g...10 - iced

[ArchivalUser]

how does alcohol produces pancratitis?

[ArchivalUser]

Alcohol increases fatty acid synthesis > CCK activation > Inc panc. secretion > prolonged activation > cell burnout ????

[ArchivalUser]

alcohol causes cytoplasmic lipid accumulationin acinar cells....cud be dur to oxidative damage alcohol does to liver.

[ArchivalUser]

CCk activation conversion of Trypsinogen to trypsin and auto digestion of pancreas

[ArchivalUser]

Ok..this is what I found out from the web:
Alcohol sensitizes pancreatic acinar cells to CCK leading to the stimulation of Zymogens (proteases) which cause audodigestion - Acute pancreatitis

Hey guys check this out:

Lerch MM, Albrecht E, Ruthenburger M, Mayerle J, Halangk W, Kruger B. Pathophysiology of alcohol-induced pancreatitis. Pancreas. 2003 Nov;27(4):291-6.


THE ROLE OF ETHANOL IN PREMATURE ZYMOGEN ACTIVATION

A continuous or excessive consumption of ethanol is one of the most common risk factors for the development of acute, and even more specifically, chronic pancreatitis in humans. The mechanisms that are involved in alcohol-induced pancreatitis in general have been extensively studied in ethanol-fed laboratory animals. Although several cell biologic changes have been reported from these studies, their relevance to the human disease is questionable because neither rats nor mice develop pancreatitis when put on a high-alcohol diet for extended periods of time. Theoretically, ethanol might promote its damaging effect on pancreatic acinar cells through 2 mechanisms. First, ethanol may directly sensitize the acinar cell to a pathologic stimulus, 58 and second, ethanol may stimulate the release of a physiological secretagogue, cholecystokinin (CCK), from duodenal I cells. 59

Recent studies in which the effect of ethanol on the intracellular activation of digestive protease zymogen was studied were rather successful in eliciting potentially disease-relevant mechanisms. Several studies found that ethanol can, indeed, sensitize acinar cells to CCK-induced procarboxypeptidase A1 processing in vitro and can sensitize to various forms of pancreatitis in vivo. 60“63 Thus, ethanol is believed to enhance the stimulation-dependent induction of pancreatitis, and this process may play a role in ethanol toxicity in the pancreas. A recent study addressed several issues relevant to zymogen activation and the effects of ethanol in isolated pancreatic acini. 64 These authors observed that trypsinogen and chymotrypsinogen exhibit distinct patterns of activation in response to supraphysiological concentrations of the CCK analogue cerulein. Moreover, they found that ethanol and other alcohols sensitized the acinar cell to cerulein-induced trypsin and chymotrypsin activation and that other short-chain n-aliphatic alcohols (methanol, propanol, and butanol) enhanced the effects of cerulein on the acinar cell. Ethanol alone, on the other hand, was not found to induce pancreatitis or zymogen activation in experimental models of pancreatitis. These studies suggest that CCK receptor activation can initiate different patterns of zymogen activation in pancreatic acinar cells and the extent of activation can be enhanced by a distinct set of short-chain alcohols. Whether ethanol and other alcohols mediate these effects by interfering with acinar cell signaling pathways or by effecting acinar cell membrane fluidity is currently being investigated.

[ArchivalUser]

thanks adrenaline...for wonderful explanation!


alcohol produces thick secretions in the duct which activates the enzymes and leads to pancreatitis.

[ArchivalUser]

hey Thank you iced...these q's are awesome...makes you understand the subject rather than just know them.

[ArchivalUser]

thanks alot for participating.....
and thanks alot adrenaline

[ArchivalUser]

thanks alot iced for ur nice Qs n adrenaline for the information

[ArchivalUser]

u are welcome..kash..