Supports pretty much all of Trick and Treat
This has got to be one of the best studies I have ever seen - as a demonstration of how to waste time and money. As well, no doubt, as providing 'evidence' to frighten the less knowledgeable of the populace into cutting down on saturated animal fats to prevent obesity and osteoporosis (NOTE: Corn oil is not an animal fat and is not saturated - but I doubt that will stop someone using it as 'evidence' against them.)
I have never been a fan of extrapolating animal dietary studies to Homo sapiens. We have quite different reactions to foods. As you can read, these 'scientists' obviously share my views. But, after admitting that animal studies like this don't mimic human conditions, these 'scientists' conduct a trial on mice which, they say, serves as a model for humans!
Can anyone, please, tell me:
1. In what way does it have any relevance to anything other than, perhaps, female C57Bl/6J mice?
2. Do female C57Bl/6J mice even suffer from osteoporsis?
3. Should we care??
4. How on earth they get this cr*p published??
The abstract is below (I've got a PDF of the whole paper if anyone would like it)
Ganesh V. Halade, M. Rahman, Paul J. Williams and Gabriel Fernandes. High fat diet-induced animal model of age-associated obesity and osteoporosis.The Journal of Nutritional Biochemistry February 2010, [Article in Press, Corrected Proof]
Osteoporosis and obesity remain a major public health concern through its associated fragility and fractures. Several animal models for the study of osteoporotic bone loss, such as ovariectomy (OVX) and denervation, require unique surgical skills and expensive set up. The challenging aspect of these age-associated diseases is that no single animal model exactly mimics the progression of these human-specific chronic conditions. Accordingly, to develop a simple and novel model of post menopausal bone loss with obesity, we fed either a high fat diet containing 10% corn oil (CO) or standard rodent lab chow (LC) to 12-month-old female C57Bl/6J mice for 6 months. As a result, CO fed mice exhibited increased body weight, total body fat mass, abdominal fat mass and reduced bone mineral density (BMD) in different skeletal sites measured by dual energy X-ray absorptiometry. We also observed that decreased BMD with age in CO fed obese mice was accompanied by increased bone marrow adiposity, up-regulation of peroxisome proliferator-activated receptor γ, cathepsin k and increased proinflammatory cytokines (interleukin 6 and tumor necrosis factor α) in bone marrow and splenocytes, when compared to that of LC fed mice. Therefore, this appears to be a simple, novel and convenient age-associated model of post menopausal bone loss, in conjunction with obesity, which can be used in pre-clinical drug discovery to screen new therapeutic drugs or dietary interventions for the treatment of obesity and osteoporosis in the human population. (Emphasis added)