Fructose-Induced Elevations in Plasma Triacylglycerols

I haven't read much about the mechanisms by which fructose increases plasma triacylglycerol levels or fatty acid synthesis in the liver, but this article shows that fructose can decrease the peroxisome proliferator-activated receptor-alpha (PPAR-alpha) mRNA content, increase fatty acid synthase and phosphatidate phosphohydrolase mRNA levels (indicating the potential for an increase in fatty acid and triglyceride synthesis), and decrease beta-oxidation of fatty acids (decrease their breakdown). This article doesn't really say anything about the actual, primary mechanism by which that would occur. Using a statin, as the researchers did, in this article, to reverse the fructose-induced decreases in PPAR-alpha mRNA is...not a good idea, in my opinion. But I won't go into that:

http://jpet.aspetjournals.org/cgi/content/full/302/1/232
(pubmed unique id: http://www.ncbi.nlm.nih.gov/pubmed/12065722?dopt=Abstract)

The effects of increases or decreases in PPAR-alpha activation are not very fun to read about, in part because of this concept that playing around with PPAR activation can magically treat liver diseases. One has to consider the scope of the damage, when it comes to liver diseases. Using a PPAR-alpha agonist can only go so far, and there's a need to address more of the actual metabolic issues in things like fatty liver disease (which is very prevalent). Things like uridine, purine nucleotides, improving one-carbon metabolism, and so on, have more potential for the treatment of liver disease than many of these other "molecular-biology-based" approaches. I could reference these statements, but there are so many references as to make it difficult. I know vitamin E activates PPAR-alpha (http://www.ncbi.nlm.nih.gov/pubmed/17388862), and that effect of vitamin E could oppose some of the effects of fructose on fatty acid synthesis. At very high doses, vitamin E can cause fatty infiltration of the liver, though, too. That doesn't occur at reasonable doses, but the "PPAR-modification" approach to treating liver disease has some shortcomings, in my opinion.