Rapid adaptation of pancreatic exocrine function to short-term alcohol feeding in rats

Dèng, Xiǎoyīng; Wood, Paul G.; Eagon, Patricia K.; Whitcomb, David C.

doi:10.1159/000085270

Cited by 12 publications

(14 citation statements)

References 53 publications

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“…Future research projects may also aim at studying the role of the brain-gut axis in the development of alcoholic chronic pancreatitis [79] . Since pancreatic exocrine secretion is controlled both by the nervous system and hormones, investigations of the effects of alcohol on the neural mechanisms in mediating pancreatic function might be important for the understanding of alcoholic pancreatitis [79][80][81][82] . In conclusion, the exact mechanisms underlying alcoholic chronic pancreatitis are not yet clarifi ed, but it is likely that several mechanisms, for example genetic predispositions or environmental factors such as smoking, act together with alcohol exposure and increase the risk to develop chronic pancreatitis.…”

Section: Future Perspectivesmentioning

confidence: 99%

Alcoholic Pancreatitis

Schneider

Singer²

2005

Dig Dis

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A history of excessive alcohol consumption is found in the majority of patients with chronic pancreatitis, and numerous research efforts revealed insights into the pathogenesis of alcohol-induced pancreatic damage. However, the exact mechanisms underlying the disease are not yet clarified, and the origin of alcoholic chronic pancreatitis continues to be the topic of speculation and investigation. This article provides an overview about the epidemiology of alcoholic chronic pancreatitis, the epidemiologic association of alcohol intake and pancreatitis and the clinical course of the disease. Finally, this article summarizes several hypothetical concepts that try to explain the early and late pathophysiological mechanisms of acute and chronic pancreatitis.

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Section: Future Perspectivesmentioning

confidence: 99%

Alcoholic Pancreatitis

Schneider

Singer²

2005

Dig Dis

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“…Chronic plus binge ethanol exposure appears to alter pancreatic functions. Ethanol exposure usually causes functional hyperstimulation of the pancreas and increases the synthesis and secretion of pancreatic proteins and digestive enzymes (Deng et al , 2005). We show here that ethanol increases the expression and secretion of pancreatic amylase, which is consistent with previous findings (Saluja and Bhagat, 2003; Huang et al , 2014).…”

Section: Discussionmentioning

confidence: 99%

“…The pancreas is sensitive to acute ethanol which inhibits acinar cell function. Chronic ethanol exposure causes a rapid adaption, resulting in an exaggerated response of the acinar cells to some secretagogue which may induce pancreatic damage (Deng et al , 2005). Intraperitoneal administration of ethanol plus palmitoleic acid produces pancreatic injury characteristic of alcoholic AP.…”

Section: Discussionmentioning

confidence: 99%

Chronic plus binge ethanol exposure causes more severe pancreatic injury and inflammation

Ren

Yang

Wang

et al. 2016

Toxicology and Applied Pharmacology

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Alcohol abuse increases the risk for pancreatitis. The pattern of alcohol drinking may impact its effect. We tested a hypothesis that chronic ethanol consumption in combination with binge exposure imposes more severe damage to the pancreas. C57BL/6 mice were divided into four groups: control, chronic ethanol exposure, binge ethanol exposure and chronic plus binge ethanol exposure. For the control group, mice were fed with a liquid diet for two weeks. For the chronic ethanol exposure group, mice were fed with a liquid diet containing 5% ethanol for two weeks. In the binge ethanol exposure group, mice were treated with ethanol by gavage (5 g/kg, 25% ethanol w/v) daily for 3 days. For the chronic plus binge exposure group, mice were fed with a liquid diet containing 5% ethanol for two weeks and exposed to ethanol by gavage during the last 3 days. Chronic and binge exposure alone caused minimal pancreatic injury. However, chronic plus binge ethanol exposure induced significant apoptotic cell death. Chronic plus binge ethanol exposure altered the levels of alpha-amylase, glucose and insulin. Chronic plus binge ethanol exposure caused pancreatic inflammation which was shown by the macrophages infiltration and the increase of cytokines and chemokines. Chronic plus binge ethanol exposure increased the expression of ADH1 and CYP2E1. It also induced endoplasmic reticulum stress which was demonstrated by the unfolded protein response. In addition, chronic plus binge ethanol exposure increased protein oxidation and lipid peroxidation, indicating oxidative stress. Therefore, chronic plus binge ethanol exposure is more detrimental to the pancreas.

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“…Alcohol may also increase susceptibility to acute pancreatitis by causing functional hyperstimulation, a complex process that is associated with physiological changes in the brainstem and acinar cell that result in an exaggerated response to a given neurohormonal stimulant [24,32] . Thus, alcohol has the double susceptibility effect lowering the threshold for pancreatitis with a given amount of stimulation and increasing the amount of pancreatic stimulation with a given stimulant.…”

Section: Alcohol As a Risk Factor For Acute And Chronic Pancreatitismentioning

confidence: 99%

“…Alcohol itself usually behaves as an anti-infl ammatory agent [32] . This concept is important since anti-infl ammatory factors (e.g.…”

Section: Alcohol As a Risk Factor For Acute And Chronic Pancreatitismentioning

confidence: 99%

Genetic Polymorphisms in Alcoholic Pancreatitis

Whitcomb¹

2005

Dig Dis

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Background: Chronic, excessive alcohol consumption is clearly associated with acute and chronic pancreatitis. However, both clinical and laboratory studies demonstrate that alcohol consumption alone does not directly cause alcoholic chronic pancreatitis. Growing evidence suggests that environmental and possibly genetic cofactors must also be present to overcome the redundant mechanisms protecting the pancreas from pancreatitis and facilitating complete recovery. Methods: The SAPE hypothesis model was used to organize potential triggering factors, susceptibility factors and disease-modifying factors based on insights from animal studies. A systematic review of genetic studies on alcoholic pancreatitis was conducted and the results were analyzed in the context of animal studies. Results: To date, no major genetic cofactors for susceptibility or progression have been identified in ∼90% of cases of human alcoholic chronic pancreatitis. Mutations have been identified in the pancreatic secretory trypsin inhibitor gene (SPINK1) in about 8% of cases, and an excess in cystic fibrosis transmembrane conductance inhibitor (CFTR) gene variants have been reported, but the details of the complex genetics with CFTR have not been clarified. None of the polymorphisms in alcohol-metabolizing genes or detoxifying genes appear to explain pancreatic susceptibility. Conclusions: New, adequately powered genetic studies are needed. Several major genetic epidemiology studies are underway in both Europe and the United States to help determine why only a subset of alcoholics develop alcoholic chronic pancreatitis.

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Rapid adaptation of pancreatic exocrine function to short-term alcohol feeding in rats

Cited by 12 publications

References 53 publications

Alcoholic Pancreatitis

Alcoholic Pancreatitis

Chronic plus binge ethanol exposure causes more severe pancreatic injury and inflammation

Genetic Polymorphisms in Alcoholic Pancreatitis

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