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Published on: August 14, 2013
Dynamic changes of pancreatic structure and function in rats treated chronically with nicotine
1Department of Medicine, Department of Veterans Affairs Medical Center, Martinez, California 94553.
Toxicology and Applied Pharmacology
|July 1, 1990
Summary
Nicotine exposure increases pancreatic digestive enzyme production and accumulation in rats. Long-term nicotine treatment leads to altered enzyme release and pancreatic cell damage.
Area of Science:
- Gastroenterology
- Toxicology
- Molecular Biology
Background:
- Nicotine is a primary component of tobacco products with known systemic effects.
- The impact of chronic nicotine exposure on pancreatic exocrine function is not fully understood.
Purpose of the Study:
- To investigate the effects of chronic nicotine administration on pancreatic enzyme biosynthesis, release, and morphology in adult male rats.
Main Methods:
- Adult male Sprague-Dawley rats were subcutaneously implanted with nicotine pellets (5, 15, or 50 mg) or placebo for 1.5, 3, 6, and 12 weeks.
- Pancreatic trypsin and chymotrypsin activities, amylase mRNA levels, and secretagogue-stimulated enzyme release were measured.
- Pancreatic morphology was examined using electron microscopy.
Main Results:
- High-dose nicotine (50 mg) significantly increased pancreatic trypsin and chymotrypsin activities and amylase mRNA levels after 12 weeks.
- Nicotine exposure altered secretagogue-stimulated enzyme release, with initial increases followed by declines below control levels.
- Electron microscopy revealed intracytoplasmic vacuoles in pancreatic acinar cells after 3 weeks of high-dose nicotine treatment.
Conclusions:
- Chronic nicotine administration induces increased pancreatic digestive enzyme biosynthesis and accumulation.
- Nicotine exposure leads to altered pancreatic acinar cell responsiveness to secretagogues.
- Long-term nicotine treatment results in morphological damage to the pancreas.
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