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At least 631 records · Page 35Linked to original sources
PubMed1979

Effect of hypothalamic extract and other factors on release of adrenocorticotropin from and adenosine 3',5'-monophosphate levels in dispersed nonpituitary tumor cells.

Tumor tissues obtained from two patients with the ectopic ACTH syndrome caused by medullary carcinoma of the thyroid and malignant epithelial thymoma were dispersed by tryptic digestion and mechanical agitation. Using the isolated cells, the effects of various agents on ACTH secretion and intracellular cAMP concentrations were studied. Addition of rat median eminence extract significantly stimulated ACTH secretion and increased levels of intracellular cAMP in both cell preparations, and a dose-response relationship appeared to exist between the dose of rat median eminence extract added and either ACTH secretion or intracellular cAMP formation in the thymic tumor cells. High concentrations of calcium also produced a marked ACTH secretion in both cases. In the thymic tumor cells, norepinephrine, serotonin, and TRH were found to be effective in increasing ACTH secretion and intracellular cAMP levels, whereas biogenic amines, hypothalamic hormones, and gastrointestinal hormones did not affect hormone secretion in the thyroid tumor cells. These results suggest that a corticortropin-releasing factor-like substance(s), as yet unspecified, may play some role in stimulating ectopic ACTH secretion by certain tumors, that both intracellular cAMP and Ca++ may be involved in ectopic hormone secretion, and that the inappropriate hormonal secretory responses of some tumors to a variety of stimuli might be mediated by altered membrane receptors of the neoplastic cells.

Adrenocorticotropic Hormone↗
PubMed1977

Effect of streptozotocin administration on somatostatin content of pancreas and hypothalamus in rats.

A radioimmunoassay (RIA) method for somatostatin (SRIF) utilizing rabbit antiserum against synthetic SRIF coupled with human serum alpha-globulin is described. Synthetic N alpha-tyrosylated SRIF was labelled with 125I using the lactoperoxidase method and purified on a Sephadex G-10 column. This assay system was highly specific for SRIF and did not cross-react with hypothalamic trophic hormones, pituitary trophic hormones or gastrointestinal hormones. The effect of streptozotocin induced diabetes on the SRIF content was examined in the pancreas, the pancreatic islets, as well as the hypothalamus of rats. SRIF content in both the pancreas and islets of the diabetic rats was shown by RIA to have significantly increased. However, content in the hypothalamus of the diabetic rats did not differ from that of the control. The physiological and pathophysiological significance of the SRIF changes remains to determined.

Animals↗
PubMedDate not supplied

[Future of endocrinology].

With regards to the future of endocrinology, the author displays a spectrum formed by the following "hot" subjects: A) From a research point of view: 1) Membrane and cytosomal molecular receptors. 2) Prohormones, with regards to: a) paraneoplastic and tumoral syndromes; and b) "messenger" or transitory hormones. 3) Metabolic clearings: a) Normal; b) in endocrine pathology and c) in pathology of transformation and elimination: liver and kidney. B) From a practical-empirical point of view: 1) Tests of fetoplacental function. 2) Clinical perspectives of the use of hormonal factors and provoked endocrinological clinics (iatrogenic endocrinology). 3) Growth factors and somatostatine. 4) Thymus hormones. 5) Gastrointestinal hormones. 6) The renine-angiotensine-aldrosterone system, the problems of hypertension and preservation of the hydric compartments. Natriuretic hormones.

Aldosterone↗
PubMed2004

Bi-directional signaling between gastrointestinal peptide hormone receptors and epidermal growth factor receptor.

The mechanisms mediating the proliferative effects of gastrointestinal (GI) peptide hormones and their cognate G protein-coupled receptors are associated intimately with epidermal growth factor (EGF) receptor-regulated signaling pathways. Although transactivation of the EGF receptor is now recognized as a critical component in GI peptide hormone regulation of mitogenic signaling and cell migration, their interactions are far more complex and include potentiation of intracellular signaling pathways, regulation of ligand expression and release, and modulation of cell surface receptor expression. Mitogen-activated protein kinases play a central role integrating the signals from these receptor systems. This review summarizes the mechanisms that intertwine GI peptide hormone receptor- and EGF receptor-activation and functions.

Animals↗
PubMed1987

Protein and energy metabolism with biosynthetic human growth hormone after gastrointestinal surgery.

