gastrins and Alcoholism

The secretory response of gastric acid to pure ethanol and alcoholic beverages may be different because the action of the non-ethanolic contents of the beverage may overwhelm that of ethanol. Pure ethanol in low concentrations (< 5% vol/vol) is a mild stimulant of acid secretion whereas at higher concentrations it has either no effect or a mildly inhibitory one. Pure ethanol given by any route does not cause release of gastrin in humans. Alcoholic beverages with low ethanol content (beer and wine) are strong stimulants of gastric acid secretion and gastrin release, the effect of beer being equal to the maximal acid output. Beverages with a higher ethanol content (whisky, gin, cognac) do not stimulate gastric acid secretion or release of gastrin. The powerful stimulants of gastric acid secretion present in beer, which are yet to be identified, are thermostable and anionic polar substances. The effect of chronic alcohol abuse on gastric acid secretion is not as predictable. Chronic alcoholic patients may have normal, enhanced, or diminished acid secretory capacity; hypochlorhydria being associated histologically with atrophic gastritis. There are no studies on the acute effect of alcohol intake on gastric acid secretion in chronic alcoholic patients. The acid stimulatory component of beer and wine needs to be characterised and its possible role in the causation of alcohol induced gastrointestinal diseases needs to be investigated.

Topics: Alcohol Drinking; Alcoholic Beverages; Alcoholism; Ethanol; Gastric Acid; Gastric Mucosa; Gastrins; Humans

The action of acute and chronic administration of ethanol on pancreatic exocrine secretion in humans and several animal species is reviewed. If the data concerning the secretory action of ethanol on the pancreas are to the property assessed, several experimental variables have to be considered. Acute intravenous administration of ethanol inhibits basal and hormonally stimulated pancreatic secretion of bicarbonate and protein in nonalcoholic humans and most species of animals tested. Oral or intraduodenal ethanol causes moderate stimulation of pancreatic bicarbonate and enzyme secretion. Since anticholinergic agents and truncal vagotomy diminish the ethanol-induced inhibition of pancreatic secretion in the intact animal, it is possible that the action of ethanol on the pancreas is at least partly mediated by inhibitory cholinergic mechanisms. The action of ethanol on the pancreas may also be mediated by release of gastrointestinal hormones. Intravenous and oral administration of ethanol releases gastrin in dogs but not in humans. Pancreatic polypeptide is unlikely to be the hormonal mediator of the ethanol-induced inhibition of exocrine pancreatic secretion in humans and dogs, since ethanol does not release pancreatic polypeptide. The main secretory changes induced by chronic alcoholism in humans and dogs are increased basal secretion of pancreatic enzymes and decreased basal bicarbonate output, and these secretory changes may favour the occurrence of protein precipitates which are believed to be the first lesion of chronic pancreatitis in man. A decrease in the concentration of "pancreatic stone protein" in pancreatic juice may favour the development of protein precipitates in chronic alcoholic patients.

Topics: Acute Disease; Alcoholism; Animals; Calcium-Binding Proteins; Cholecystokinin; Chronic Disease; Dogs; Duodenum; Ethanol; Food; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Lithostathine; Nerve Tissue Proteins; Pancreas; Pancreatic Juice; Pancreatic Polypeptide; Pancreatitis; Secretin; Sphincter of Oddi; Stomach

Topics: Acute Disease; Alcoholism; Animals; Autoradiography; Bicarbonates; Chronic Disease; Dogs; Enzyme Inhibitors; Ethanol; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Pancreas; Pancreatic Juice; Pancreatitis; Proteins; Rabbits; Rats; Secretory Rate; Sphincter of Oddi

Male Wistar rats, (2 months old), randomly divided according to the diet offered to four groups (C-control; A- alcoholized, PD-protein-deprived, A-PD- alcoholized protein-deprived). In group A and A-PD rats, the number of gastrin producing G-cells was significantly lower. The volume density of G-cells was significantly decreased in alcoholic rats. Fasting serum gastrin level (FSGL) significantly raised due to combined effect of alcohol consumption and protein malnutrition. In group A rats, the profile area of G-cells and their nuclei increased. In PD rats, the profile area of G cells also increased. There were no differences in nucleus/cell ratio due to alcohol ingestion alone, but it decreased significantly in PD and A-PD rats. Pale and lucent types of granules were predominantly seen in G-cells of animals of group A and A-PD. Mean diameter of granules increased in A, PD and A-PD rats. Other endocrine cells (ECL, D, EC) also decreased in number in A rats. Somatostatin producing D-cells decreased significantly in A-PD rats, both in fundic and pyloric mucosa.

