laevis was determined. The sequence was composed of 705 bp of coding region, accounting for 234 amino acids, 58 bp of 5'-untranslated region and 158 bp of 3'-untranslated region containing two putative poly(A) signals. It coded for four caerulein peptides interspersed with three 147 bp segments (intercaerulein segment; ICS). Analyses of several caerulein encoding cDNAs revealed some interesting features of caerulein mRNA species, which were highly heterogeneous and consisted of a repetition of two fundamental RNA sequences, a 45-nucleotide caerulein fragment and a 147-nucleotide ICS. The result of Northern blotting indicated that caerulein mRNA was only present in frog skin, not in stomach, upper intestine or liver. It appears that caerulein has different physiological function(s) from mammalian gastrin and cholecystokinin-pancreozymin (CCK). The relationship of caerulein to mammalian gastrointestinal hormones is discussed.

Amino Acid Sequence↗
PubMed1999

In ovo peptide YY administration improves growth and feed conversion ratios in week-old broiler chicks.

The effects of in ovo Peptide YY (PYY) administration on growth and feed conversion ratios in a commercial broiler line were investigated. Six hundred Ross male x Cobb female eggs were administered either 0.9% saline (control) or 600 microg/kg egg weight PYY in ovo at Day 18 of incubation. On day of hatching, 210 birds from each treatment group were randomly placed by sex into pens. Body weights at placement were not different between treatment groups. Average chick body weight and adjusted pen feed conversion ratios were improved by PYY in ovo treatment at 7 d posthatch (165.7 vs. 170.2 g, P<0.02; and 1.55 vs. 1.49, P<0.04, respectively). No significant differences between treatments were noted for these parameters at 21 or 42 d of age. These results suggest that in ovo treatment of broiler chicken eggs with gastrointestinal hormones that increase intestinal nutrient absorption, such as PYY, may enhance chick performance.

Animals↗
PubMed1976

Release of immunoreactive serotonin following acid perfusion of the duodenum.

Cannulas were placed in the portal vein, hepatic vein, and infrarenal vena cava in eight anesthetized dogs. The duodenum of each dog was irrigated with saline (control) and 0.1 N HCI (50 ml in 10 min). Heparinized blood samples were taken from each cannula 5 min before, and 1, 5, 10, 30 and 60 min after each irrigation for measurement of immunoreactive serotonin concentrations. Serotonin concentrations did not change during saline irrigation of the duodenum. In contrast, serotonin release was consistently observed after duodenal acidification (pH 1.5-2.0). Portal venous serotonin concentrations were increased at 1 min (356 +/- 147 ng/ml) and following a biphasic pattern remained elevated at 30 and 60 min (499 +/- 131 and 489 +/- 187 ng/ml, respectively). Concentrations in the hepatic vein rose more slowly and to a lower peak (357 +/- 123 ng/ml at 10 min). Caval serotonin concentrations were increased at 10 min (342 +/- 121 ng/ml) but promptly returned to baseline levels. In the canine gastrointestinal tract, immunoreactive serotonin concentrations were highest in the duodenal bulb (15.4 mug/gm). This study demonstrated serotonin release from the duodenum following acid perfusion and documented that some of the released serotonin escaped hepatic inactivation. These findings support the possibility that serotonin may be a gastrointestinal hormone involved in the feedback inhibition of gastric acid secretion.

Animals↗
PubMed1979

Glucagon or insulin suppressed biliary lipid excretion in dog and man.

The possibility that gastrointestinal hormones influence biliary lipid secretion was studied further in chronic bile fistula dogs and subsequently in a patient with a balloon-occludable t-tube. After stabilization of bile flow in the dog by infusing 500 mg/hr sodium taurocholate, glucagon and insulin increased bile flow, decreased cholesterol output, and had no effect on phospholipid or bile salt output. Similarly, during reinfusion of bile in the human subject, glucagon increased bile flow, decreased cholesterol output and had no effect on bile salt output. Phospholipid secretion decreased, as had occurred at a lower bile salt infusion rate in the chronic bile fistula dog. These findings suggest that glucagon or insulin may play a role in regulating cholesterol secretion in dog and man, and that mechanisms other than simple dilution of micelles are operative.

Animals↗
PubMed1986

Water and electrolyte absorption from a human Thiry-Vella ileal loop. Responses to systemic administration of gastrin, glucagon, secretin, and cholecystokinin.

Water and electrolyte flux in response to systemic administration of four different gastrointestinal hormones were studied in a human with a chronic Thiry-Vella ileal loop. Gastrin infusion with a pharmacological dose of 4 micrograms/kg-hr has no effect. Responses to glucagon were proportional to infused doses with directly increased absorption of water and electrolytes (except bicarbonate). However, when gastrin was infused simultaneously with glucagon, the enhanced absorption was inhibited. Secretin only transiently increased absorption of fluid and electrolytes. In contrast to its effects on jejunum, CCK increased both water and electrolyte absorption from the ileum.

