How diets made from purified ingredients influence the phenotypes of the MS in commonly used rodent models.
A quick look at a crowd of people shows that many of our fellow humans are carrying around too much excess weight. The prevalence of obesity is at epidemic levels in the developed world, and obesity may be the root cause of or precursor to other diseases such as insulin resistance, abnormal blood lipid levels (hypertriglyceridemia and reduced high density lipoprotein cholesterol), and hypertension (high blood pressure). The term ‘metabolic syndrome’ (MS) is used to describe the simultaneous occurrence of these diseases and people with the MS are at increased risk for type 2 diabetes, cardiovascular disease, cancer, and nonalcoholic fatty liver disease. It is estimated that individuals with the MS spend over $4000 per year in treatment and to make matters worse, the prevalence of the MS is growing at an alarming rate, even in obese children.
The costs of treating the MS are clearly growing, and it is no surprise that the research community is seeking animal models that mimic the human phenotype so that potential therapies can be tested. Because of the pivotal role that diet plays in causing the MS in humans, most metabolic disease animal models do (and we believe should) use diet as a way to precipitate this syndrome. Though this was not the case decades ago, today, most diet-driven animal disease models are generated using open source, purified ingredient diets. The open source nature of purified ingredient diets allows researchers around the world to compare data from different studies, since the diet formulas are generally freely available to the public (this is in contrast to chow diets, which are generally ‘closed,’ meaning the formulas are generally kept secret). In addition, purified ingredient diets have very little variability from batch to batch (compared to chows), and so help to minimize data variability. To read more, see our Product Literature.
See full table with references in product literature.