Colloquially phrased: do all animals of an experimental group get fat and diseased when exposed to an obesogenic environment which simulates contemporary human environments (i.e. ad libitum availability of high-fat food AND the availability of running wheels), or is there a percentage of animals which resist the obesity outcome, e.g. by increasing voluntary wheel running?
Hi Lutz Kraushaar,
Some animals (in the same strain) are resistance to obesity, even when administered high-fat diet. some experiments identify resistant animals and exclude or create a new group of resistances.
You can identify this animals In the second week of diet (for rodents), they do not gain body mass.
I dont know if this is really what you asked.
Andre, Thanks for sharing your insights. Is it correct to say that resistance is due to lower caloric intake and/or higher physical activity energy expenditure compared to the obese animals? Or is it a difference in metabolism which protects the animals against obesity even when their caloric excess is similar to the ones which become obese? I'd be very interested in finding published references to the first type.
Lutz, is correct to say that resistance is due to higher physical activity however, this is not a consistent effect, in literature you gone find resistance to obesity without higher physical activity, and is not correct to say that is due to lower caloric intake ( is very common animals eat the same amount and not become obese)
The obesity resistance occurs due to changes related to energetic balance controlled by the hypothalamus (i.e. Arcuate nucleus, paraventricular nucleus, lateral hypotalamic nucleus, etc). This energetic balance involves energy expenditure, food intake, physical activity and thermogenesis.
These two attached articles are related to that theme. But do not believe the resistance is caused by a single factor (such as increased physical activity), it is multifactorial.
Thanks for the 2 papers, Andre. I fully agree with your remark that caloric intake is not the sole contributor, or that it might not contribute at all to obesity resistance. I see food intake and physical activity as summary behavioral phenotypic responses to a complex interaction of neurohormonal molecular constituents. That seems to be corroborated in the Teske paper. Thanks again, Andre.
Dear All,
I made a lot of experiments in HFD mice, and as colleagues reported, some mice didn't get weight... For our paper, we tested different strains of immunodeficient mice,but the good one was RAG2 Mice.
i would think that in highly inbred lab rats (as opposed to wild caught rats and used for obesity studies), overt energy metabolic differences are unlikely.
If a group of rats are kept in one cage, they tend to establish a dominance hierarchy and even in the presence of unrestricted access to food, one or two will always weigh less. To exclude this possibility, it may be necessary to house 1 animal per cage. If difference in the amount of food consumed is studied, one needs metabolic cages.
Dear all,
what about leptin receptor? the ativation of leptin receptors might be a reason for the animals are obese or not?
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