|(Un!)Surprising results: The "healthy" soy oil is the only fat in the study at hand that causes NAFLD.|
That being said, let's stick with what we have and take a look at the results, Yoko Hashimoto and her colleagues published in a recent issue of the medical journal Lipids (Hashimoto. 2013).
The "obesity resistant" wistar rat and it's reaction to different dietary fats
I promise, the results are interesting and probably highly relevant, because the strain of Wistar rats (Slc:Wistar/ST) used in this study does not become obese simply because there is some fat in their chow. In fact, this is exactly the reason why the Japanese researchers picked the Wistar/STs. They wanted to examine the effects of various high-fat diets on plasma and hepatic lipid parameters and lipid metabolism in an obesity "resistant" rodent strain (everyone and every rat can become obese, but these don't get obese just by feeding them fatty chow) who were kept on either standard low fat chow or 3 different high-fat diets for 4 weeks (45% of the energy from fat) .
|Figure 1: Fatty acid composition of the different diets (Hashimoto. 2013)|
|Figure 2: Food intake, organ/body weight (Hashimoto. 2013)|
|Figure 3: Serum an liver lipid profiles (Hashimoto. 2013)|
The changes in the blood lipid levels the researchers observed went hand in hand with a few, but statistically significant differences in the local expression of important epigenetic regulators of fatty acid oxidation Acat1 / Acox1, in particular in the "fish oil rats":
Interestingly enough, the fish oil group was yet not the only group with metabolically relevant changes in the genetic landscape of the liver:
"Nineteen genes involved in inﬂammation response genes as well as lipid metabolism-related genes were selected and their mRNA expression levels were measured by qRT-PCR. No signiﬁcant differences were detected between the groups in the expression levels of genes encoding microsomal triglyceride transfer protein (MTP), ACAT2, 3-hydroxy-3-methylglutaryl-Coenzyme A reductase (HMG- CoA R, EC 126.96.36.199), and prostaglandin-endoperoxide synthase 1 (PTGS1, COX-1). In contrast, the expression levels of Acat1 and Acox1 mRNAs were the most abundant (p < 0.01) in the livers of the [fish] group." (Hashimoto. 2013)
Suggested read on the effects of fish oil on liver fat: "TTA + Fish Oil - Fat Burning Superfats or Hepatoxic Pro-Oxidants?" (read more)
"Lipogenesis was not signiﬁcantly increased in the [soy] group [...] Moreover, the level of VLDL secretion in the [soy] group was lower than that in the [lard] group group, because the mRNA expression levels of Apob and Mttp were not up-regulated in the [soy] group. The normal levels of VLDL secretion contributed to hepatic lipid accumulation in the [soy] group"(Hashimoto. 2013)Overall, the results of the study at hand do not simply highlight the differential effects of various forms of fatty acids on the development of metabolic derangements, they are also testimony to the fact that their effects on the metabolism of obesity-resistant Slc:Wistar/ST rats are much different from those of the obesity-susceptible animals that are usually used in studies like that. The latter become hyperphagic (ravenously hungry => overeating) and acquire hepatic lipid accumulation, almost irrespective of the source of dietary fat. The results of Hashimoto et. al. on the other hand demonstrate that "obesity-resistant Slc:Wistar/ST rats are isocaloric and do not exhibit hepatic lipid accumulation even when consuming high-fat diets, except one that includes soybean oil." (Hashimoto. 2013)
|These results remind me of another SuppVersity article with the telling title "If You Go 'High Carb', You Better Go Really High! Seven Meals/Day, More than 800g of Carbs, Less Than 50g of Fat & 1000kcal Over Maintenance and Still Lean Gains!" (read more)|
- Hashimoto Y, Yamada K, Tsushima H, Miyazawa D, Mori M, Nishio K, Ohkubo T, Hibino H, Ohara N, Okuyama H. Three Dissimilar High Fat Diets Differentially Regulate Lipid and Glucose Metabolism in Obesity-Resistant Slc:Wistar/ST Rats. Lipids. 2013 Aug;48(8):803-15