Human adenovirus_36 improves insulin sensitivity, lipid profiles and increases inflammatory markers in wistar rats

Fatemeh Shirani dastjerdi,1,* Ali teimoori,2 Mohammad rashno,3 Mehdi zarei,4 Seyed mahmoud latifi,5 Majid karandish,6

1. Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
2. Infectious and Tropical Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
3. Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
4. Department of Food Hygiene, School of Veterinary Medicine, ShahidChamran University, Ahvaz, Iran.
5. Department of Statistics and Epidemiology, Faculty of Public Health, Diabetes Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
6. Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University, of Medical Sciences, Ahvaz, Iran.

Abstract

Introduction

Obesity, as excess body fat accumulation, is a major public health epidemic in the world. recent evidence has shown a positive correlation between obesity and viral infections. human adenovirus 36 (ad-36), is a possible cause of obesity through increasing adiposity and metabolic inflammatory cytokines though paradoxically improves glycemic control and lipid profile; the results, however, are not consistent. in the present study, the effects of ad-36 infection on insulin resistance, lipid metabolism and inflammatory markers in wistar rats was investigated.

Methods

Sixty male wistar rats (eight-week-old, weighing 170-240 gram) were randomly divided into two groups, infection group (48 rats) and a control group (12 rats). ad-36 virus suspension (50% cell culture infective dose (5 × 105 ccid50)) was injected in the left hind paw of the experimental group rats. all rats were given free access to a chow diet and water and were weighed weekly. blood samples were collected at beginning of the study and 3 months later in both groups. routine measurement of metabolic indices and inflammatory markers were performed.

Results

The mean ± sd of body weight was not significantly different between the infected and control groups at the baseline and 12 weeks after infection. at the beginning of the study, there were no significant differences in glucose, lipid profiles and inflammatory markers between groups. after 12 weeks, fasting blood glucose (95.3 ± 17.4 vs. 107.5 ± 13.6 mg/dl, p = 0.013), and fasting serum insulin (55.2 ± 21.3 vs. 73.6 ± 24.6 μu/ml, p = 0.016) were significant lower in the infected group compared with the control group. the homa index showed significantly higher insulin sensitivity in the infected group (p = 0.002). serum triglycerides (51.4 ± 16.1 vs. 60.2 ± 10.8 mg/dl, p = 0.026) and total cholesterol concentrations (46.5 ± 8.9 vs. 53.6 ± 14.8 mg/dl, p = 0.036) were significant lower in the infected group than the control group at 12 weeks after infection. tumor necrosis factor-α (p = 0.034) interleukine-6 (p = 0.071) and monocyte chemoattractant protein-1 (p = 0.022) were significant higher in the infected group compared with the control group.

Conclusion

In the present study, ad-36 had no significant effect on weight gain but had a favorable effect on glycemic and lipid control in infected rats. a significant increase was observed in the inflammatory markers in the infected group. the mechanism of change in glucose and lipid metabolism attributable to ad-36 has not yet been fully understood. ad-36 infections could be a potential new way of developing novel anti-diabetic and anti-hyperlipidemic therapeutic agents. further investigations are required.

Keywords

Adenovirus-36, glucose, lipid metabolism, inflammatory markers, wistar rats.