OK, here's some of the medical literature on the topic:
J Nutr. 2002 Oct;132(10):3155-60. Related Articles, Links
Human adenovirus Ad-36 promotes weight gain in male rhesus and marmoset
monkeys.
Dhurandhar NV, Whigham LD, Abbott DH, Schultz-Darken NJ, Israel BA, Bradley
SM, Kemnitz JW, Allison DB, Atkinson RL.
Department of Nutrition and Food Science and the Center for Molecular
Medicine and Genetics, Wayne State University, Detroit, MI, USA.
[log in to unmask]
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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2: Diabetes Obes Metab. 2001 Oct;3(5):367-80. Related Articles, Links
Effects of adenovirus-mediated liver-selective overexpression of protein
tyrosine phosphatase-1b on insulin sensitivity in vivo.
Wang J, Cheung AT, Kolls JK, Starks WW, Martinez-Hernandez A, Dietzen D,
Bryer-Ash M.
University of Tennessee, Memphis, TN, USA.
AIM: Protein tyrosine phosphatase-1B (PTP-1B) is an intracellular PTP known
to dephosphorylate and inactivate upstream tyrosine phosphoproteins in the
insulin signalling cascade. We and others reported increased abundance of
catalytically impaired PTP-1B in tissue lysates from obese human subjects
with and without type 2 diabetes, while genetic knockout of PTP-1B improves
insulin sensitivity and prevents nutritionally mediated insulin resistance
and obesity. The aim of the present work was to further elucidate the role
of PTP-1B in glucose metabolism in vivo. METHODS: We used adenoviral
constructs incorporating cDNAs for either wild-type (W/T) or a catalytically
inactive C(215)S (C/S) mutant PTP-1B to achieve liver-selective PTP-1B
overexpression in young Sprague-Dawley rats using tail vein injection, based
on the high degree of hepatotropism of adenovirus 5 (Ad5). An Ad5-lacZ
construct encoding beta-galactosidase was used as a control for viral
effects alone. A hyperinsulinaemic euglycaemic clamp was used to study whole
body glucose disposal and endogenous glucose production rates. RESULTS:
Control studies in HIRcB cells confirmed catalytic activity and inactivity
of W/T and C/S respectively. Mean PTP-1B abundance was 2.24 +/- 0.02- and
2.33 +/- 0.04-fold of saline-treated control in liver lysates of W/T and C/S
rats respectively. Liver selective overexpression was confirmed by analysis
of tissue lysates from liver, fat and muscle tissues. Ad5 treatment did not
result in a statistically or clinically significant liver injury, as
determined by serum alanine aminotransferase and histological examination.
Seven days post injection, no significant difference in rate of weight gain,
fasting blood glucose or insulin levels were seen in any group. Similarly,
under steady-state glucose clamp conditions, glucose disposal rate (R(d)),
endogenous glucose production rate (EGP) and serum insulin levels were
similar in all groups. CONCLUSION: We conclude that moderate medium-term
overabundance, to a degree resembling that seen in insulin-resistant states,
of PTP-1B in liver tissue does not alter insulin action on glucose
metabolism and that the major site of action of PTP-1B is presumably at
insulin-responsive target tissue or tissues other than the liver.
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3: J Nutr. 2001 Oct;131(10):2794S-2797S. Related Articles, Links
Infectobesity: obesity of infectious origin.
Dhurandhar NV.
The Department of Nutrition and Food Science and the Center for Molecular
Medicine and Genetics, Wayne State University, Detroit, MI 48202, USA.
[log in to unmask]
In the U.S., the prevalence of obesity increased by 30% from 1980 to 1990,
and this increase appears to be continuing. Although obesity has multiple
etiologies, an overlooked possibility is obesity of an infectious origin.
Six pathogens are reported to cause obesity in animals. Canine distemper
virus was the first virus reported to cause obesity in mice, followed by
Rous-associated virus-7, an avian retrovirus, which has been shown to cause
stunting, obesity and hyperlipidemia in chickens. Next, the
obesity-promoting effect of Borna disease virus was demonstrated in rats.
Scrapie agents were reported to induce obesity in mice and hamsters. The
final two reports were of SMAM-1, an avian adenovirus, and Ad-36, a human
adenovirus that caused obesity in animals. Additionally, an association with
human obesity is the unique feature of SMAM-1 and Ad-36. Although the exact
mechanism of pathogen-induced obesity is unclear, infection attributable to
certain organisms should be included in the long list of potential
etiological factors for obesity. In addition, the involvement of some
pathogens in etiology of obesity suggests the possibility of a similar role
for additional pathogens.
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4: US News World Rep. 2000 Aug 7;129(5):64. Related Articles, Links
'Catching' the fat bug. Can obesity be caused by exposure to a virus?
Sobel RK.
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5: Int J Obes Relat Metab Disord. 2000 Aug;24(8):989-96. Related Articles,
Links
Comment in:
Int J Obes Relat Metab Disord. 2001 Jan;25(1):143-5.
Increased adiposity in animals due to a human virus.
Dhurandhar NV, Israel BA, Kolesar JM, Mayhew GF, Cook ME, Atkinson RL.
Department of Nutrition and Food Science, Wayne State University, Detroit,
MI, USA. [log in to unmask]
BACKGROUND: Four animal models of virus-induced obesity including adiposity
induced by an avian adenovirus have been described previously. This is the
first report of adiposity induced in animals by a human virus. OBJECTIVE: We
investigated the adiposity promoting effect of a human adenovirus (Ad-36) in
two different animal models. DESIGN: Due to the novel nature of the findings
we replicated the experiments using a chicken model three times and a mammal
model once. In four separate experiments, chickens and mice were inoculated
with human adenovirus Ad-36. Weight matched groups inoculated with tissue
culture media were used as non-infected controls in each experiment. Ad-36
inoculated and uninfected control groups were housed in separate rooms under
biosafety level 2 or better containment. The first experiment included an
additional weight matched group of chickens that was inoculated with CELO
(chick embryo lethal orphan virus), an avian adenovirus. Food intakes and
body weights were measured weekly. At the time of sacrifice blood was drawn
and visceral fat was carefully separated and weighed. Total body fat was
determined by chemical extraction of carcass fat. RESULTS: Animals
inoculated with Ad-36 developed a syndrome of increased adipose tissue and
paradoxically low levels of serum cholesterol and triglycerides. This
syndrome was not seen in chickens inoculated with CELO virus. Sections of
the brain and hypothalamus of Ad-36 inoculated animals did not show any
overt histopathological changes. Ad-36 DNA could be detected in adipose
tissue, but not skeletal muscles of randomly selected animals for as long as
16 weeks after Ad-36 inoculation. CONCLUSIONS: Data from these animal models
suggest that the role of viral disease in the etiology of human obesity must
be considered.
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