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Gene
For 'Sweet Tooth' Identified
NEW
YORK (Reuters Health) - New research findings may help shed light
on why some people react to a piece of chocolate cake with a craving
for more, while others are content with just a bite. Two separate
teams of researchers have identified a gene in mice that appears
to regulate a sweet receptor--a protein on nerve cells in taste
buds that responds to sweetness.
The researchers
used data from the recently completed mapping of the human genome
to locate a similar gene in humans. The findings could lead to
the development of artificial sweeteners with a more authentic
taste than current products, as well as ways to regulate cravings
for sweets.
They researchers
used two sets of mice-tasters--one group that preferred drinking
sweetened water and another group that was more ambivalent about
the sugar water--to locate the so-called ``sweet tooth'' gene.
One study,
published in the May issue of Nature Genetics, found that mice
that were unable to taste most sugars had a mutation in the T1R3
gene, which blocked the function of the taste receptor.
``Differences
in this gene from one person to another may determine their particular
preference for candies, cakes and other sweets,'' Dr. Robert Margolskee
of Mount Sinai School of Medicine in New York and a senior author
of one study, said in an interview. ``Decreasing the activity
of this gene may enable people to control their urges to overindulge
in sweets.''
Researchers
of another study, published in the May issue of Nature Neuroscience,
found that mice with certain mutations in the same gene were less
drawn to sweetened water, compared with mice whose T1R3 gene did
not have mutations.
``The results
presented here identify T1R3 as a candidate taste receptor in
mouse and human,'' Dr. Linda Buck of Harvard University in Boston,
Massachusetts and colleagues, write.
However, researchers
of both studies note that more study is needed.
``We believe
that this receptor actually binds sugars and sweeteners, although
this remains to be directly shown,'' Margolskee said.
SOURCE:
Nature Neuroscience 2001;4:492-498; Nature Genetics 2001;28:58-
Reference
Source 89
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