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| Heidelberg, 5 June 2007 |
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| Uncovering the molecular basis of obesity
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Researchers discover the molecule that links spontaneous physical activity
and food intake in mice
Press
Release 5 June 2007 [PDF]
Why does the same diet make some
of us gain more weight than others? The answer could be a
molecule called Bsx, as scientists from the European
Molecular Biology Laboratory [EMBL], the German Institute
for Nutrition [DIFE], Potsdam, and the University of
Cincinnati report in the current issue of Cell Metabolism. Bsx
is the molecular link between spontaneous physical activity
and food intake. Mice lacking the molecule show less spontaneous
physical activity, perceive hunger signals differently and
have a lower concentration of feeding hormones in their brain
than normal mice. Being conserved across species, Bsx might
be a promising target for controlling diet-induced obesity in
humans.
Spontaneous physical activity, subconscious movements we
make such as fidgeting while working at the computer, and
food intake are two crucial factors regulating our body weight.
Both are controlled by the same part of the brain, called hypothalamus,
and they are intrinsically linked. When we are hungry,
our spontaneous activity increases and provides us with
the drive to go out and find food. Mathias Treier and his group
at EMBL have now discovered the molecule that brings about
this link between locomotor activity and food intake in mice.
"The molecule is called Bsx and is required for spontaneous
activity," Treier says. "Mice that lack Bsx in their hypothalamus
are a lot lazier than normal mice. They show less spontaneous
activity and less food seeking behaviour, which is based
on locomotor activity."
Bsx brings about its effect by regulating the expression of NPY
and AgRP, hormones of the hypothalamus that promote feeding.
Without Bsx less hormones are made with the result that
only rarely the mice go looking for food even if they have been
starving for an extended period. The scientists suggest Bsx is
also needed to enable brain cells to sense and respond to specific
hunger signals from the body – without it the mice do not
feel hunger.
"Bsx is is conserved across species and very
likely plays a similar role in controlling body weight in
humans," says Maria Sakkou, who carried out the research
in
Treier's lab. "Differences in Bsx activity between individuals
could help explaining why some people are intrinsically more
active than others and less susceptible to diet-induced obesity.
Bsx might be the key to why the same diet makes one person
fat, while leaving another unaffected."
The insights gained into the molecular mechanisms regulating
body weight in mice might serve as a basis for new ways to
prevent obesity and resulting diseases such as cardiovascular
conditions and diabetes in humans. Bsx is a promising candidate
drug target and further research might suggest how it
could be used to modulate basic physical activity as a way to
protect against diet-induced obesity.
Source Article
Sakkou, M., Wiedmer, P., Anlag, K., Hamm, A, Seuntjens, E., Ettwiller, L., Tschöp, M.H. and Treier, M., A role for brain-specific
homeobox factor Bsx in the control of hyperphagia and locomotory behavior, Cell Metabolism, 5 June 2007
Press Contact
Anna-Lynn Wegener
Press Officer
EMBL Heidelberg
Tel: +49 6221 387-8452
Email: wegener@embl.de |
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