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PubMed2005

Effect of chemotherapy on circulating gastrointestinal hormone levels in ovarian cancer patients: relationship to nausea and vomiting.

OBJECTIVE: The introduction of 5-HT3 receptor antagonists greatly reduced the problems associated with nausea and vomiting immediately after cancer chemotherapy. However, delayed nausea and vomiting is still a major problem and the underlying mechanism is obscure. MATERIAL AND METHODS: We studied the effect of cisplatin-containing combination chemotherapy in 14 ovarian cancer patients on the levels of gastrin and a panel of other hormones as well as glucose and prostaglandin F2a. Blood samples were obtained once daily in the morning before chemotherapy and for 4 days after chemotherapy. RESULTS: Concentrations of many hormones including gastrin were generally high. A pronounced increase in plasma insulin levels occurred on the day after chemotherapy accompanied by a modest increase in plasma glucose concentrations. Minor increases were observed for gastrin, oxytocin and prostaglandin F2a. In contrast, a transient decrease after chemotherapy was observed for motilin. Plasma cortisol decreased markedly after chemotherapy as expected since betamethasone was given as an antiemetic prophylaxis. Certain trends concerning the relationship between some hormones and nausea and vomiting were noted. A high plasma gastrin concentration before chemotherapy was related to delayed vomiting. Relative day-to-day variability of cholecystokinin tended to correlate positively with delayed nausea, whereas an inverse relationship was observed for gastrin variability. CONCLUSIONS: Changes in hormone plasma levels were found but only few could be distinguished as possible mediators of delayed nausea and vomiting.

Adult↗

PubMed1982

Pancreatic and gastrointestinal hormones in chronic pancreatitis.

Pancreatic and gut hormones have been measured in 39 patients with chronic pancreatitis, 16 of whom had severe pancreatic insufficiency. Patients with pancreatic insufficiency had significantly diminished fasting levels and postprandial rises of pancreatic polypeptide which were less than 20% of normal. Patients with chronic pancreatitis, with or without exocrine insufficiency, had two- to threefold higher plasma levels of motilin and enteroglucagon than controls. Plasma levels of insulin, pancreatic glucagon, gastric inhibitory polypeptide and gastrin were similar to normal in these patients. The pattern of response of these hormones to a test breakfast differs markedly from those seen in other gut disease states and may reflect pathophysiological mechanisms.

Adult↗

PubMed1994

Glucagonlike peptide 1: a newly discovered gastrointestinal hormone.

Glucagonlike peptide (GLP) 1, a peptide of 30 amino acids with 50% sequence homology to glucagon, results from expression of the glucagon gene in the L cells of the distal intestinal mucosa. It is secreted early in response to mixed meals by mechanisms involving the presence of unabsorbed nutrients in the gut lumen or the absorptive process itself, but other mechanisms may also be involved. GLP-1 has two important actions. First, it stimulates insulin secretion and inhibits glucagon secretion and thereby inhibits hepatic glucose production and lowers blood glucose levels. It may have effects on glucose clearance independent of its pancreatic effects. It acts on recently cloned G protein-coupled specific receptors and seems to increase insulin secretion via cyclic adenosine monophosphate-dependent increases in intracellular calcium. It has been suggested that activation of the beta cells by GLP-1 is a prerequisite for glucose-induced insulin secretion. Second, it also potently inhibits gastrointestinal secretion and motility and is likely to act as an "ileal brake," possibly after activation of cerebral receptors. Therefore, GLP-1 physiologically seems to signal nutritional abundancy and enhance deposition of nutrients. Because of these effects, however, the peptide can completely normalize blood glucose levels in type 2 diabetics and is therefore of considerable pharmaceutical interest.

Blood Glucose↗

PubMedDate not supplied

[The effect of balneotherapy on the gastrointestinal hormone level of patients with digestive organ diseases subjected to small doses of radiation exposure].

Balneotherapy with several mineral waters at health resorts proved effective in 228 patients with GI diseases. All of them were exposed to low-dose radiation as a result of the Chernobyl accident. Such treatment promoted a decrease in initially elevated basal level of insulin, improved production of gastrin and C-peptide.

Accidents↗

PubMed1978

Endocrine control of appetite: gastrointestinal hormonal effects on CNS appetitive structures.

