Related Experiment Video
Updated: Jul 30, 2026
08:18
A Model of Chronic Nutrient Infusion in the Rat
Published on: August 14, 2013
Altered exocrine pancreatic function in rats treated with nicotine
M A Dubick1, R Palmer, P P Lau
1Department of Medicine, Veterans Administration Medical Center, Martinez, California 94553.
Toxicology and Applied Pharmacology
|October 1, 1988
Summary
Nicotine treatment significantly increased digestive enzyme content and release in rat pancreas. This suggests potential impacts on exocrine pancreatic function in moderate cigarette smokers.
Area of Science:
- Gastroenterology
- Endocrinology
- Toxicology
Background:
- Exocrine pancreatic function is crucial for digestion.
- Nicotine is a major component of tobacco products with known systemic effects.
Purpose of the Study:
- To investigate the impact of nicotine on exocrine pancreatic function in rats.
- To determine if nicotine affects digestive enzyme levels and secretion.
Main Methods:
- Adult male Sprague-Dawley rats received nicotine via time-release pellets for 3 weeks.
- Assessed pancreatic enzyme activities (amylase, trypsin, chymotrypsin), mRNA levels, and enzyme secretion from isolated pancreatic acini.
- Stimulated enzyme release using CCK-8, secretin, and carbachol.
Main Results:
- Nicotine treatment increased pancreatic amylase, trypsin, and chymotrypsin activities by 51%, 29%, and 35%, respectively.
- Elevated levels of immunoreactive cationic trypsin(ogen) and amylase mRNA were observed in nicotine-treated rats.
- Basal and stimulated enzyme secretion from pancreatic acini were significantly higher in nicotine-exposed rats.
Conclusions:
- Nicotine exposure increases digestive enzyme content within the rat pancreas.
- Nicotine enhances both basal and stimulated exocrine pancreatic secretion.
- These findings suggest nicotine may alter pancreatic digestive capacity at levels relevant to human smokers.
Related Concept Videos
01:23Drugs Acting on Autonomic Ganglia: Stimulants
Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
01:27Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Insulin and C-peptide are co-secreted in...
01:25Chronic Pancreatitis I: Introduction
Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...
01:21Chronic Pancreatitis II: Pathophysiology
Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...