This paper came up in comments to the last post:
Dietary Stearic Acid Leads to a Reduction of Visceral Adipose Tissue in Athymic Nude Mice
I think we can say that, at least in athymic nude mice (which do not seem to be derived from the C57Bl/6 strain), omega 6 PUFA do not cause obesity when compared to either a low fat or high stearic acid synthetic diet (ie the low fat arm is equally synthetic, not more "food-like" ie not chow). At least when you look at total body weights:
So omega 6 PUFA appear to get a free pass here. The actual composition of the diets is in Table 1 of this previous paper and all four contain generous amounts of starch and equal amounts of sucrose:
Dietary Stearate Reduces Human Breast Cancer Metastasis Burden in Athymic Nude Mice
However if you dexa scan the mice you find that the low fat, corn oil and safflower oil groups all have reduced lean mass (probably muscle) and increased visceral fat mass compared to the stearate group. A picture is worth a thousand words so here are some postmortem images with the size of the inguinal fat pads outline by the authors of the paper (no need for me to doodle on this one!). Fig 3:
I really like these images.
Now, cavenewt questioned the relevance of weight/fat alterations from stearate compared to other potential health effects, particularly its affect on cancer metabolism.
The third paper from this same group is
Prevention of carcinogenesis and inhibition of breast cancer tumor burden by dietary stearate
I've been through all three papers and searched on "insulin". The group appears to have no concept that insulin has anything to do with adipocyte size or cancer progression.
A slight handicap when it comes to insight.
In the stearate-visceral fat paper there is a single measurement made of plasma insulin/glucose. Insulin does not vary between diet groups but glucose is significantly lower in the stearate group. I have been unable to work out if the measures were fasting or fed, or even what time of day the samples were taken (ie when the mice were killed). I think that with glucose values in to 200-250mg/dl range these were probably "fed" glucose and insulin levels. The paper does not give us the measured insulin levels, merely that there was no statistically significant difference between groups. But insulin levels come with such huge standard deviations that getting a p value below 0.05 with small group sizes is not going to happen. A ns result does not automatically mean that there were no differences.
Of course a single insulin measurement at one terminal time point tells us nothing about the long term 24h exposure to insulin of the mice, of their adipocytes or of their cancer cells.
So we have to, once again, look at the significance of the changes in fat distribution to attempt to gain insight in to overall insulin exposure. I spent quite some time looking at visceral fat and its significance early last year in this post:
On phosphorylation of AKT in real, live humans. They're just like mice!
and on how stearate might avoid systemic hyperinsulinaemia here:
Dairy and diabetes
Visceral fat is a surrogate for chronic hyperinsulinaemia, particularly fasting hyperinsulinaemia. While I consider non-inflamed visceral fat to be completely benign, or even beneficial for controlling the hunger of fasting, the insulin which maintains that visceral lipid storage is not benign. Chronically elevated insulin (or, more accurately, insulin signalling) should drive both visceral fat storage and xenograft tumour growth in the mice. Probably in humans too.
Happy Solstice and assorted mid-Winter celebrations. If you live in the northern hemisphere that is. Not that I envy those with a Solstice-on-the-beach-without-wooly-hats-and-gloves situation!