Permanent semi-microelectrodes were implanted in the ventromedial hypothalamus (VMH), lateral hypothalamus (LH), amygdala (AMYG), medial forebrain bundle (MFB), anterior hypothalamus (AH), inferior colliculus (IC), and caudate nucleus (CN). Average evoked responses were recorded simultaneously from the above sites in freely behaving rats before and after administration of pentagastrin (100 microgram/kg), secretin 1 microgram/kg or cholecystokinin octapeptide (CCK-OP) (1 microgram/kg) in search of satiety signal. Gastrin and secretin had little effect while it appears that CCK may perform a regulatory function in a neurohumoral feedback mechanism.

Amygdala↗

PubMed1986

Reduced glycemic response to beet-fibre meal in non-insulin-dependent diabetics and its relation to plasma levels of pancreatic and gastrointestinal hormones.

Standardized breakfasts with or without beet-fibre were given, in random order, to non-insulin-dependent diabetics. The blood glucose levels were monitored continuously and hormonal responses were determined at regular intervals for 3 hr. After the beet-fibre breakfast including 10.8 g dietary fibre from the sugar beet, the glucose plateau level and the area below the curve were lower than after the control meal. The rate of glucose decrease was also slower after the beet-fibre meal. There were no notable differences with regard to the plasma levels of insulin, C-peptide or glucagon. The gastric inhibitory polypeptide response was greater during the first part of the curve, while the somatostatin response after the beet-fibre meal displayed a significantly larger total area below the curve. The results suggest that the diminished glycemic response after the beet-fibre meal is associated with an increased response of somatostatin, giving a reduced glucose absorption and a delayed gastrointestinal transit time.

Aged↗

PubMed1989

Effects of gastrointestinal hormones on the growth of human intestinal epithelial cells in vitro.

The growth of cultured epithelium like cells from human normal embryonic intestine was studied in response to various hormones using a method that quantifies the number of cells by the amount of dye that they bind after fixation. Gastrin and neurotensin in the pg/ml range and higher caused small increases in cell growth. Glucagon and VIP were stimulatory in the low ng/ml range, whereas somatostatin and bombesin had no effect at the lower concentrations but were stimulatory at the highest concentration tested (10 and 100 ng/ml respectively). Secretin and pancreozymin (cholecystokinin) seemed to be ineffective.

Cell Division↗

PubMed1990

[Gastrointestinal hormones--function and clinical significance. 1: The classical enterohormones gastrin, cholecystokinin and secretin].

Gastrointestinal endocrinology is undergoing a variety of different changes. Thus, many of the known hormones are seen no longer to fit the definition of endocrinology--rather, their regulation mechanism may be of a paracrine, neurocrine, neuroendocrine or autocrine nature, or the peptide may be a neurotransmitter. A better term than hormone would thus be regulatory peptide. A knowledge of the physiological mode of regulation of a peptide impacts not only on our understanding of pathophysiological processes, but also on the therapeutic use of peptides. In this Part, the classical gut hormones gastrin, secretin and cholecystokinin are described with the above aspects in mind. The well-known hormones have also been shown to have previously unsuspected biological actions, whose biological significance is, as yet, unknown. For example, cholecystokinin is now being considered as a regulator of glucose homeostasis, satiety and pancreatic growth.

Cholecystokinin↗

PubMed1988

Human gastric lipase: variations induced by gastrointestinal hormones and by pathology.

Secretin and cholecystokinin-pancreozymin had no effect on the secretion of human gastric lipase, in contrast to pentagastrin, which increased the gastric lipase output but not the enzyme concentration in gastric juice. The secretion of gastric lipase was not significantly different in patients with duodenal ulcer or chronic pancreatitis and in controls. In contrast, basal gastric lipase concentration was significantly lower in children with cystic fibrosis than in normal children. This shows that neither in adults nor in children is there a compensation for a decreased lipase secretion by an increased gastric lipase secretion.

Adolescent↗

PubMed1985

Role of endogenous prostaglandins in somatostatin-induced inhibition of gastrointestinal hormone secretion.

