Also, knocking out
the leptin gene in mice showed that this hormone regulated appetite.
Not exact matches
When similar analysis was performed on the db
mice, it was found that the disrupted db
gene was responsible for encoding a protein that functions as a
leptin receptor: When it binds circulating
leptin at the cell surface, it sets
in motion a biochemical cascade inside the cell.
Scientists had been searching
in vain for such a
gene since 1994 when Rockefeller University scientist Jeffery Friedman found that lab
mice with a specific genetic mutation fail to produce
leptin and as a result have uncontrollable appetites, and become huge.
One team has found
in two children mutations
in the
gene for the metabolic hormone
leptin, which
in mice tells the body it's satiated; defects
in this
gene had not previously been found
in obese people.
Mice without the
leptin gene, called ob / ob, overeat, weigh
in at three to four times normal, and develop symptoms similar to the obesity - related diabetes seen
in humans.
In a remote Turkish village, researchers have located a family with a mutation in the leptin gene similar to the one found in lab mice, and — just like the mice — adults with two copies of the mutation are grossly overweight and don't ever go through pubert
In a remote Turkish village, researchers have located a family with a mutation
in the leptin gene similar to the one found in lab mice, and — just like the mice — adults with two copies of the mutation are grossly overweight and don't ever go through pubert
in the
leptin gene similar to the one found
in lab mice, and — just like the mice — adults with two copies of the mutation are grossly overweight and don't ever go through pubert
in lab
mice, and — just like the
mice — adults with two copies of the mutation are grossly overweight and don't ever go through puberty.
The revolution
in obesity research began less than five years ago with the landmark discovery of a
gene for
leptin, the weight - regulating hormone found
in both
mice and people.
In 1994 scientists discovered that
mice missing both copies of their
leptin gene develop excessive body fat, extreme hunger, and sterility.
This
gene therapy resulted
in high - fat diet
mice having a reduced body weight, building up less fat, expending more energy, and showing evidence of improved
leptin - signalling.
Much of our knowledge of
leptin comes from the study of two brands of lab
mouse: the ob / ob
mouse, deficient
in genes responsible for
leptin production; and the db / db
mouse, deficient
in the
leptin receptor
gene.