Cholecystokinin↗
PubMed2000

Leptin and the gastrointestinal tract.

The discovery of leptin in 1990 was the culmination of earlier work which recognized that communication between the adipocyte and the hypothalamus was important in maintaining body weight. Leptin, which is a 16 kilodalton protein-encoded by the OB gene, is involved in the regulation of food intake, body composition, and energy expenditure through a central feedback mechanism. Initially thought to be adipocyte-specific, the OB gene, as well as the leptin receptor, have been found in a variety of other tissues. Relevant to this review, the leptin gene and its receptor have been identified in the stomach, intestine, liver, and pancreas. Recent data also suggest that leptin may act locally within the gastrointestinal tract to influence intestinal function. This review emphasizes the concept that leptin may be a new gastrointestinal hormone and the need to expand the focus of leptin research to include all phases of weight maintenance, such as nutrient absorption and utilization, in addition to food intake.

Journal Article↗
PubMed2006

Serum ghrelin levels in children with celiac disease.

OBJECTIVES: Ghrelin, a gastrointestinal hormone, has effects on nutrient intake and growth. Because celiac disease (CD) has intestinal histopathologic alterations and subsequent malnutrition and/or growth failure, we hypothesized that there would be alterations in serum ghrelin levels of those patients. In this study, we aimed to determine serum ghrelin levels in childhood CD, to observe probable alterations under gluten-free diet (GFD), and to see whether there is a relationship between ghrelin levels and the presentation of the disease and/or diet compliance. METHODS: Thirty-six children with CD and 10 healthy children were included. Serum fasting ghrelin level was measured using radioimmunoassay method. After 6 months under GFD, sera of 19 patients were retested for ghrelin level. RESULTS: Mean serum ghrelin levels in children with CD and in controls were 478.2+/-154.6 and 108.3+/-49.1 pg/mL, respectively (P<0.001). Serum ghrelin level was not different in different clinical presentations. Ghrelin was negatively correlated with body mass index, both in healthy children and in children with CD on admission (P<0.01). Ghrelin level was lower after 6 months under GFDcompared with the level detected on admission (P<0.001), but was still higher compared with that of healthy children (P<0.001). Strict diet compliance lowered ghrelin level, although not statistically. CONCLUSIONS: Ghrelin is increased in childhood CD and is responsive to GFD. Further studies are needed to clarify the mechanism underlying its action in CD.

Adolescent↗
PubMed1995

Involvement of gene expressions of cholecystokinin and secretin in luminal feedback regulation in conscious rats.

Pancreatic exocrine secretion in conscious rats in regulated by bile and pancreatic juice in the proximal intestinal lumen; exclusion of bile and pancreatic juice produces release of cholecystokinin (CCK) and pancreatic hypersecretion (luminal feedback regulation). In the present study, we examined the changes of gene expressions of CCK and secretin, another representative gastrointestinal hormone in the intestine, and found that exclusion of bile and pancreatic juice significantly enhanced gene expressions of both CCK and secretin. These results suggested involvement of both CCK and secretin in luminal feedback regulation.

Animals↗
PubMed1995

The role of CCK and its analogues in the organogenesis of the fetal rat pancreas.

The gastrointestinal peptide cholecystokinin (CCK) has been shown to stimulate pancreatic growth in the adolescent and adult rat. However, little is known about the role of gastrointestinal hormones in the regulation of organ formation during fetal development. We therefore examined the effects of the CCK receptor antagonist devazepide (25 micrograms/h) and an antigastrin/CCK monoclonal immunoglobulin G on the maternal and fetal rat pancreas. These substances were infused subcutaneously with minipumps in female rats during the entire period of gestation. At the end of gestation, the rats were killed and the pancreata of the dams and their litter were examined for DNA and protein. In the dams, the receptor antagonist and the antibody against CCK/gastrin had no effect. In the newborns, the CCK receptor antagonist led to a significant reduction of the protein and DNA concentration [protein in controls, 105.0 +/- 3.75 micrograms/mg pancreatic tissue; in the antagonist group, 91.9 +/- 4.2 micrograms/mg pancreatic tissue (p < 0.05); DNA in controls, 1.28 +/- 0.19 micrograms/mg pancreatic tissue; in the antagonist group, 0.48 +/- 0.06 micrograms/mg pancreatic tissue (p < 0.05) (mean +/- SEM)]. Immune neutralization of CCK/gastrin in the maternal-fetal circulation induced a reduction of the protein concentration in the fetal pancreas (85.3 +/- 3.06 micrograms/mg pancreatic tissue; p < 0.01) but had no effect on fetal pancreatic DNA. Additional experiments indicated effective concentrations of the CCK receptor antagonist in fetal pancreatic tissue and free binding sites of the circulating antibody. In conclusion, the study provides evidence that CCK and its analogues are involved in fetal pancreatic organogenesis.

Animals↗