Topics: Alcoholism; Animals; Dietary Proteins; Gastrin-Secreting Cells; Gastrins; Male; Microscopy, Electron; Nutrition Disorders; Rats; Rats, Wistar

To gain further insight on the effects of alcohol on human pancreatic enzyme secretion, we tested the effects of a 12% (v/v) alcohol solution, wine, and a glucose solution added to a meal on trypsin output in duodenal aspirate of nonalcoholic volunteers and compared the results to those of chronic alcoholics. Plasma concentrations of gastrin, cholecystokinin, and pancreatic polypeptide were monitored pre- and postprandially. Similar blood alcohol concentrations were determined in nonalcoholics and alcoholics following wine and the alcohol solution. Nonstimulated trypsin output (basal) was higher in alcoholics but not significantly so when compared to nonalcoholics. However postprandial trypsin output, 2014 +/- 301 mg/5 hr was significantly greater in alcoholics (P < 0.05) compared to nonalcoholics 1271 +/- 118 mg/5 hr. Alcohol and wine when added to the meal significantly (P < 0.05) inhibited trypsin output in both groups. Basal and postprandial levels of gastrin and cholecystokinin were similar in nonalcoholics and alcoholics. Basal plasma pancreatic polypeptide levels were similar in both groups, but the postprandial increments in pancreatic polypeptide levels observed in nonalcoholics were not observed in alcoholics. We conclude that chronic alcoholics have increased postprandial pancreatic enzyme secretion, and that this secretion, as that of nonalcoholics, can be affected by alcohol or wine. The postprandial hypersecretion of enzymes in alcoholics is not related to increased plasma levels of cholecystokinin or gastrin. It is possible that the impaired release of pancreatic polypeptide may participate in the mechanism for increased pancreatic enzyme secretion in chronic alcoholics.

Topics: Adult; Alcoholism; Cholecystokinin; Duodenum; Eating; Ethanol; Gastrins; Humans; Male; Middle Aged; Pancreas; Pancreatic Polypeptide; Trypsin; Wine

Basal and maximum gastrin levels were measured in 81 patients with various stages of chronic alcoholism and different periods of alcohol intake, in 23 patients with chronic gastritis of nonalcohol etiology, and in 12 normal subjects. The findings permit a conclusion on the depressive effect of alcohol on the function of gastrin-producing G-cells, this resulting in lowered levels of both basal and maximal gastrin. A direct correlation between the degree of alcohol depression of gastric gastrin production and the length of alcohol consumption was revealed.

Topics: Adult; Alcoholism; Gastrins; Humans; Middle Aged

It has been claimed that plasma cholecystokinin (CCK) concentrations are raised in patients with pancreatic insufficiency. We have measured plasma CCK concentrations in 32 patients with pancreatic insufficiency (22 alcoholic pancreatitis and 10 cystic fibrosis) and in 30 normal subjects by radioimmunoassays using antibodies with different specificities. Antibody 1703 binds to COOH-terminal forms of CCK containing at least 14 amino acid residues and does not cross-react with gastrins. Antibody T204 binds to all CCK-peptides containing the sulfated tyrosyl region and shows low cross-reactivity with sulfated gastrins but no binding to nonsulfated gastrins. Antibody 5135 binds to all COOH-terminal CCK-peptides and shows full cross-reactivity with gastrins. In patients with pancreatic insufficiency, plasma CCK concentrations (1.2 +/- 0.1 pmol/liter, antibody 1703; 2.0 +/- 0.2 pmol/liter, antibody T204; 12.5 +/- 1.4 pmol/liter, antibody 5135) were not significantly different from those in normal subjects (1.1 +/- 0.1 pmol/liter, antibody 1703; 2.2 +/- 0.3 pmol/liter, antibody T204; 10.5 +/- 0.9 pmol/liter, antibody 5135). Furthermore, plasma CCK concentrations in patients with pancreatic insufficiency due to alcoholic pancreatitis (1.2 +/- 0.1 pmol/liter, antibody 1703; 1.9 +/- 0.2 pmol/liter, antibody T204; 14.0 +/- 1.9 pmol/liter, antibody 5135) were not significantly different from those in patients with cystic fibrosis (1.2 +/- 0.2 pmol/liter, antibody 1703; 2.4 +/- 0.4 pmol/liter, antibody T204, 9.1 +/- 1.0 pmol/liter, antibody 5135). Cross-reactivity with gastrin accounted for almost all CCK-like-immunoreactivity measured with antibody 5135.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Alcoholism; Antibodies; Antibody Specificity; Binding Sites, Antibody; Cholecystokinin; Cross Reactions; Cystic Fibrosis; Diabetes Mellitus; Exocrine Pancreatic Insufficiency; Female; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Radioimmunoassay

