Only during the last 15 years have systematic and controlled studies on the action of pure ethanol and some commonly ingested alcoholic beverages on gastric acid secretion and release of gastrin in humans been published (1)(2)(3)(4)(5)(6)(7)(8). Pure ethanol in low concentrations (≤4% vol/vol) is a mild stimulant of gastric acid output, whereas at higher concentrations, it has either no effect or a mildly inhibitory one (5). Alcoholic beverages with low ethanol content (beer and wine) are powerful stimulants of gastric acid output and gastrin release; the effect of beer is equal to the maximal acid output (5-8). Beverages with a higher ethanol content (e.g., whisky, gin, cognac) do not stimulate gastric acid output or release of gastrin (5, 7).The ethanol content in beer (4% vol/vol) and wine (10% vol/vol) can be only partially or not at all responsible for the marked gastric acid secretory responses to beer and wine. Thus, nonalcoholic ingredients in beer or wine are most likely responsible for the stimulatory gastric action of these alcoholic beverages. The intensive search for the stimulatory substances in beer has proved that none of the known nonalcoholic stimulants of gastric acid output present in beer either alone or in combination can be implicated (6).In a recent study (7), we reported that alcoholic beverages produced by fermentation (such as beer, wine, champagne, and sherry), but not by distillation (such as whisky, cognac, calvados, armagnac, Bacardi, Pernod, Cointreau, and Campari), are powerful stimulants of gastric acid output and release of gastrin. In addition, we found that the alcoholic beverage constituents that stimulate gastric acid output and release of gastrin are produced during the process of fermentation and removed during the following process of distillation (7).We used yeast-fermented glucose as a simpler model of beer in order to look for the powerful stimulants of gastric acid output produced during the process of alcoholic fermentation (6, 9). Alcoholic fermentation is the catabolism of glucose to pyruvate (e.g., glycolysis) and of pyruvate to ethanol by yeast. Yeast-fermented glucose (11.5% wt/vol) has been shown to mimic the effects of beer on gastric acid output and release of gastrin (6, 9). Whereas beer has a great number of unknown substances, yeastfermented glucose is a relatively pure solution.The aim of the present investigation was to separate and identify the substances in fermented glucose and alcoholic beverages that are responsible for their powerful stimulatory action on gastric acid output and release of gastrin in nonalcoholic healthy humans.
Methods
SubjectsThirty-five healthy young male (n = 20) and female (n = 15) volunteers (age, 21-37 years; body weight, 50-87 kg) were studied. All subjects were in good health and had a normal physical examination, electrocardiogram, and laboratory tests, including blood count, platelets, prothrombin time, aspartate aminotransferase, alanine aminotransferase, γ-glutamyltransferase, amylase, lipase, creatinine, electrolytes...