Pathophysiology of alcoholic pancreatitis: An overview

Chowdhury, Parimal; Gupta, Priya

doi:10.3748/wjg.v12.i46.7421

Cited by 57 publications

(45 citation statements)

References 92 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Ethanol is known to cause acute and chronic injury to the pancreas in humans and in some experimental animal models (Chowdury and Gupta 2006). Clearly, a rat experimental model is per se a limitation if one wants to extrapolate results to humans.…”

Section: Discussionmentioning

confidence: 99%

Ethanol induces secretion of oxidized proteins by pancreatic acinar cells

2007

View full text Add to dashboard Cite

The pancreas is vulnerable to ethanol toxicity, but the pathogenesis of alcoholic pancreatitis is not fully defined. The intracellular oxidative balance and the characteristics of the secretion of isolated rat pancreatic acinar cells stimulated with the cholecystokinin analogue cerulein were assayed after acute oral ethanol (4 g/kg) load. Pancreatic acinar cells from ethanol-treated rats showed a significant (p < 0.02) lower content of total glutathione and protein sulfhydryls, and higher levels of oxidized glutathione (p < 0.03), malondialdehyde, and protein carbonyls (p < 0.05). Ethanol-intoxicated acinar cells showed a lower baseline amylase output compared to controls, with the difference being significantly exacerbated by cerulein stimulation. After cerulein, the release of protein carbonyls by ethanol-treated cells was significantly increased, whereas that of protein sulfhydryls was significantly decreased. In conclusion, ethanol oxidatively damages pancreatic acinar cells; cerulein stimulation is followed by a lower output of amylase and by a higher release of oxidized proteins by pancreatic acinar cells from ethanol-treated rats. These findings may account for the decreased exocrine function, intraductular plug formation, and protein precipitation in alcoholic pancreatitis.

show abstract

Section: Discussionmentioning

confidence: 99%

Ethanol induces secretion of oxidized proteins by pancreatic acinar cells

2007

View full text Add to dashboard Cite

show abstract

“…It has been known that excessive alcohol consumption is associated with increased risk of many diseases, including pancreatitis, which is an inflammatory disease [1]. It was reported in an animal study that the mortality from alcohol-induced pancreatitis was caused by a transient increase of pancreatic amylase output and plasma cholecystokinin (CCK) levels [2].…”

Section: Introductionmentioning

confidence: 99%

Relationships among Iron, Protein Oxidation and Lipid Peroxidation Levels in Rats with Alcohol-induced Acute Pancreatitis

Kiziler

Aydemir

Gülyaşar

et al. 2008

Biol Trace Elem Res

View full text Add to dashboard Cite

It has been previously shown that alcohol induces the damage of pancreatic parenchyma tissue, but the mechanism of this damage is still poorly understood. Assuming that oxygen radical damage may be the involved, we measured markers of oxidative damage in pancreatic tissue, blood serum, plasma, and whole blood of rats with early-stage alcohol-induced acute pancreatitis. Thirty-eight male Wistar rats were divided into three groups: the control group (group 1), the acute pancreatitis group 1 day (group 2), and 3 days (group 3) after the injection of ethyl alcohol into the common biliary duct, respectively. The levels of Fe in tissue and serum, whole blood viscosity, plasma viscosity, fibrinogen and homocysteine (Hcy) levels, erythrocyte and plasma malondialdehyde (MDA), and tissue and plasma protein carbonyl levels were found to be significantly higher in groups 2 and 3 than in group 1. However, the levels of reduced glutathione (GSH) in tissue and erythrocytes were significantly lower in groups 2 and 3 than in group 1. These results suggest that elevated Fe levels in serum and pancreatic tissue in rats with early-stage alcohol-induced acute pancreatitis is associated with various hemorheological changes and with oxidative damage of the pancreas.

show abstract

“…Etanol powoduje zmniejszoną produkcję lipostatyny i wodorowęglanów, zmniejsza wydzielanie polipeptydu trzustkowego oraz zwiększa wrażliwość komórek trzustkowych na cholecystokininę, a w efekcie wywołuje produkcję gęstego, lepkiego, wysokobiałkowego soku trzustkowego, skutecznie czopującego drobne przewody trzustkowe, co doprowadza do uszkodzenia miąższu trzustki. Ta teoria nie jest uznawana przez wszystkich badaczy, ponieważ nie u wszystkich osób uzależnionych obserwuje się wyżej opisane zmiany, a zmniejszone stężenie lipostatyny występuje również u alkoholików, u których nie stwierdza się przewlekłego zapalenia trzustki [91][92][93][94][95].…”

Section: Wpływ Napojów Alkoholowych Na Trzustkęunclassified

Alcohol and the digestive system – should it always be blamed?

Kasicka-Jonderko¹

2012

View full text Add to dashboard Cite

Pathophysiology of alcoholic pancreatitis: An overview

Cited by 57 publications

References 92 publications

Ethanol induces secretion of oxidized proteins by pancreatic acinar cells

Ethanol induces secretion of oxidized proteins by pancreatic acinar cells

Relationships among Iron, Protein Oxidation and Lipid Peroxidation Levels in Rats with Alcohol-induced Acute Pancreatitis

Alcohol and the digestive system – should it always be blamed?

Contact Info

Product

Resources

About