Article

Human adenovirus Ad-36 promotes weight gain in male rhesus and marmoset monkeys

Department of Nutrition and Food Science and the Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, USA.
Journal of Nutrition (Impact Factor: 4.23). 10/2002; 132(10):3155-60.
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ABSTRACT Although obesity has multiple etiologies, an overlooked possibility is an infectious origin. We previously identified two viruses, SMAM-1, an avian adenovirus (Ad), and Ad-36, a human adenovirus, that produce a syndrome of visceral obesity, with paradoxically decreased serum cholesterol and triglycerides in chickens and mice. In the two studies presented in this paper, we used nonhuman primates to investigate the adiposity-promoting potential of Ad-36. In study 1, we observed spontaneously occurring Ad-36 antibodies in 15 male rhesus monkeys, and a significant longitudinal association of positive antibody status with weight gain and plasma cholesterol lowering during the 18 mo after viral antibody appearance. In study 2, which was a randomized controlled experiment, three male marmosets inoculated with Ad-36 had a threefold body weight gain, a greater fat gain and lower serum cholesterol relative to baseline (P <0.05) than three uninfected controls at 28 wk postinoculation. These studies illustrate that the adiposity-promoting effect of Ad-36 occurs in two nonhuman primate species and demonstrates the usefulness of nonhuman primates for further evaluation of Ad-36-induced adiposity.

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    • "The detection of significantly higher BMI and leptin, lower adinopectin, and paradoxically insignificantly lower levels of serum cholesterol and triglyceride levels in the obese group with positive Ad-36 antibodies, as compared to the obese group with negative Ad-36, showed similarity with the animal model studies of Dhurandhar et al. [12] [13] [15] and with the human studies of Atkinson et al. [16] and Jiao et al. [10]. However, in line with the relationship between morbid obesity and Ad-36 level described by Almgren et al. [6], even less number, we detected BMI ! "
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    ABSTRACT: Obesity which developes due to multifactorial reasons, was associated recently with human Adenovirus-36 (Ad-36). The aim of this study was to investigate the prevalence of Ad-36 antibodies in obese adults and also to investigate the DNA of Ad-36 in their adipose tissue. In this cross-sectional and case-control based study, 49 obese adults, with BMI ≥30 kg/m(2), and 49 non-obese adults, with BMI ≤25 kg/m(2), applied for esthetic purposes and were included in this study as patient and control groups, respectively. Adipose tissue samples, obtained by the lipoaspiration method, were studied by single-step PCR and nested-PCR methods. Simultaneously, the presence of Ad-36 antibodies and serum leptin and adiponectin levels were assessed by serum neutralization assay (SNA) and ELISA, respectively. Serum samples which didn't cause a cytopathic effect at ≥1:8 were accepted as positive. Ad-36 antibody was detected in 6 (12.2%) of 49 patients by SNA and was statistically significant (p < 0.05). Ad-36 DNA was not detected in any of the adipose tissue samples of the patient or control groups. Mean BMI and leptin levels were higher in the Ad-36-positive group, while adiponectin levels were found to be lower in the Ad-36-positive group. Although no statistically significant difference was found in cholesterol and triglyceride levels between the two groups (p > 0.05), lower mean serum cholesterol and triglyceride levels were found in the Ad-36-positive patients. In conclusion, we couldn't detect Ad-36 DNA in adipose tissue; however, we detected significantly higher Ad-36 antibody levels in the obese group compared to the non-obese group, according to the both univariant and multivariant analyses, suggesting that Ad-36 may play a role in obesity. There is a need for new and extended serial, particularly cohort and human-based, studies in order to have a clear understanding of the Ad-36-obesity relationship. Copyright © 2015. Published by Elsevier Ltd.
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    • "Studies involving animals confirmed a strong association between adenovirus 36 (AdV36) and increased predisposition to excessive accumulation of visceral fat[14] [19] [20] [21] [22]. However, although experimental infections in animals or model cell lines showed an adipogenic potential of some AdV types, there are only few controversial reports on the role of these viruses in the development of obesity in humans and the knowledge about engagement of other AdV types is still limited[14] [19] [20] [21] [23] [24] [25] [26] [27] [28]. The study including 502 participants from the USA showed a significantly greater prevalence of AdV36 in obese people (30%) than in non-obese (11%). "
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    • "Species in which spontaneous or diet-induced obesity in a captive setting have been described include macaques (Kemnitz, 1984; Bodkin et al., 1993; Wagner et al., 2006), vervet monkeys (Kavanagh et al., 2007), baboons (Comuzzie et al., 2003), squirrel monkeys (Ausman et al., 1981) and marmosets (Tardif et al., 2009; Wachtman et al., 2011). Weight gain associated with infection of adult macaques and marmosets with human adenovirus AD36 has been reported (Dhurandhar et al., 2002). Sequelae to obesity are described in most of these cases that mirror those seen in humans, including insulin resistance, diabetes, dyslipidemia , lipid accumulation in the liver and atherosclerotic changes (Hansen and Bodkin, 1993; Wagner et al., 2006; Tardif et al., 2009; Wachtman et al., 2011). "
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    ABSTRACT: While much is known about adult obesity in nonhuman primates, very little is known regarding development of childhood adiposity. As small monkeys that are easy to handle and have a relatively fast life history, common marmoset monkeys (Callithrix jacchus) offer interesting opportunities to examine the question of fat versus lean mass growth in a nonhuman primate. This article provides an overview of our understanding of early life growth in mass in marmoset monkeys, based primarily upon our past 20 years of research, culminating in our recent findings on early life obesity in this species. Common marmosets display variance in early life growth patterns that is related to both pre- and postnatal factors and the marmoset uterine environment is exquisitely designed to reflect resources available for the gestation of multiple offspring, making them an interesting model of developmental programming. We have demonstrated that obesity can be generated in very early life in captive marmosets, with excess adiposity evident by one month of age, making this species a potentially valuable model in which to study pediatric obesity and its sequelae. Birth weight is associated with adiposity in animals vulnerable to obesity. Early life exposure to higher fat diets enhances the chances of postweaning obesity development. However, overall higher food consumption is also associated with obesity development at later ages. One unexpected finding in our studies has been the relatively high body fat percentage of neonatal (12-18%) marmosets suggesting that hypotheses regarding the uniqueness of high human neonatal adiposity merit further examination. Am J Phys Anthropol, 2013. © 2012 Wiley Periodicals, Inc.
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