There is too much in the Italian rat study for a single post. Here's the easy bit discussing the rats fed the lard based diet.
Obesity is associated with hypothalamic injury in rodents and humans
which provides this gem. These are the *daily* caloric intakes of rats on bog standard lab chow, in grey, or during the sudden onset of feeding lard based D12492, in black:
These are Long-Evans rats weighing 300-350g. I drag this up because Protons suggests that on day 1 of exposure to D12492 the rats immediately sequester approximately 70kcal of energy in to adipocytes (ignoring processing losses) while still maintaining the basal (when chow fed) intake of 75kcal which are needed to run the rat's metabolism.
This immediate significant fat gain on day one (seen in section F of the same figure) raises adipocyte diameter, so increases basal lipolysis, so reduces hunger, such that on day two the extra food intake needed is lower and eventually, by day seven, excess food intake is no longer significantly increased and by day 14 it is normalised. Simple, yes?
Now let's return to the current study of interest discussed by Tucker, which I think of as the "Italian" study:
This used Sprague-Dawley rats weighing 250g, so probably more actively growing than the rats in the Schwartz lab study. They were measured as consuming 90kcal/d (380kJ/d) of chow assessed over the time before the study started. So we can plot the food intake of rats in the Italian study on a modification of graph H of the Schwartz study. I've left the chow fed line from the Schwartz study as an imaginary chow fed control line which was omitted by this group and I've renumbered the y axis to reflect the values of caloric intake actually reported in the Italian study:
We know that the red line for the lard fed group is close to correct from the methods section:
"Rats were divided in two groups with the same mean body weight (250 ± 5 g) and were pair fed with 380 kJ [90kcal] metabolisable energy (ME)/day (corresponding to the spontaneous energy intake of the same rats, that was assessed [on chow] before the start of the experiment) of a lard-based (L) or safflower-linseed oil based (S) diet for two weeks."
The Italian rats, without any access to the luxurious amounts of D12492 provided to the Schwartz rats, still got fat.
If you view this from my perspective this is not surprising. The Italian rats still lost calories in to adipocytes but, without access to extra food, had an hypocaloric crisis. They ended up with a reduced percentage of protein mass in their carcass, despite an increased fat mass. Obese and sarcopaenic.
However, by two weeks on a diet which sequesters lipid in to adipocytes at the cost of reduced growth, a few of the rats will have achieved a sufficient increase in basal lipolysis to normalise hunger, as per the Schwartz rats, at the "cost" of obesity. It is very simple to multiply 380kJ/d by 14 days and get 5320kJ of offered food over 14 days. The mean of the actual food intake over the study was measured as 5286kJ in total for the lard fed rats. We don't have individual data but any rat still hungry on day 14 will have eaten all of its 380kJ, but no extra, because none was on offer. Adequately obese rats will have, via increased basal lipolysis, not needed to eat all of the 380kJ offered, ie these rats will have slightly reduced the mean total energy intake, by 34kJ, probably in the last few days of the study.
These rats are in a difficult position, they must maintain an adequate fat mass for increased basal lipolysis to offset increased insulin mediated lipid sequestration induced by the linoleic acid component of their diet. As they grow they will have to increase fat mass to maintain adequate basal lipolysis to function.
Running on basal lipolysis derived FFAs at a time when you have access to dietary glucose is the basic definition of metabolic syndrome.
If you keep adipocytes small by forcibly keeping insulin low (ie caloric restriction) you will completely side step increased basal lipolysis, side step insulin resistance, side step or delay many diseases and *increase* the duration of the miserable, hungry existence which will be your extended life.
The Influence of Dietary Fat Source on Life Span in Calorie Restricted Mice
An isocaloric moderately high-fat diet extends lifespan in male rats and Drosophila
An isocaloric moderately high-fat diet extends lifespan in male rats and Drosophila
There is no way in which you can transfer sufficient the FFAs from insulin sensitive but non-adequately distended adipocytes to hepatocytes as is needed to maintain a fatty liver. Caloric restriction is highly protective. Just ask any obesity researcher, the cure for fatty liver is hunger. Oops, I mean weight loss rather than hunger, in obesity doublespeak.
Safflower/linseed oil next.
Peter
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