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.
«Cani and his team found that
genetically obese mice had 3,300 times less A. muciniphila in their intestines than healthy mice.
Astonishingly, when germ - free mice are colonized with the gut microbiota from
genetically obese mice (ob / ob), the otherwise lean mice dramatically increase body weight.
«[Certain
genetically obese mice] will fatten excessively regardless of how much they eat.
To make their discovery, Jin and colleagues used
both genetically obese mice and mice with diet - induced obesity as models.
In addition, administration of a recently discovered adiponectin receptor agonist, AdipoRon, to
genetically obese mice led to improved glucose intolerance and longer lifespans.
Not exact matches
Back then, Harrison restricted calories for
genetically modified
obese mice, which remained extremely fat even when food was cut.
The
genetically obese and diabetic
mice showed similar metabolic benefits from both WBV and exercising on the treadmill.
In fact, metabolic benefits were almost the same for
genetically obese and diabetic
mice from both WBV and those exercising on the treadmill.
As a result, these researchers found that one strain of
mice which were
genetically prone to become
obese became resistant to excess weight gain after their populations of gut microbiota were transformed simply by an sharing an environment with other
mice.
In
genetically programed insulin - resistant
obese mice with increased appetite and reduced physical activity, targeted restoration of Pomc function only within 5 - hydroxytryptamine 2c receptor containing cells induces sex differences in energy balance (267).
In 1994, it was discovered that a protein hormone called leptin, which is released from fat cells and monitored by the brain, was deficient in a certain strain of
genetically mutated
obese mice.
Male C57BL / 6J
obese mice fed a high - fat diet for 12 weeks and
genetically diabetic db / db
mice at an age of 6 weeks received dietary C3G supplementation (0.2 %) for 5 weeks.
in 2016,
genetically identical
mice that consumed a high - fat diet were more likely to produce
obese offspring with impaired glucose tolerance, an early sign of type 2 diabetes.
The researchers gave vitamin D supplements to
obese and non-
obese mice genetically engineered to be predisposed to endometrial cancer.
Nicotine can stabilize blood sugar and insulin sensitivity in both
genetically obese and diet - induced
obese mice (source).