DLS posted a link to this paper in the comments on the last post.
Overfeeding Polyunsaturated and Saturated Fat Causes Distinct Effects on Liver and Visceral Fat Accumulation in Humans
It's really fascinating. It's rather the flip side to the rodent study in the post itself. They took reasonably healthy humans and over-fed them muffins based on palm oil or sunflower oil.
The core findings, here from the conclusions:
"The fate of SFA [saturated fat] appears to be ectopic and general fat accumulation, whereas PUFA instead promotes lean tissue in healthy subjects. Given a detrimental role of liver fat and visceral fat in diabetes, the potential of early prevention of ectopic fat and hepatic steatosis by replacing some SFA with PUFA in the diet should be further investigated".
And the most important finding from the results:
"the MRI assessment showed that the SFA group gained more liver fat, total fat, and visceral fat, but less lean tissue compared with subjects in PUFA group (Table 2)".
This is pay dirt. It completely justifies saturated fat avoidance at even modest overeating. As Tom Naughton has commented recently:
Jane Brody And The American Heart Association Bravely Admit They’ve Been Right All Along
Well. I guess we can all just pack up and go home right now.
But, ultimately, you have to try to understand what is going on.
So let's have a think about it. We have two populations of adipocytes in the two study groups. Each is being provided with an excess of fatty acids to store under the influence of insulin. One population is being exposed to palmitic acid. Palmitic acid provides the maximum FADH2 of all FFAs excepting stearic acid. So it predisposes to generating insulin resistance via reverse electron transport (RET). In adipocytes this means that they are less likely to accumulate triglyceride, ie palmitic acid stops you getting fat. It does this by limiting fat storage under peak insulin. My presumption is that, under free feeding situations, this information about the state of adipocytes is transmitted to the brain, either through plasma fatty acids, hormones or via the autonomic nervous system, resulting in a cessation of eating. But there is no cessation of eating allowed in the study. If you don't gain weight you are made to eat more muffins. You have to eat. If the excess fat in the diet is not going in to the adipocytes it is going to end up somewhere else. Liver and visceral fat are good places if you have nowhere else. Sticking it in muscles might well limit the anabolic action of insulin at this site.
The PUFA group are asked to eat more too. The linoleic acid in the muffins allows easy distention of this population of adipocytes (less FADH2 per unit NADH). Insulin acts easily because peak RET is blunted and adipoctes accept more fat. Excess dietary fat ends up in adipocytes, the adipocytes don't care. At 1.6kg weight gain in a young, fit Swede there is insufficient adipocyte distention to raise FFAs in the face of insulin. Eating surplus PUFA appears to be metabolically easier to deal with than eating palmitate beyond acute needs. With sequestration of fatty acids in adipocytes rather than in to muscle we have the possibility for the anabolic effect of insulin actually working at increasing lean muscle mass.
We know that the groups were carefully managed to reach a very tightly controlled target of weight gain. Week by week the number of muffins fed per day was adjusted to give us the desired target gain of 1.6kg in each group. It took, on average, 3.1 muffins per day in each group to achieve this over seven weeks.
What we don't know is what the pattern of weight gain was during the study. Did the PUFA group gain weight easily in the early weeks and need less and less muffins later in the study to avoid excess weight gain, with the risk of overshooting the 1.6kg target?
Did the palmitic acid group show a steady weight gain, almost all of it ending up in ectopic sites because subcutaneous adipocytes didn't want to accept more fat throughout the study?
These are interesting thoughts. It is an interesting paper!
BTW There are a whole stack more questions regarding the role of fructose in the paper but I think the basics are probably covered in the differential effects of of fatty acids on the electron transport chain.