Catching Obesity:
Identifying Viruses That May Make Us Fat
Do
human adenoviruses cause obesity? Is a vaccine possible?Researcher advises:
‘Eat right, exercise, wash your hands’
BETHESDA, Md. (Jan. 30, 2006) – There is a lot of good
advice to help us avoid becoming obese, such as “Eat less,” and “Exercise.”
But here’s a new and surprising piece of advice based on a promising area of
obesity research: “Wash your hands.”
There is accumulating evidence that certain viruses may
cause obesity, in essence making obesity contagious, according to Leah D.
Whigham, the lead researcher in a new study, “Adipogenic potential of
multiple human adenoviruses in vivo and in vitro in animals,” in the January
issue of the American Journal of Physiology-Regulatory, Integrative and
Comparative Physiology published by the American Physiological
Society.
The study, by Whigham, Barbara A. Israel and Richard L.
Atkinson, of the University of Wisconsin, Madison, found that the human
adenovirus Ad-37 causes obesity in chickens. This finding builds on studies
that two related viruses, Ad-36 and Ad-5, also cause obesity in animals.
Moreover, Ad-36 has been associated with human obesity,
leading researchers to suspect that Ad-37 also may be implicated in human
obesity. Whigham said more research is needed to find out if Ad-37 causes
obesity in humans. One study was inconclusive, because only a handful of
people showed evidence of infection with Ad-37 – not enough people to draw
any conclusions, she said. Ad-37, Ad-36 and Ad-5 are part of a family of
approximately 50 viruses known as human adenoviruses.
Researchers now must:
Screening test and vaccine
still a long way off
The Whigham et al. study prompted an editorial in the
same issue of AJP-Regulatory, Integrative and Comparative Physiology
by Frank Greenway, professor in the
Department of Clinical Trials, Pennington Biomedical Research Center,
Louisiana
State University, Baton Rouge.
“If Ad-36 is
responsible for a significant portion of human obesity, the logical
therapeutic intervention would be to develop a vaccine to prevent future
infections,” Greenway wrote. “If a vaccine were to be developed, one would
want to ensure that all the serotypes of human adenoviruses responsible for
human obesity were covered in the vaccine.”
“If one could
predict the potential of an adenovirus to cause human obesity by using an in
vitro assay or even by animal testing, screening of the approximately 50
human adenoviruses might be accelerated, shortening the time required for
vaccine formulation," Greenway wrote. “Human antibody prevalence in obese
and lean human populations appears to be the only reliable method to screen
adenoviruses for their potential to cause obesity in humans at the present
time,” he noted.
Obesity contagion theory
slow to catch on
The notion that viruses can cause obesity has been a
contentious one among scientists, Whigham said. And yet, there is evidence
that factors other than poor diet or lack of exercise may be at work in the
obesity epidemic. “The prevalence of obesity has doubled in adults in the
United States in the last 30 years and has tripled in children,” the study
noted. “With the exception of infectious diseases, no other chronic disease
in history has spread so rapidly, and the etiological factors producing this
epidemic have not been clearly identified.”
“It makes people feel more comfortable to think that
obesity stems from lack of control,” Whigham said. “It’s a big mental leap
to think you can ‘catch’ obesity.” However, other diseases once thought to
be the product of environmental factors are now known to stem from
infectious agents. For example, ulcers were once thought to be the result of
stress, but researchers eventually implicated bacteria, Helicobacter pylori, as a
cause.
“The nearly simultaneous increase in the prevalence of
obesity in most countries of the world is difficult to explain by changes in
food intake and exercise alone, and suggest that adenoviruses could have
contributed,” the study said. “The role of adenoviruses in the worldwide
epidemic of obesity is a critical question that demands additional
research.”
Ad-37 third virus
implicated in animal obesity
The theory that viruses could play a part in obesity
began a few decades ago when Nikhil Dhurandhar, now at Pennington Biomedical
Research Center at LSU, noticed that chickens in India infected with the
avian adenovirus SMAM-1 had significantly more fat than non-infected
chickens. The discovery was intriguing because the explosion of human
obesity, even in poor countries, has led to suspicions that overeating and
lack of exercise weren’t the only culprits in the rapidly widening human
girth. Since then, Ad-36 has been found to be more prevalent in obese
humans.
In the current study, Whigham et al. attempted to
determine which adenoviruses (in addition to Ad-36 and Ad-5) might be
associated with obesity in chickens. The animals were separated into four
groups and exposed to either Ad-2, Ad-31, or Ad-37. There was also a control
group that was not exposed to any of the viruses. The researchers measured
food intake and tracked weight over three weeks before ending the experiment
and measuring the chickens’ visceral fat, total body fat, serum lipids, and
viral antibodies.
Chickens inoculated with Ad-37 had much more visceral
fat and body fat compared with the chickens infected with Ad-2, Ad-31 or the
control group, even though they didn’t eat any more. The Ad-37 group was
also generally heavier compared to the other three groups, but the
difference wasn’t great enough to be significant by scientific standards.
The authors concluded that Ad-37 increases obesity in
chickens, but Ad-2 and Ad-31 do not. “Ad-37 is the third human adenovirus to
increase adiposity in animals, but not all adenoviruses produce obesity,”
the study concluded.
There is still
much to learn about how these viruses work, Whigham said. “There are people
and animals that get infected and don’t get fat. We don’t know why,” she
said. Among the possibilities: the virus hasn’t been in the body long enough
to produce the additional fat; or the virus creates a tendency to obesity
that must be triggered by overeating, she said.
Mass screening for these viruses is impractical right
now because there is no simple blood test available that would quickly
identify exposure to a suspect virus, Whigham et al. said. More work is
needed to develop such a test, Whigham said.
Source, funding and disclosure
“Adipogenic
potential of multiple human adenoviruses in vivo and in vitro in animals,”
by Leah D. Whigham and Richard L. Atkinson of the Departments of Medicine
and Nutritional Sciences at the University of Wisconsin, Madison, and
Barbara A. Israel of the Department of Pathobiological Sciences, University
of Wisconsin, Madison, is in the January issue of the American Journal of
Physiology - Regulatory, Integrative and Comparative Physiology
published by the American Physiological Society.
Research was supported by grants from the National
Institute of Diabetes and Digestive and Kidney Diseases, and the
Beers-Murphy Clinical Nutrition Center, University of Wisconsin. Atkinson,
now at the Virginia Commonwealth University, owns all shares of Obetech LLC,
a company that markets assays to detect infection with human adenovirus-36
and owns patent rights for these assays.
Editor’s note: The media may obtain a copy of
Whigham et al. by contacting
Christine Guilfoy, American Physiological Society, (301) 634-7253 or
cguilfoy@the-aps.org.
* * *
The
American Physiological Society was founded in 1887 to foster basic and
applied bioscience. The Bethesda, Maryland-based society has more than
10,000 members and publishes 14 peer-reviewed journals containing almost
4,000 articles annually.
* * *
APS
provides a wide range of research, educational and career support and
programming to further the contributions of physiology to understanding the
mechanisms of diseased and healthy states. In May 2004, APS received
the Presidential Award for Excellence in Science,
Mathematics and Engineering Mentoring (PAESMEM).
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