The effect of biosynthetic human growth hormone (BSHGH) on postoperative protein and energy metabolism has been studied in patients who had major gastrointestinal surgery. Seven patients received placebo and seven patients received BSHGH, 0.1 mg/kg/24 h, for the first six postoperative days. Mean total nitrogen excretion was significantly lower with BSHGH (31.5 +/- 2.4 g N) (2287 +/- 160 mmol) than with placebo (42.7 +/- 3.1 g N) (3049 +/- 219 mmol) over the 6-day study period. The mean daily measured energy expenditure over days 3-6 was higher with BSHGH (31.3 +/- 1.8 kcal/kg LBM/24 h) (131 +/- 7 kJ/kg LBM/24 h) than with placebo (27.6 +/- 0.8 kcal/kg LBM/24 h) (114 +/- 2 kJ/kg LBM/24 h). Fat oxidation with BSHGH (2.05 +/- 0.26 mg/kg LBM/24 h) was greater than with placebo (1.5 +/- 0.17 mg/kg LBM/24 h) and protein oxidation was less with BSHGH (0.68 +/- 0.07 g/kg LBM/24 h) than with placebo (0.9 +/- 0.09 g/kg LBM/24 h) on days 1-6. Postoperative nitrogen turnover (BSHGH 943 +/- 174 mg N/kg LBM/24 h, placebo 557 +/- 50 mg N/kg LBM/24 h) (BSHGH 67 +/- 13 mmol/kg LBM/24 h, placebo 40 +/- 4 mmol/kg LBM/24 h), protein synthesis (BSHGH 5.31 +/- 1.09 g prot/kg LBM/24 h, placebo 2.54 +/- 0.33 g prot/kg LBM/24 h) and protein breakdown (BSHGH 5.90 +/- 1.09 g prot/kg LBM/24 h, placebo 3.48 +/- 0.31 g prot/kg LBM/24 h) were greater with BSHGH. On the first postoperative day serum insulin and blood glucose levels were higher with BSHGH than with placebo, and on days 4 and 7 serum somatomedin-C levels were significantly elevated. This study shows that BSHGH alters postoperative protein and energy metabolism by reducing protein oxidation and increasing fat oxidation with raised rates of whole body nitrogen turnover.

Adult↗
PubMed1982

[Somatostatin in the medical treatment of fistula of the pancreas and the small intestine].

Somatostatin is a peptide hormone which inhibits the secretion of the growth hormone and certain gastrointestinal hormones. Its main effect is to reduce the gastric acid output and inhibit the exocrine function of the pancreas. It was therefore used as an adjuvant therapy in the conservative treatment of ten patients presenting with fistulas of the small intestine or pancreas. The treatment was successful in eight cases. The short halflife of the hormone makes continuous application of the somatostatin as important as the carrying on of the conservative treatment itself.

Adult↗
PubMed1981

Gastrointestinal insulinotropic hormones in normal and gestational-diabetic pregnancy: response to oral glucose.

The responses of gastric inhibitory polypeptides (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, and pancreatic glucagon to a 50-g oral glucose load were studied in late pregnancy and postpartum in 11 normal women, 10 normal weight gestational diabetics, and 10 overweight gestational diabetics. The GIP response to glucose was impaired in pregnancy in all three groups. In pregnancy, the GIP response was smaller in both groups of gestational diabetics than in normal women, whereas postpartum, the GIP response was lower than normal in the normal weight gestational diabetics only. In pregnancy, the gut GLI response to glucose was reduced in the overweight gestational diabetics and abolished in the normal women. The insulin response to glucose was increased in pregnancy in all three groups. Moreover, it was higher in the overweight gestational diabetics than in the other two groups in pregnancy and postpartum. In the normals, the suppression of glucagon levels after glucose ingestion was more marked in pregnancy than postpartum, whereas no such effect was seen in gestational-diabetic pregnancy. It is concluded that pregnancy--normal as well as gestational-diabetic--is accompanied by profound changes in the secretion of gastrointestinal insulinotropic hormones after glucose ingestion. These findings may be important for the understanding of changes in metabolism and gastrointestinal physiology in gestation.

Blood Glucose↗
PubMed1988

Evidence for a peripheral action of thyrotropin releasing hormone on gastrointestinal transit in mice.

The effect of the two analogs of thyrotropin-releasing hormone (TRH), namely MK-771 and DN-1417, administered peripherally, on the actions of morphine and loperamide on gastrointestinal transit, was investigated in mice. The actions of naltrexone and methyl naltrexone on these effects were also determined in order to assess the central or peripheral mechanism of action. The administration of morphine sulfate (5 mg/kg) inhibited gastrointestinal transit, as measured by the charcoal meal test. The effect of morphine was potentiated by MK-771 and DN-1417 at the 10 mg/kg dose. The peripheral administration of DN-1417 inhibited gastrointestinal transit but MK-771 had no effect. Naltrexone antagonized the potentiating effect of the peptides on the effect of morphine on gastrointestinal transit. Methyl naltrexone, which crosses the blood-brain barrier with difficulty, also antagonized the potentiating effect of the peptides on the action of morphine on gastrointestinal transit. A subthreshold dose (0.5 mg/kg) of loperamide, a peripherally acting opiate, which had no effect on gastrointestinal transit by itself, when combined with MK-771 or DN-1417 significantly inhibited gastrointestinal transit. The administration of methyl naltrexone had little effect on loperamide-induced inhibition of gastrointestinal transit but antagonized the potentiating effect of MK-771 and DN-1417. It is concluded that the effects of analogs of thyrotropin releasing hormone on gastrointestinal transit involve peripheral sites of action, the effect of DN-1417 was not antagonized by naloxone and that the inhibitory effect of DN-1417 on gastrointestinal transit is not mediated by opiate receptors.

