In the brief report by Pisabarro et. al, the authors examine a potential connection between a diet high in trans and saturated fatty acids and individuals with the Ala allele for peroxisome proliferator-activated receptor (PPAR) γ2 and incidience of type 2 diabetes. PPAR functions as a transcription factor and plays a role in the regulation of cell differentiation, development, and metabolism, and the Ala allele is a common polymorphism. Aside from the fact that the authors never suggest a mechanism for why carriers of the Ala allele are more likely to develop type 2 diabetes as a result of a diet high in trans and saturated fatty acids, their statistics to argue that a connection exists are even weaker.
According to their results, only 50% of the individuals found to have this polymorphism had impaired glucose metabolism, and while that may sound encouraging, this equates to 6 individuals. Furthermore, the data that suggests that type 2 diabetes occurs at a younger age, lower BMI, lower insulin levels, and lower waist circumference was not found to be significant. In general, it makes sense that a diet high in trans and saturated fatty acids could be suspected to be correlated to incidence of type 2 diabetes, yet the results presented in this paper and the lack of a mechanism raise significant questions about the validity of the authors’ claims. I am curious as to what other work has been done in examining a connection between diets high in trans and/or saturated fatty acids, genetic polymorphisms, and incidence of type 2 diabetes, but as of this point, I remain skeptical of a direction relationship between the Ala allele and such diets based on this evidence (or lack thereof) alone.
While the Ala conclusions are not the most convincing, it's nice to see people trying to pinpoint why some people get fat while others get fat and develop diabetes. On the Trans fat issue, http://jn.nutrition.org/cgi/content/abstract/135/3/562 That may be an interesting read. I don't have access to the UofA network right now, so I can't grab the whole article.
ReplyDeleteMaybe we could find a more rigorous study on the Ala substitution and diabetes?
We recently discussed genetic mutations of the insulin receptor gene that can cause insulin resistance in my endocrinology class. Some of them were mutations that decrease insulin receptor production through inhibition of translation, impairing receptor translocation into the cell membrane, reduction of insulin binding affinity, inhibition of the receptor's tyrosine kinase activity, and increasing the rate of receptor turnover. While an individual with these mutations may not necessarily develop diabetes, an unhealthy diet in conjunction with the above mutations may make them more susceptible.
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