Scientists found that mice with a faulty internal Clock (right) gained more body
fat than normal mice (left).
Mice with a disrupted biological clock slept less, ate more, and gained more body
fat than normal mice, indicating that, when it comes to understanding the molecular basis of obesity, timing may be key.
On the other hand, as they aged, these «knockout mice» grew
fatter than the normal mice, especially when fed a high - fat diet.
Not exact matches
Three groups of middle - aged
mice (about a year old) were studied: one group ate a
normal diet, in which fewer
than 30 percent of calories came from
fat, while two others were fed high - calorie diets in which 60 percent of the calories came from
fat.
Moreover,
mice engineered to generate smaller
than normal quantities of SIRT1 carried relatively little
fat in their blood, indicating that their cells hung onto it.
As a result, they have less
than half of the
fat tissue found in
normal, aged
mice.
When they exposed these
mice to the cold, the animals developed far fewer beige
fat cells
than did
normal animals, suggesting that macrophages were key to browning of white
fat.
To investigate, Akhtar deleted the gene for Rac1 in female
mice; their first litter of pups survived, but they were smaller
than normal — probably because the milk they received contained less
fat and protein
than normal.
Fat mice fed huge quantities of it lived longer and aged more slowly
than normal.
That research showed that
mice on a
normal diet who were exposed to low doses of antibiotics throughout life, similar to what occurs in commercial livestock, packed on 10 to 15 percent more
fat than untreated
mice and had a markedly altered metabolism in their liver.
And, consistent with other studies, when these
mice ate a high -
fat diet, they gained weight faster
than their
normal counterparts.
During this period, the
mice on the high -
fat diet gained 30 to 50 percent more body mass
than mice fed a
normal diet, and they developed more intestinal tumors
than mice on a
normal diet.
First, they found that the
mice on a high -
fat diet had many more intestinal stem cells
than mice on a
normal diet.
Some studies have identified a number of regions of methylated DNA (one key way in which epigenetic changes occur) that are different in
fat cells of
mice fed high -
fat diets
than in cells of
mice with
normal diets.
Over an eight - week period, a control group of
mice fed a high -
fat diet predictably became obese, but the
mice whose Hedgehog pathway had been activated didn't gain any more weight
than another control group fed on a
normal diet.
The reason for this response, Gordon says, was twofold: Firmicutes bacteria transplanted from the
fat mice produced more of the enzymes that helped the animals extract more energy from their food, and the bacteria also manipulated the genes of the
normal mice in ways that triggered the storage of
fat rather
than its breakdown for energy.