Introduction: In animal models, infection with human adenovirus (Ad36) is associated with increased adiposity but improved glycemic control.
Methods: The longitudinal observational study involved 1,400 Mexican American adults enrolled in the San Antonio Family Heart Study. Serum samples taken at baseline were assessed for Ad36 infection. Measurements of obesity (body mass index and body fat percentage) and glycemic control (fasting glucose and insulin levels) were taken at baseline and 10 years later.
Results: Approximately 15% of this sample was seropositive for Ad36 infection. Infected subjects were more likely to have a greater body fat percentage at baseline than noninfected subjects. Infection also was associated with better glycemic control at baseline in patients of normal weight (ie, BMI ≤25 kg/m2). The longitudinal analysis showed greater adiposity indices but lower fasting insulin levels in seropositive patients. Subgroup analyses linked infection with Ad36 to lower fasting insulin levels over time in patients of normal weight and greater adiposity in the overweight and obese men. The authors noted that the differences between seropositive and seronegative groups in adiposity and glycemic control were modest in magnitude.
Conclusion: Infection with Ad36 is associated with greater adiposity and less deterioration in glycemic control over time in Mexican American men and women.
Commentary by Louis Kuritzky MD
The adenovirus story line goes way back, but for the moment let’s look at it right now. Lin et al provide data from the San Antonio Heart Study of Mexican American adults (n=1,400) in whom adenovirus 36 (Ad36) antibodies were measured at baseline. Concordant with national data, about 15% of enrollees were Ad36-antibody positive at the time of enrollment.1
At the 10-year follow up of these subjects, a counterintuitive relationship between Ad36 antibody status and adiposity/glycemia was discerned: compared with Ad36 seronegative individuals, there was significantly greater weight gain amongst Ad36 seropositive individuals. However, despite the greater degree of adiposity, there was lower A1c and fasting glucose in the Ad36-seropositive group. The authors posit contrasting activities of Ad36 in obesity and glucose modulation.
The history of a relationship between Ad36 and weight change goes back to Bombay, India, where it was reported that an Ad36 infection in chicks resulted in unexpected weight gain, confirmed shortly afterwards by observations that within 3 weeks of Ad36 injection, chicks gained weight.2 In a follow-up study comparing lean and obese patients, Ad36 antibody was found in 23 out of 154 obese individuals, versus 0 out of 45 lean subjects.3 Before we dismiss the potential role of Ad36 infection as implausible, recall that through the 1980s the discovery of Helicobacter pylori as the cause of peptic ulcer disease was similarly dismissed because it was considered common knowledge that no bacteria could possibly survive the acid environs of the stomach!