Animals↗
PubMed2006

Gut-brain axis: regulation of glucose metabolism.

Obesity and type II diabetes mellitus have reached epidemic proportions. From this perspective, knowledge about the regulation of satiety and food intake is more important than ever. The gut releases several peptides upon feeding, which affect hypothalamic pathways involved in the regulation of satiety and metabolism. Within the hypothalamus, there are complex interactions between many nuclei of which the arcuate nucleus is considered as one of the most important hypothalamic centres that regulates food intake. The neuropeptides, which are present in the hypothalamus and are involved in regulating food intake, also play a key role in regulating glucose metabolism and energy expenditure. In synchrony with the effects of those neuropeptides, gastrointestinal hormones also affect glucose metabolism and energy expenditure. In this review, the effects of the gastrointestinal hormones ghrelin, cholecystokinin, peptide YY, glucagon-like peptide, oxyntomodulin and gastric inhibitory polypeptide on glucose and energy metabolism are reviewed. These gut hormones affect glucose metabolism at different levels: by altering food intake and body weight, and thereby insulin sensitivity; by affecting gastric delay and gut motility, and thereby meal-related fluctuations in glucose levels; by affecting insulin secretion, and thereby plasma glucose levels, and by affecting tissue specific insulin sensitivity of glucose metabolism. These observations point to the notion of a major role of the gut-brain axis in the integrative physiology of whole body fuel metabolism.

Appetite Regulation↗
PubMed1992

Gut hormones and gastrointestinal motility in children with cystic fibrosis.

Intestinal dysmotility may be an important factor contributing to various gastrointestinal complications associated with cystic fibrosis. Motilin, enteroglucagon, neurotensin, and peptide YY may each play a role as endocrine hormones influencing gastrointestinal motor activity. Fasting children with cystic fibrosis (N = 8) and controls (N = 18) received a liquid nutrient test meal (fat 4 g/100 ml, protein 4 g/100 ml, carbohydrate 20 g/100 ml, 125 kcal/100 ml; 200 ml/m2) containing lactulose (5 g/100 ml), and the plasma concentrations of these peptides were studied. Mouth-to-cecum transit time was simultaneously studied using the breath H2 technique. Fasting levels of peptide YY and the postprandial response of all four peptides were significantly increased in those with cystic fibrosis. In repeat studies on those with cystic fibrosis after a period of altered pancreatic enzyme supplementation, no significant changes in peptide concentrations were observed. A rise in breath H2 permitting estimation of mouth-to-cecum transit time was noted in 17 control subjects (70-220 min, median 140). In contrast, a rise occurred in only two with cystic fibrosis after low-dose enzyme (70 and 180 min), and four after high-dose enzyme replacement (120-230 min, median 155). Altered gut hormone secretion may play a role in the pathophysiology of intestinal dysmotility in patients with cystic fibrosis.

Adolescent↗
PubMedDate not supplied

Comparison of the functional and morphological changes in the pancreatic remnant between pylorus-preserving pancreatoduodenectomy and pancreatoduodenectomy.

BACKGROUND/AIMS: Pylorus-preserving pancreatoduodenectomy preserves the secretion of gastrointestinal hormones from the distal stomach and duodenum, whereas after pancreatoduodenectomy they are no longer secreted. It has been suggested that some gastrointestinal hormones exert a trophic effect on the pancreas, although this effect has not been documented in man. It was postulated that the ablation of gastrointestinal hormones, such as gastrin by pancreatoduodenectomy is an important cause of postoperative pancreatic atrophy and, since pylorus-preserving pancreatoduodenectomy preserves the secretion of these hormones, it would be more effective than pancreatoduodenectomy for the maintenance of postoperative pancreatic function. METHODOLOGY: We measured postoperative pancreatic function, parenchymal thickness of pancreas and the release of gastrin in patients who underwent pancreatoduodenectomy or pylorus-preserving pancreatoduodenectomy who had survived > 1 year without tumor recurrence. RESULTS: After pylorus-preserving pancreatoduodenectomy, exocrine pancreatic function, parenchymal thickness of pancreas and gastrin release were significantly greater than after pancreatoduodenectomy. CONCLUSIONS: We concluded that postoperative atrophy of the distal pancreas after pancreatoduodenectomy occurs, in part because of resections of the duodenum and distal stomach, which is the source of trophic stimuli, gastrin.

Ampulla of Vater↗