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).
Not exact matches
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 our previous study we found that a high fat diet containing comparable amounts of soybean oil to what Americans are currently consuming caused
mice to become
obese, diabetic and insulin
resistant and to have large lipid droplets and hepatocyte ballooning in their livers.
Mice on the high - fat diet become much more
obese and more insulin -
resistant compared to their peers on the glucose diet.
This idea is supported by animal studies, showing that
mice without any bacteria in their intestines had lower amounts of body fat, and did not become
obese or insulin
resistant when put on a high - fat diet.
mouse studies, macrophages taken from
obese mice were less receptive to insulin than normal (in other words insulin
resistant to a degree).
One - half of the
mice on the HF diet developed obesity (diet - induced
obese (DIO)
mice), whereas the remaining
mice were diet
resistant (DR).
This study has examined the effect of alpha - lipoic acid on glucose uptake by cultured L6 muscle cells and different types of skeletal muscles in normal lean (+ / +) and severely insulin -
resistant,
obese - diabetic (ob / ob)
mice.
The healthy
mice developed low - grade intestinal inflammation and a metabolic disorder that caused them to eat more, becoming
obese, hyperglycemic, and
resistant to insulin.