Endogenous prostaglandins have been reported to be essential for the inhibitory effect of somatostatin on acid secretion. From these results it could be suggested that the effect of somatostatin on the secretion of gastroentero-pancreatic hormones may also be medulated by prostaglandins. This hypothesis was investigated in man and in the rat. Somatostatin-induced inhibition of postprandial gastrin, cholecystokinin, pancreatic polypeptide, and insulin release was not influenced by indomethacin pretreatment in healthy subjects. Using the isolated perfused rat stomach preparation, inhibition of acetylcholine-stimulated gastrin secretion by somatostatin was found to be unchanged by indomethacin treatment. It is concluded that endogenous prostaglandins are unlikely to be indispensable for the inhibitory effect of somatostatin on gastroentero-pancreatic endocrine cells.

Adult↗

PubMed1979

Effects of gastrointestinal hormones on fasting gallbladder storage patterns in man.

Gallbladder storage and emptying patterns were studied in fasting normal subjects by a duodenal perfusion technique using indocyanine green as a biliary marker. Fasting gallbladder storage patterns were very variable but a more uniform biliary output with net storage of about 40% of the biliary marker was observed during a simulated interprandial state (2--4 h after meals) produced by a low dose intravenous infusion of secretin and caerulein. With this background hormonal stimulation, infusion of bovine pancreatic polypeptide to achieve physiological interprandial levels promoted further gallbladder storage of bile. Bovine pancreatic polypeptide produced storage by a major effect on the gallbladder rather than on the liver, common bile duct or sphincter of Oddi since a reduction of biliary output was not observed during bovine pancreatic polypeptide infusion in cholecystectomized subjects. Bovine pancreatic polypeptide had a separate effect on the pancreas, reducing trypsin output in both normal and cholecystectomized subjects.

Adult↗

PubMed1975

Pharmacologic effects of gastrointestinal hormones on intestinal oxygen consumption and blood flow.

The vasoactive effects of cholecystokinin-octapeptide (CCK-OP), pentagastrin, synthetic secretin, glucagon, and acetylcholine were assessed in the intestinal circulation of the dog. In pharmacologic doses of glucagon, CCK-OP, and, to a lesser degree, pentagastrin significantly increased blood flow and oxygen consumption. Atropine blocked the vasodilator effects of CCK-OP, pentagastrin, and acetylcholine but did not block those of glucagon. Neither the alpha-adrenergic blocker, phenoxybenzamine, nor the beta-adrenergic blocker, propranolol, blocked the vasodilator response to pentagastrin. Synthetic secretin had no significant effect on either blood flow or oxygen consumption in the intestinal segment. The vasodilator response to CCK-OP and pentagastrin appears to be mediated specifically through cholinergic receptors.

Acetylcholine↗

PubMed1975

Hepatic, vascular and biliary responses to infusion of gastrointestinal hormones and bile salts.

The effects of secretin, cholecystokinin, synthetic pentagastrin, sodium dehydrocholate and sodium taurocholate on hemodynamics of the canine liver were studied in a total of 57 dogs. Bile flow was also measured. Dehydrocholate and cholecystokinin significantly decreased systemic arterial pressure while the other substances did not. Hepatic arterial vessels were dilated by pentagastrin and the bile salts; however, flow was not increased in the latter case. Intraheptic portal venous resistance was decreased by pentagastrin and increased by the bile salts. Portal flow was decreased by the bile salts and increased by pentagastrin. Apart from this, mean changes in portal venous flow and portal pressure were not statistically significant. All were potent choleretic agents except pentagastrin which produced only a relatively small transient increase in bile flow.

Animals↗

PubMed1988

[Diurnal profile of gastrointestinal hormones following pancreatectomy].

A long-term follow-up study revealed that diabetes, diarrhea and dumping syndrome were the major complications after pancreaticoduodenectomy. The PABA recovery rate in PFD test was markedly decreased in patients with pancreaticoduodenectomy, suggesting that impaired exocrine pancreatic function is the main cause of the complications. A 24-hour profile of pancreatic juice secretion more than 1.5 months after operation, showed that pancreatic juice was rich in protein and amylase, and secretion was increased following a meal and early in the morning. Gastrin, CCK and VIP were not detected during these periods; however, secretin and motilin were increased. These results suggest that pancreatic exocrine function recovered in patients with pancreaticoduodenectomy and secretin and motilin played an important role in the regulation of these functions.

Circadian Rhythm↗

PubMed1985

Release of gastrointestinal hormones in cardiodepressive shock.

