6: Harv Mens Health Watch. 1998 Jun;2(11):8.  Related Articles, Links

I heard on the radio that infections can make people fat. Is it true?
--------------------------------------------------------------------------------

7: Obes Res. 1997 Sep;5(5):464-9.  Related Articles, Links

Association of adenovirus infection with human obesity.

Dhurandhar NV, Kulkarni PR, Ajinkya SM, Sherikar AA, Atkinson RL.

Department of Medicine, University of Wisconsin, Madison 53706, USA.

We previously reported that chickens infected with the avian adenovirus
SMAM-1 developed a unique syndrome characterized by excessive
intra-abdominal fat deposition accompanied by paradoxically low serum
cholesterol and triglyceride levels. There have been no previous reports of
avian adenoviruses infecting humans. We screened the serum of 52 humans with
obesity in Bombay, India, for antibodies against SMAM-1 virus using the agar
gel precipitation test (AGPT) method. Bodyweights and serum cholesterol and
triglyceride levels were compared in SMAM-1-positive (P-AGPT) and
SMAM-1-negative (N-AGPT) groups. Ten subjects were positive for antibodies
to SMAM-1, and 42 subjects did not have antibodies. The P-AGPT group had a
significantly higher bodyweight (p < 0.02) and body mass index (p < 0.001)
(95.1 +/- 2.1 kg and 35.3 +/- 1.5 kg/m2, respectively) compared with the
N-AGPT group (80.1 +/- 0.6 kg and 30.7 +/- 0.6 kg/m2, respectively). Also,
the P-AGPT group had significantly lower serum cholesterol (p < 0.02) and
triglyceride (p < 0.001) values (4.65 mmol/L and 1.45 mmol/L, respectively)
compared with the N-AGPT group (5.51 mmol/L and 2.44 mmol/L, respectively).
Two subjects positive for SMAM-1 antibodies had antibodies against each
others' serum, suggesting the presence of antigens in one or both. When
these two serum samples were inoculated into chicken embryos, macroscopic
lesions compatible with SMAM-1 infection developed. The inoculation of serum
from N-AGPT subjects did not produce such lesions. The presence of increased
obesity, antibodies to SMAM-1, reduced levels of blood lipids, and viremia
that produces a typical infection in chicken embryos suggests that SMAM-1,
or a serologically similar human virus, may be involved in the cause of
obesity in some humans.
--------------------------------------------------------------------------------

8: Drug News Perspect. 2004 Jun;17(5):307-13.  Related Articles, Links

Contribution of pathogens in human obesity.

Dhurandhar NV.

Department of Nutrition and Food Science and the Center for Molecular
Medicine and Genetics, Wayne State University, Detroit, Michigan 48202, USA.
[log in to unmask]

Obesity is increasing rapidly in the United States as well as in other
countries. The World Health Organization considers obesity a worldwide
epidemic that poses a major public health threat. In humans, obesity causes
or exacerbates a number of other diseases and co-morbidities. Etiology of
obesity includes genetic, metabolic, social, behavioral and cultural
factors. Although obesity has multiple causes, an often overlooked
possibility is that of obesity due to an infection. Over the past two
decades, seven pathogens are reported to cause obesity in animals. Canine
distemper virus was the first reported obesity-promoting virus.
Rous-associated virus-7, an avian retrovirus, causes stunted growth, obesity
and hyperlipidemia in chickens. Borna disease virus was noted to cause
obesity in rats. Scrapie agents were reported to induce obesity in mice.
These pathogens appear to produce obesity by damaging the central nervous
system. Next, three adenoviruses were reported to promote obesity, but their
mechanisms are not clear. Animals experimentally infected with SMAM-1, an
avian adeno-virus, or two human adenoviruses, adenovirus type 36 (Ad-36) and
Ad-37, developed adiposity. Notably, SMAM-1 and Ad-36 were associated with
obesity in humans. Although more research is needed to further define the
mechanisms and the role of pathogens in the etiology of obesity, they should
be included in the long list of potential etiological factors for obesity.
Determination of the role of pathogens in human obesity is critical for its
successful treatment and prevention. (c) 2004 Prous Science. All rights
reserved.
--------------------------------------------------------------------------------

9: Obes Res. 2004 May;12(5):770-7.  Related Articles, Links

A human adenovirus enhances preadipocyte differentiation.

Vangipuram SD, Sheele J, Atkinson RL, Holland TC, Dhurandhar NV.

Department of Nutrition and Food Science, Wayne State University, Detroit,
MI 48202, USA.

OBJECTIVE: Adenovirus 36 (Ad-36) has been shown to increase adiposity in
experimentally infected chickens, mice, and marmosets (nonhuman primates).
Neutralizing antibodies to Ad-36 are associated with obesity in humans. The
metabolic and molecular mechanisms responsible for Ad-36-induced
adipogenesis are unknown. As a potential adipogenic mechanism, this study
examined if Ad-36 enhanced differentiation of preadipocytes. RESEARCH
METHODS AND PROCEDURES: To determine the suitability of 3T3-L1 cells (murine
preadipocyte cell line) as a model, the first experiment determined if Ad-36
attaches and initiates replication in the cells. Next, effects of Ad-36 on
the number of differentiated adipocytes, glycerol 3-phosphate dehydrogenase
(GPDH) levels, and cellular lipid accumulation were determined. The last
experiment determined the effect of Ad-36 on human primary preadipocyte
differentiation. Ad-2, a known nonadipogenic human adenovirus, was used as a
negative control in these experiments. RESULTS: Immunofluorescence studies
showed adenoviral attachment to 3T3-L1 cells, and reverse
transcriptase-polymerase chain reaction showed expression of the Ad-36 E1A
gene in the infected cells. Ad-36, but not Ad-2, increased the number of
differentiated adipocytes, GPDH enzyme levels, and the total cellular lipid
content. Also, Ad-36, but not Ad-2, increased GPDH levels in human
preadipocytes. DISCUSSION: Taken together, these experiments showed that
Ad-36 enhanced differentiation of preadipocytes, which may be a contributory
mechanism to its adipogenic effect in vivo. The lack of effect of Ad-2 on
differentiation demonstrated that the observed findings were not a common
characteristic of all adenoviruses. Future understanding of the molecular
interactions of cellular and viral genes responsible for enhanced
differentiation may reveal novel signaling pathways and controls of
preadipocyte differentiation. Copyright 2004 NAASO