Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 41 GP77 | DOI: 10.1530/endoabs.41.GP77

ECE2016 Guided Posters Diabetes (10 abstracts)

Pancreatic damage induced by cigarette smoke: How does smoking affect the pancreatic functions?

Senay Topsakal 1 , Ozlem Ozmen 2 , Rahime Aslankoc 3 & Demet Hancer Aydemir 4


1Department of Endocrinology and Metabolism, Pamukkale University, Faculty of Medicine, Kinikli Campus, Denizli, Turkey; 2Department of Pathology, Mehmet Akif Ersoy University, Faculty of Veterinary Medicine, Istiklal Yerleskesi, 15030, Burdur, Turkey; 3Department of Physiology, Faculty of Medicine, Suleyman Demirel University, 32200, Isparta, Turkey; 4Department of Medical Laboratory, Health Vocational Schools, Suleyman Demirel University, 32200, Isparta, Turkey.


Background: Studies have shown that smoking may increase the risk of pancreatic disorders. This study aimed to evaluate the oxidative stress status, biochemical, pathological and immunohistochemical findings of rats exposed to the cigarette smoke, pathogenesis of smoking related pancreatic damage and usability of Alpha Lipoic Acid (ALA) for amelioration of cigarette’ harmful effects on rat pancreas.

Methods: Twenty eight female, Sprague Dawley rats were randomly distributed into three groups. Sham group (S) (n=8), rats given 0.1 ml of physiological serum by oral gavage for 8 weeks. Cigarette smoke exposed group (CSE) (n=10), rats exposed to successive periods of cigarette smoke for 2 hours/day/8 weeks and given 0.1 ml of physiological serum by orally during the study. Cigarette smoke exposed and ALA treated group (CSE+ALA) (n=10), animals exposed to cigarette smoke (2 hours/day/8 weeks) and simultaneously treated by 100 mg/kg/day ALA orally during the study. Total oxidant status (TOS), total antioxidant status (TAS) levels and oxidative stress index (OSI) were evaluated at the pancreas samples. Immunohistochemically insulin, glucagon, calcitonin gene related protein (CGRP), Caspase-3, hypoxia inducible factor-1 (Hif-1), Hif-2 and TNF-α expressions of pancreas were examined.

Results: Cigarette smoke caused statistically significant increase in serum amylase and glucose levels. At the histopathological examination the pancreases slight degenerative and apoptotic cells noticed both endocrine and exocrine part of the pancreas in CSE group. Immunohistochemical examination revealed marked increase in caspase-3, glucagon, Hif-1 and Hif-2, CGRP and TNF-α expressions while decrease in insulin secretion in some Langerhans islets in CSE group. ALA ameliorated biochemical and pathological findings in CSE+ALA group.

Conclusion: These findings clearly demonstrated that cigarette can cause damage in rat pancreas and ALA has ameliorative effect of cigarette induced lesions.

Keywords: Cigarette smoke, pancreas, pathology, biochemistry.

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