In previous studies increased plasma levels of vasoactive intestinal polypeptide (VIP), somatostatin and pancreatic polypeptide (PP) were demonstrated in a porcine endotoxin shock model. Unchanged levels of gastric inhibitory polypeptide (GIP) and secretin point to a specific shock reaction of peptide release and not to a diffuse mucosal leakage. A porcine model of cardiodepressive shock was developed to enable discrimination to be made between a general low-flow state and endotoxin reaction. Infusion of the tricyclic antidepressive agent nortriptyline 15 mg/kg bodyweight resulted in a grave shock state. Increased plasma levels of somatostatin, PP and insulin were found. No increase in VIP levels could be demonstrated. Endotoxin given after nortriptyline administration resulted in the increase of VIP levels regularly seen during endotoxinaemia. VIP release during endotoxin shock is related to endotoxin and not to a general low flow state.

Animals↗

PubMed2000

Gastrointestinal hormones.

Solomon A. Berson, M.D., the first Murray M. Rosenberg Professor and Chair of the Department of Medicine at Mount Sinai from 1968 until his death in 1972, and Rosalyn S. Yalow, Ph.D., 1977 Nobel Laureate in Medicine or Physiology and Solomon A. Berson Distinguished Professor-at-Large, brought meticulous quantitation and new vistas to all of clinical medicine and biomedical science through the application of their technique of radioimmunoassay. I was fortunate to know and work with them for many years. In 1972, while I was an NIH Fellow in gastroenterology at Mount Sinai, Dr. Berson suggested that I pursue my research in their laboratory at the Bronx Veterans Administration Hospital. Dr. Berson died one month after I began my research in the Bronx. Yalow and Berson had already discovered big gastrin (G-34), but much work with gastrin remained to be done. Challenging work with secretin, cholecystokinin, and a host of other gut peptides, would keep the Mount Sinai group at the forefront of this exciting field.

Gastrointestinal Hormones↗

PubMed1994

Role of the duodenum in postprandial release of pancreatic and gastrointestinal hormones.

In previous studies we found that duodenectomy abolished the interdigestive cycles of plasma motilin and pancreatic polypeptide (PP). In the current studies, we tested the hypothesis that an intact duodenopancreatic axis is necessary for normal postprandial release of pancreatic (PP, insulin) and gut peptides (gastric inhibitory peptide, GIP; cholecystokinin octapeptides, CCK-8; neurotensin; and gastrin). Consequently, we measured plasma concentration of pancreatic and gut hormones in normal and duodenectomized dogs after gavage feeding of a 250-ml liquid formula diet in conscious animals. After completing the experiments, pancreatic tissue concentrations of PP and insulin were measured. Removal of the duodenum was associated with decreases in postprandial plasma concentrations of PP (p < 0.05) and insulin (p < 0.05) and in pancreatic tissue concentrations of insulin (p = 0.01). Duodenectomy, however, did not alter postprandial plasma concentrations of GIP, CCK-8, neurotensin, or gastrin nor pancreatic tissue concentrations of PP. These effects of duodenectomy may be due to disruption of duodenopancreatic neural connections or loss of vagus sensitive (non-GIP) humoral factors. Decreased postprandial insulin concentrations may be due to lack of a neural or humoral insulinotropic factor arising from the duodenum.

Animals↗

PubMed1984

Chronic renal failure: effect of hemodialysis on gastrointestinal hormones.

Fifteen patients with chronic renal failure (serum creatinine level greater than 5 mg/dl) of long duration (more than 2 years) requiring hemodialysis were studied. Blood samples before and after 4 hours of hemodialysis were assayed for creatinine, blood urea nitrogen, potassium, calcium, glucose, insulin, gastrin, gastric inhibitory polypeptide, vasoactive intestinal polypeptide, pancreatic polypeptide, somatostatin, motilin, and neurotensin levels. Before dialysis, serum gastrin was minimally increased whereas gastric inhibitory polypeptide and pancreatic polypeptide were grossly increased compared with normal fasting values. Hemodialysis produced no changes in serum gastric inhibitory polypeptide, vasoactive intestinal polypeptide, pancreatic polypeptide, somatostatin, motilin, and neurotensin. Slight increases in serum insulin and gastrin levels may have occurred secondary to a dialysis-induced increase in the serum calcium level. The kidneys appear to be a major site of inactivation of insulin, gastrin, gastric inhibitory polypeptide, and pancreatic polypeptide. The gastrin level, although elevated in renal failure patients, may be suppressed by very high circulating levels of gastric inhibitory polypeptide.

Adult↗