Gordon and his team found several years ago that genetically obese mice (the animals lacked the ability to make leptin, a hormone that limits appetite) had 50 percent fewer Bacteroidetes bacteria and 50 percent more Firmicutes
bacteria than normal mice did.
Not exact matches
Researchers led by Emory University pathologist Andrew Gewirtz found that
mice genetically deficient in an immune system receptor have altered gut
bacteria, eat more
than normal mice do, and develop features of metabolic syndrome.
The older
mice fed a diet containing extra amounts of vitamin E, the equivalent to about 200 IU / day consumed by humans — about 10 times the Recommended Daily Allowance but well below the upper limit — were far more resistant to the
bacteria than the older
mice that had a
normal amount of vitamin E in their diet.
Female
mice and male
mice that had been treated with estrogen were able to clear the
bacteria from their lungs more rapidly
than normal male
mice.
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.