Ethanol-stimulated acid secretion in the isolated whole stomach of the rat

Bunce, K.T.; Parsons, M E

doi:10.1111/j.2042-7158.1980.tb12843.x

Cited by 4 publications

(2 citation statements)

References 13 publications

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“…Ethanol can stimulate gastric acid secretion. 78–81 The increased acid load delivered to the duodenum will result in increased secretin release 80 which will, in turn, augment ductal secretion of a bicarbonate-rich fluid. 80 Therefore, drinking alcoholic beverages will result in an increase in the concentration of both secretin and ethanol.…”

Section: Effects Of Ethanol On the Exocrine Pancreasmentioning

confidence: 99%

The acinar-ductal tango in the pathogenesis of acute pancreatitis

Hegyi

Pandol

Venglovecz

et al. 2010

Gut

103

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There is an unacceptably high mortality in acute pancreatitis, which is due to the lack of specific treatments for the disease. A major reason stated to account for the inability to develop effective treatments is that there are multiple pathobiologic pathways activated in the acinar cell mediating pancreatitis making it difficult to choose molecular targets for therapeutic strategies. However, this reasoning limits opportunities for therapeutic development because it does include another important participant in pancreatitis - the pancreatic duct cells. The most recent advance in pancreatitis research is that depletion of both glycolytic and oxidative ATP synthesis is a common event in both acinar and ductal cells. Although ATP has a very short half-life in the blood and is hydrolysed to ADP, there is clear evidence that encapsulating ATP into liposomes can effectively drive ATP into the cells which can be effective in protecting them from necrosis. In this review, we will examine the effects of different insults associated with pancreatitis on both the acinar and ductal components of the exocrine pancreas pointing out the role of the ductal epithelial responses in both attenuating and increasing the severity of pancreatitis. In addition, we propose that exogenous ATP administration may restore ductal and acinar function providing therapeutic benefit.

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Section: Effects Of Ethanol On the Exocrine Pancreasmentioning

confidence: 99%

The acinar-ductal tango in the pathogenesis of acute pancreatitis

Hegyi

Pandol

Venglovecz

et al. 2010

Gut

103

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“…It is not secondary to increased calcium or increased gastrin [I]. Ethanol also influences other biologic processes either directly, such as nonpancreatic amylase secretion [2] and gastric acid secretion [3] or indirectly, such as secretin production in humans [4,5]. It does not, however, stimulate the release of cholecystokinin or pancreatic polypeptide in humans [6].…”

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confidence: 99%

Effect of ethyl alcohol on the TSH‐receptor‐cyclase system in thyroid and nonthyroid tissues

Clark

Gerend

1986

World j. surg.

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Alcohol has been documented to be an excellent stimulator of calcitonin secretion in patients with C‐cell hyperplasia and medullary thyroid carcinoma (MTC). We, therefore, investigated the effects of 3–9% ethyl alcohol (ethanol) on the binding of tracer quantities of125I‐labeled bovine thyroid‐stimulating hormone (125I‐bTSH) to its receptor in normal and neoplastic thyroid tissue as well as its effects on adenylate cyclase (AC) stimulation in an 8,000 × g particulate fraction from normal and neoplastic nonmedullary thyroid tissue from 10 patients (20 specimens). We also studied the effect of ethanol on AC activity in 16 other nonthyroidal tissues (5 parathyroid adenoma, 1 pheochromocytoma, 1 sarcoma, and normal and neoplastic breast, kidney, parotid, and colon). These studies demonstrated that ethanol increased the binding of125I‐bTSH to normal and neoplastic thyroid tissue. It also increased AC activity in all but 3 of the 20 thyroid tissues and in all but 3 of the 16 nonthyroid tissues [thyroid basal 20.9±7.1, ethanol maximum 45.9±12.3 (p<0.025); nonthyroid basal 83.0 ±21.5, ethanol maximum 137±31.1 (p<0.01) in picomoles/30 min per mg protein]. This increase was dose dependent over a range of 3–9% ethanol. There was no difference in the degree of ethanol stimulation of AC between normal (28.7±16.3) and neoplastic (21.4±7.8) thyroid or between normal (89.0±8.9) and neoplastic (75.2±23.7) nonthyroid tissues. When ethanol (5%) was given along with TSH, sodium fluoride, Gpp(NH)p, or forskolin, there was a greater increase in AC activity than when no alcohol was present. The combined effect of TSH and ethanol (140.1±49.4) at maximal concentrations was comparable or greater than the result when TSH and ethanol were added separately (121.5±41.8). Thus, ethanol stimulates TSH binding and also activates AC in nearly all normal and neoplastic human tissues. This may be important biologically as well as experimentally since some compounds used in AC assays (in particular, forskolin) are dissolved in ethanol.

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The in vitro effect of ethanol on the histamine-sensitive adenylate cyclase system

Szücs

Karnushina

1981

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The effect of low concentrations (1-5%) of ethanol on the histamine-sensitive adenylate cyclase system was examined in guinea pig gastric mucosa and hippocampus homogenate. Ethanol in these concentrations caused a dose-dependent increase of the adenylate cyclase activity, and this effect was not inhibited by histamine antagonists. Phosphodiesterase activities were not affected by these concentrations of alcohol. Our in vitro findings agree well with the results of BUNCE and PARSONS [10].

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Ethanol-stimulated acid secretion in the isolated whole stomach of the rat

Cited by 4 publications

References 13 publications

The acinar-ductal tango in the pathogenesis of acute pancreatitis

The acinar-ductal tango in the pathogenesis of acute pancreatitis

Effect of ethyl alcohol on the TSH‐receptor‐cyclase system in thyroid and nonthyroid tissues

The in vitro effect of ethanol on the histamine-sensitive adenylate cyclase system

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