Human adenovirus Ad-36 induces adipogenesis via its E4 orf-1 gene

Rogers, Pamela M.; Fusinski, K A; Rathod, Miloni; Loiler, Scott A.; Pasarica, Magdalena; Shaw, Michael K.; Kilroy, Gail; Sutton, Gregory M.; McAllister, E J; Mashtalir, Nazar; Gimble, Jeffrey M.; Holland, Thomas C.; Dhurandhar, Nikhil V.

doi:10.1038/sj.ijo.0803748

Cited by 98 publications

(106 citation statements)

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“…The effect of Ad-36 on adipose tissue cannot be attributed simply to any viral infection. Ad-2, another human adenovirus, which is nonadipogenic in vivo and in vitro (23,33), was used as a negative control. In addition, we conducted a plaque-forming unit assay in hASCs.…”

Section: Resultsmentioning

confidence: 99%

Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

et al. 2008

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OBJECTIVE-Experimental infection of rats with human adenovirus type 36 (Ad-36) promotes adipogenesis and improves insulin sensitivity in a manner reminiscent of the pharmacologic effect of thiozolinediones. To exploit the potential of the viral proteins as a therapeutic target for treating insulin resistance, this study investigated the ability of Ad-36 to induce metabolically favorable changes in human adipose tissue. RESEARCH DESIGN AND METHODS-We determinedwhether Ad-36 increases glucose uptake in human adipose tissue explants. Cell-signaling pathways targeted by Ad-36 to increase glucose uptake were determined in the explants and human adipose-derived stem cells. Ad-2, a nonadipogenic human adenovirus, was used as a negative control. As a proof of concept, nondiabetic and diabetic subjects were screened for the presence of Ad-36 antibodies to ascertain if natural Ad-36 infection predicted improved glycemic control.RESULTS-Ad-36 increased glucose uptake by adipose tissue explants obtained from nondiabetic and diabetic subjects. Without insulin stimulation, Ad-36 upregulated expressions of several proadipogenic genes, adiponectin, and fatty acid synthase and reduced the expression of inflammatory cytokine macrophage chemoattractant protein-1 in a phosphotidylinositol 3-kinase (PI3K)-dependent manner. In turn, the activation of PI3K by Ad-36 was independent of insulin receptor signaling but dependent on Ras signaling recruited by Ad-36. Ad-2 was nonadipogenic and did not increase glucose uptake. Natural Ad-36 infection in nondiabetic and diabetic subjects was associated with significantly lower fasting glucose levels and A1C, respectively. CONCLUSIONS-Ad-36 proteins may provide novel therapeutic targets that remodel human adipose tissue to a more metabolically favorable profile.

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Section: Resultsmentioning

confidence: 99%

Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

et al. 2008

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“…5 An indirect evidence of the relationship between eating habits and weight gain come from the literature on the (negative) effect of fast food prices on adolescent BMI (see Chou et al, 2005;Powell et al, 2007;Auld and Powell, 2008;Powell and Bao, 2009). See also Cutler et al (2003) which relates the declining relative price of fast food and the increase in fast food restaurant availability over time to increasing obesity in the U.S. 6 We acknowledge that some recent studies have pointed that obesity might be partially due to a virus ad-36 (see Rogers et al, 2007). 7 Of course, having obese peers may influence a student's tolerance for being obese and therefore his weight management behaviours.…”

Section: Introductionmentioning

confidence: 99%

Peer effects, fast food consumption and adolescent weight gain

Fortin

Yazbeck

2015

Journal of Health Economics

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This paper aims at opening the black box of peer effects in adolescent weight gain. Using Add Health data on secondary schools in the U.S., we investigate whether these effects partly flow through the eating habits channel. Adolescents are assumed to interact through a friendship social network. We first propose a social interaction model of fast food consumption. Our approach allows to control for correlated effects at the network level and to solve the simultaneity (reflection) problem. We exploit results by Bramoullé, Djebbari and Fortin (2009) which show that if there are two agents who are separated by a link of distance 3 within a network (i.e., two adolescents who are not friends but are linked by two friends), peer effects are identified. The model is estimated using maximum likelihood and generalized 2SLS strategies. We also estimate a panel dynamic weight gain production function relating an adolescent's Body Mass Index (BMI) to his current fast food consumption and his lagged BMI level. Results show that there are positive significant peer effects in fast food consumption among adolescents belonging to a same friendship school network. The estimated social multiplier is 1.59. Our results also suggest that, at the network level, an extra day of weekly fast food restaurant visits increases BMI by 2.4%, when peer effects are taken into account.

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“…Adipogenesis and lipid accumulation decreased when Ad36 E4 orf-1 was knocked down by RNAi (58). Therefore, Ad36 E4 orf-1 could play an important role in inducing adipogenesis.…”

Section: The Mechanism Of Ad36-induced Obesitymentioning

confidence: 94%

Infectobesity: a New Area for Microbiological and Virological Research

Nam

2011

J Bacteriol Virol

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Obesity is connected with numerous diseases, such as type 2 diabetes, atherosclerosis, cancer, and nervous system dysfunctions. Obesity is affected by genetic, environmental, and cultural factors. However, numerous studies indicate that several pathogens might cause obesity. This review discusses recent data and the characteristics of pathogens that are implicated in obesity. In particular, human adenovirus 36 (Ad36) is the most clearly implicated virus in human obesity. It was recently shown that obese groups from the USA, Korea, and Italy have a higher prevalence of serum antibodies against Ad36. The mechanisms of Ad36-induced obesity remain unclear. However, glucose uptake and inflammation are possible mechanisms of Ad36-induced obesity. Overall, this new understanding of causes of obesity has developed into the concept of 'infectobesity' and the possibility of developing a 'vaccine' or 'therapeutic agents' for obesity. million women were considered to be obese (Fig. 1A and 1B). Thus, more than one in ten of the world's adult population was obese. Close to 35 million overweight children live in developing countries and eight million in developed countries, which means that overweight children are a problem in all countries. Overweight and obesity also account for 44% of the diabetes burden, 23% of the ischemic heart disease burden, and between 7% and 41% of certain cancer burdens. Recently, the obesity rate among Koreans has increased drastically (Fig. 1C). In 1995, 11.7% of women and 18% of men were considered to be obese.However, 29.4% of women and 32.6% of men were considered obese in 2001 and the obese ratio recently increased further. There was also a noticeable increase in the ratio of obese children and adolescents (1).The costs of treating obesity and obesity-related metabolic disease account for 40% of total health expenditure in the USA and this recent trend is dramatically increasing (2).The social and economic cost of obesity therapy is more than 1 billion dollar and diabetes treatments account for 19.2% of the national medical insurance premium in Korea (3). Thus, obesity-related diseases are a severe loss to the national economy.There are many causes for obesity, such as genetics, medical problems, or psychiatric illness. Simply put, obesity is a result of an energy imbalance, where the energy intake is greater than energy expenditure (4) and excess energy accumulates in adipose tissue. Increasing rates of obesity at the societal level are attributed to easy access to a palatable diet, increased dependence on cars, and mechanized manufacturing. However, the recent increase in obesity might be

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Human adenovirus Ad-36 induces adipogenesis via its E4 orf-1 gene

Cited by 98 publications

References 44 publications

Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

Peer effects, fast food consumption and adolescent weight gain

Infectobesity: a New Area for Microbiological and Virological Research

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