Post-prandial plasma gastrointestinal hormone profiles were measured in nine chronic alcoholics, one and fourteen days after complete alcohol withdrawal. Basal plasma pancreatic polypeptide concentration (PP--mean +/- SE mean) was significantly greater in alcoholics (control, 28 +/- 5 pmol/l; alcoholics, post-withdrawal day 1, 62 +/- 14 pmol/l, P less than 0.05; and post-withdrawal day 14, 89 +/- 17 pmol/1, P less than 0.005). The total integrated (TIR) PP response following a test breakfast was similarly elevated (control, 442 +/- 63 units; alcoholics, day 1, 1310 +/- 231 units, P less than 0.005; day 14,1066 +/- 66, P less than 0.005). Basal and TIR values for gastrin, gastric inhibitory peptide, insulin and glucagon were similar in alcoholics and controls. As PP has been shown to inhibit pancreatic exocrine enzyme secretion, these findings may help explain the abnormal pancreatic function seen frequently in alcoholics.

Topics: Adult; Alcoholism; Food; Gastric Inhibitory Polypeptide; Gastrins; Glucagon; Humans; Insulin; Male; Pancreatic Polypeptide; Time Factors

Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.

Topics: Adult; Alcoholism; Chronic Disease; Duodenum; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Stomach

Fasting serum gastrin and gastrin response to a protein meal were measured in a group of patients with chronic pancreatitis and in controls. No significant differences were found between the two groups of subjects. In patients with chronic pancreatitis no relation was found between gastrin release and the severity of pancreatic exocrine insufficiency.

Topics: Adult; Alcoholism; Chronic Disease; Fasting; Female; Food; Gastrins; Humans; Male; Middle Aged; Pancreatitis

Topics: Adult; Alcoholism; Female; Gastrins; Gastritis; Humans; Male; Middle Aged

Plasma gastrin levels were measured by radioimmunoassay before and after a test meal associated with 40 ml ethanol in 21 patients presenting with chronic calcifying pancreatitis, in 10 apparently normal subjects drinking since at least 5 years 100 g alcohol a day, in 14 subjects presenting hepatic alcoholic cirrhosis and in 18 apparently normal non alcoholic controls. Post-stimulation gastrin concentration were higher in chronic pancreatitis patients or in normal alcoholics (peak post-stimulation value: 74 +/- 41 and 74 +/- 43 pg/ml respectively) than in cirrhotics or non alcoholic controls (45 +/- 26 and 41 +/- 15 pg/ml respectively) (m +/- SD).

Topics: Adult; Alcoholism; Chronic Disease; Ethanol; Fasting; Food; Gastrins; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Pancreatitis

On the basis of some experimental observations of hypergastrinemia in animals chronically intoxicated with ethanol, both fasting and after meals serum gastrin were determined in patients affected by chronic alcoholic pancreatitis. A significant increase in serum gastrin levels was observed in patients with chronic pancreatitis compared with controls, both in basal conditions and following food stimulation. The physiopathological hypotheses and possible aetiopathogenetic implications suggested by such gastrin behaviour are discussed.

Topics: Adult; Aged; Alcoholism; Chronic Disease; Gastrins; Humans; Male; Middle Aged; Pancreatitis

Fifty patients with cirrhosis of the liver had gastrin concentrations in serum above normal when measured in the fasting state. Hypergastrinaemia predominated in non-alcoholic cirrhosis. In both groups of patients, serum gastrin levels were higher in patients with inactive cirrhosis than when cirrhosis was slightly active.

Topics: Aged; Alcoholism; Female; Gastrins; Humans; Liver Cirrhosis; Male; Middle Aged

Topics: Alcoholism; Amylases; Anemia, Pernicious; Atrophy; Bicarbonates; Gastrins; Gastritis; Humans; Pancreas; Pancreatic Juice; Pancreatic Neoplasms; Pancreatitis; Secretin; Zollinger-Ellison Syndrome

Gastirn blood levels after the ingestion of a meat meal, either alone or associated with ethanol (1.0 gm./kg.), are higher and better sustained in dogs treated chronically with alcohol than in control animals. This greater gastrin-releasing capacity of the dog gastric antrum would be responsible for the increased parietal cell mass and gastric acid secretion shown by animals subjected to chronic alcohol intoxication.

Topics: Alcoholism; Animals; Chronic Disease; Dogs; Ethanol; Fasting; Gastric Mucosa; Gastrins; Humans; Radioimmunoassay; Time Factors

Topics: Alcoholism; Depression; Gastrins; Humans; Lithium; Male; Personality Disorders; Schizophrenia

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Alcoholism; Aspirin; Blood Circulation; Body Constitution; Endocrinology; Gastrins; Genetics, Medical; Humans; Infections; Pepsin A; Peptic Ulcer; Phenylbutazone; Psychosomatic Medicine; Research; Stress, Physiological; Toxicology; Tuberculosis; Tuberculosis, Pulmonary