Re: obesity may develop because of ordinary Virus

"ghyti" <Nutrition.tips@xxxxxxxxx> wrote in message
news:1189076011.692714.21140@xxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
U.S. researchers revealed that an ordinary virus caused human adult
stem cells to become fat cells and could clarify why some people grow
to be obese...
http://personalhealthcare.googlepages.com/study_revealed_that_a_common_virus_may_c



Hi ghyti,
here is the (free) original article :

http://www.nature.com/ijo/journal/v31/n1/pdf/0803366a.pdf

Int J Obes (Lond). 2007 Jan;31(1):87-96. Epub 2006 May 16.
Adipogenic human adenovirus-36 reduces leptin expression and secretion and
increases glucose uptake by fat cells.

OBJECTIVE: Human adenovirus Ad-36 causes adiposity in animal models and
enhances differentiation and lipid accumulation in human and 3T3-L1
preadipocytes, which may, in part, explain the adipogenic effect of Ad-36.
We determined the consequences of Ad-36 infection on leptin and glucose
metabolism in fat cells. DESIGN: 3T3-L1 preadipocytes were used to determine
the effect of infection by human adenoviruses Ad-36, Ad-2, Ad-9 and Ad-37 on
leptin secretion and lipid accumulation. Rat primary adipocytes were used to
determine the effect of Ad-36 infection on leptin secretion and glucose
uptake in vitro. Furthermore, the effect of Ad-36 on expressions of leptin
and selected genes of de novo lipogenesis pathway of visceral adipose tissue
were compared ex vivo, between Ad-36 infected and uninfected control rats.
RESULTS: Ad-36 suppressed the expression of leptin mRNA in 3T3-L1 cells by
approximately 58 and 52% on days 3 and 5 post-infection, respectively.
Leptin release normalized to cellular lipid content was 51% lower (P<0.002)
in the Ad-36 infected 3T3-L1 cells. Lipid accumulation was significantly
greater and leptin secretion was lower for the 3T3-L1 cells infected with
other human adenoviruses Ad-9, Ad-36, or Ad-37. Whereas, human adenovirus
Ad-2 did not influence cellular lipid accumulation or the leptin release. In
rat primary adipocytes, Ad-36 reduced leptin release by about 40% in
presence of 0.48 (P<0.01) or 1.6 nM insulin (P<0.05) and increased glucose
uptake by 93% (P<0.001) or 18% (P<0.05) in presence of 0 or 0.48 nM insulin,
respectively. Next, the adipose tissue of Ad-36 infected rats showed two to
fivefold lower leptin mRNA expression, and 1.6- to 21-fold greater
expressions for acetyl Co-A carboxylase-1 and 1.2- to 6.3-fold greater
expressions for fatty acid synthase, key genes of de novo lipogenesis,
compared to the uninfected weight and adiposity matched controls.
CONCLUSION: The in vitro and ex vivo studies show that Ad-36 modulates
adipocyte differentiation, leptin production and glucose metabolism. Whether
such a modulation contributes to enhanced adipogenesis and consequent
adiposity in Ad-36 infected animals or humans needs to be determined.

PMID: 16703005

By the same author (not free) :

Adv Food Nutr Res. 2007;52:61-102.
Infectobesity: obesity of infectious origin.

The rapid increase in obesity and the associated health care costs have
prompted a search for better approaches for its prevention and management.
Such efforts may be facilitated by better understanding the etiology of
obesity. Of the several etiological factors, infection, an unusual causative
factor, has recently started receiving greater attention. In the last two
decades, 10 adipogenic pathogens were reported, including human and nonhuman
viruses, scrapie agents, bacteria, and gut microflora. Some of these
pathogens are associated with human obesity, but their causative role in
human obesity has not been established. This chapter presents information
about the natural hosts, signs and symptoms, and pathogenesis of the
adipogenic microorganisms. If relevant to humans, "Infectobesity" would be a
relatively novel, yet extremely significant concept. A new perspective about
the infectious etiology of obesity may stimulate additional research to
assess the contribution of hitherto unknown pathogens to human obesity and
possibly to prevent or treat obesity of infectious origins.

PMID: 17425944

hth
Gys


.

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