Here is the next study.
α‐Tocopherol suppresses hepatic steatosis by increasing CPT‐1 expression in a mouse model of diet‐induced nonalcoholic fatty liver disease
We might also take note of the caloric intake per day which comes out as exactly what anyone would expect for mice on an high fat diet, in contrast to the last post. The current study calorie intake is picked out in blue:
α‐Tocopherol suppresses hepatic steatosis by increasing CPT‐1 expression in a mouse model of diet‐induced nonalcoholic fatty liver disease
From the methods:
"Experiment 1: Mice were divided into seven groups (n = 10 in each) and given the following diets for 8 weeks: standard diet (control group; 30% protein, 68% carbohydrate, and 12% fat including vitamin E acetate [500 IU/g]; Research Diet); HF diet (HF group; 20% protein, 20% carbohydrate, and 60% fat including vitamin E acetate [500 IU/g]; Research Diet) and HF diet with α‐tocopherol (α‐Toc) which is one of the natural vitamin E forms supplementation (20, 50, 100, 150, and 200 mg/kg)."
"Experiment 1: Mice were divided into seven groups (n = 10 in each) and given the following diets for 8 weeks: standard diet (control group; 30% protein, 68% carbohydrate, and 12% fat including vitamin E acetate [500 IU/g]; Research Diet); HF diet (HF group; 20% protein, 20% carbohydrate, and 60% fat including vitamin E acetate [500 IU/g]; Research Diet) and HF diet with α‐tocopherol (α‐Toc) which is one of the natural vitamin E forms supplementation (20, 50, 100, 150, and 200 mg/kg)."
Okay, a ghastly typo.
We have no idea which of the Research Diets these mice were fed on. I am going to assume that the chow resembles PicoLab Rodent Diet 20/LabDiet 5053 and contains, as per my last post, ~100iu/kg of synthetic vitamin E acetate yielding, also as per last post, 44.5mg/kg of active vitamin E in the food.
The typo is to state that this chow contains 500iu/g. That's quite a lot of vitamin E. The correct amount is (almost certainly) 100iu/kg, not 500,000iu/kg.
I feel it is reasonable to assume the high fat diet was something similar to, or in fact was, D12942 which also probably contains around 100iu/kg vitamin E. Obviously the mice would eat less weight of D12942 than chow because they eat to caloric need. This will be met by a lower weight of D12942 so their intake of d-α-tocopherol would also be a little lower than if they ate the chow. More like 40mg/kg if you taken in to account the reduced weight of food eaten.
I am also going to assume that they added their supplementary vitamin E to this standard high fat diet so we're looking at intakes based on diets containing totals of 60mg/kg to 240mg/kg of d-α
-tocopherol per kilogram.
Anyhoo. For the time being I'm going to ignore the changes in everything other than total body weight.
There are no data presented for the effects of most of the supplement levels used, though these were recorded as per the methods. I think it's safe to assume that the effect on weight was consistent across all vitamin E intakes used, otherwise they would have mentioned it. This is what they actually presented:
There are, undoubtedly, effects from vitamin E supplementation on parameters other than total body weight. People may find the liver damage induced by high dose vitamin E fascinating. I do. But that's another story.
So I think we can say that, in a poorly described study, vitamin E supplementation has absolutely no effect on the body weight of mice over eight weeks of feeding an high fat diet. Over a wide range of dose rates.
To continue the catalogue of appalling vitamin E focused studies, it's now time to look at this one:
Effects of d-α-tocopherol supplements on lipid metabolism in a high-fat diet-fed animal model
How bad is it? It's this bad:
"After the adaptation period, the mice were randomly divided into three groups. Nine mice were placed in the control group [CON, regular diet (10% of calories derived from corn oil) and distilled water as a vehicle (0.1 ml, p.o.)]. Another set of nine mice were placed in the high-fat group [HF, high-fat diet (45% of calories derived from lard) with distilled water as a vehicle (0.1 ml, p.o.)], while the rest of the mice were placed in the high-fat diet with daily oral administration of 100 IU/kg B.W. of d-α-tocopherol group [HF-E, high-fat diet (45% of calories derived from lard)]."Effects of d-α-tocopherol supplements on lipid metabolism in a high-fat diet-fed animal model
How bad is it? It's this bad:
So we know nothing about anything. We have no idea of the vitamin E levels of the control chow or of the high fat diet. We don't even know if the high fat diet was manufactured specifically or whether they just added lard to chow to make 45% of calories from the lard which diluted the chow's vitamin E. We don't know what the lard was composed of in terms of LA either. Or even if it was Japanese or from the USA. We *do* know it was high enough in LA to make the mice fat.
None of this matters too much because the vitamin E supplementation was given by oral gavage of 100iu/kg once daily. This was pure d-α-tocopherol so the arithmetic is easy. The 100iu gavage provided 67mg of active d-α-tocopherol, not the racaemic mix and not the acetate ester. The mice weighed 32g so each got ~2mg/d by the end of the study.
If we reverse engineer to translate this in to how much vitamin E would need to be added to food to deliver that same dose we can do this. We can say that a mouse eats ~2.8g/d of high fat diet. So there would need to have been 2mg in 2g of food or 1000mg/kg of food. Though if you used the synthetic acetate ester then around twice that. This is a massive dose of vitamin E and guess what effect it had on body weight? You're waaay ahead of me:
We might also take note of the caloric intake per day which comes out as exactly what anyone would expect for mice on an high fat diet, in contrast to the last post. The current study calorie intake is picked out in blue:
I hope you're not getting too bored with this. I suffered for weeks with these studies. Now it's your turn.
I guess I'm not selling you vitamin E as a weight loss hack. That's good.
So how do we square these studies (and many others, it's been a rough three weeks of reading) with the results from
where there is a marked decrease in weight gain on an high fat diet with modest vitamin E supplementation?
I absolutely accept that these data are correct as reported.
These are the sorts of findings which test your hypothesis of obesity. It's what makes slogging through the typos and brain farts and shifting definitions of high vs low vs unspecified levels of vitamin E in diet trials worthwhile.
Ultimately we are looking for circumstances where reducing ROS with vitamin E allows weight loss. Some weight loss anyway.
I think there might be an explanation.
Peter



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