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Using rats as a research model to investigate the effect of human adenovirus 36 on weight gain

Document Type : Original Article(s)

Authors

1 PhD Candidate, Nutrition and Metabolic Diseases Research Cente AND School of Paramedical, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

2 Assistant Professor, Health Research Institute, Infectious and Tropical Diseases Research Center AND School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

3 Assistant Professor, Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

4 Lecturer, Diabetes Research Center AND Department of Statistics and Epidemiology, School of Public Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

5 Professor, Nutrition and Metabolic Diseases Research Center AND School of Paramedical, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Abstract

BACKGROUND: Recent evidence has shown a positive correlation between obesity and viral infections with a particular emphasis on the human adenovirus-36 (Ad-36). Ad-36 is the first human virus that may increase adiposity in animals, and it is considered as a possible risk factor for obesity in humans; however, the results were not consistent across all the studies. The present study was conducted to examine the influence of Ad-36 infection on obesity in a rat model. METHODS: Eight-week-old male Wistar rats weighing 170-240 gram (g), were randomly divided into two groups, infection group (48 rats) and a control group (12 rats). The rats in the infection group were infected with human Ad-36. All rats were given free access to a normal chow diet and water. They were weighed weekly. RESULTS: The mean ± standard deviation (SD) body weights were 229.0 ± 25.9 g and 232.3 ± 16.6 g in the infection and control groups, respectively at the time of infection. The mean ± SD body weight of the infection group (304.0 ± 39.0 g) was higher than the control group (301.0 ± 36.5 g) at 12 weeks post-infection (P = 0.82). Although two groups had approximately same food intakes, the mean change in body weight was greater in the infection group than the control group (75.8 ± 27.9 g vs. 70.8 ± 24.5 g) but it was not significant (P = 0.57). CONCLUSION:We did not find a statistically significant association between weight gain and Ad-36 infection in the rat model. It seems that longer follow-up duration is needed to develop a significant weight gain in the infected rats. Rats can be used as a good animal model for further investigations about Ad-36-induced obesity, provided not to rely merely on weight measurements. Evaluating body composition or histopathological assessments are suggested. 

Keywords

References
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ARYA Atherosclerosis Journal
Volume 13, Issue 4 - Serial Number 4
July and August 2017
Pages 167-171
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