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MINIREVIEW

Pathophysiological Effects of Nicotine on the Pancreas: An Update¹

Parimal Chowdhury^2,*, Stewart MacLeod, Kodetthor B. Udupa^*, and Phillip L. Rayford^*

^* Departments of Physiology and Biophysics,
Surgery, and
Geriatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205

Epidemiological evidence strongly suggests an association between cigarette smoking and pancreatic diseases. It is well recognized that nicotine, a major component in cigarette smoke, is an addictive agent and, therefore, reinforces smoking behavior. The current review update focuses on the genetics of nicotine dependence and its role on the development of pancreatic diseases. The role of smoking and nicotine in pancreatitis and pancreatic cancer development is also discussed. Exposure of laboratory animals to nicotine clearly supports the notion that nicotine can induce pancreatic injury. The mechanism by which nicotine induces such effects is perhaps mediated via signal transduction pathways in the pancreatic acinar cell, leading to enhanced levels of intracellular calcium release, resulting in cytotoxicity and eventual cell death. The induction of pancreatic injury by nicotine may also involve activation and expression of protooncogene, H-ras, which can increase cytosolic calcium via second messenger pathways. Development of pancreatic carcinoma in cigarette smokers as observed in human populations may be the result of activation and mutation of the H-ras gene. A possible pathogenetic mechanism of nicotine in the pancreas activating multiple signal transduction pathways is schematically summarized in Figure 1.

View larger version (37K): [in this window] [in a new window]   Figure 1. Pancreatic acinar cell model showing induction of multiple Ca2+ regulated signal transduction pathways (Printed with permission from Lippincott Williams & Wilkins. Eur J Gastroenterol Hepatol 12(8):869–877, 2000).

Key Words: nicotine • gastrointestinal function • pancreas • pancreatic injury • mechanism of action

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