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Saturated Fat Is More Metabolically Harmful For The Human Liver Than Unsaturated Fats Or Sugars (?)

_lppaiva

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Jul 30, 2019
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114
Saturated Fat Is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars

[JUST SAW THAT THIS STUDY WAS ALREADY POSTED IN MAY 2018 MY BAD]

"We overfed 38 overweight subjects (age 48 ± 2 years, BMI 31 ± 1 kg/m2, liver fat 4.7 ± 0.9%) 1,000 extra kcal/day of saturated, unsaturated fat or simple sugars for 3 weeks. We measured intrahepatic triglycerides (1H-MRS), pathways contributing to it (lipolysis ([2H5]glycerol) and de novo lipogenesis (2H2O) basally and during euglycemic hyperinsulinemia), insulin resistance, endotoxemia, plasma ceramides, and adipose tissue gene expression at 0 and 3 weeks.

Overfeeding saturated fats increased intrahepatic triglycerides more (+55%) than unsaturated fats (+15%, P < 0.05). Carbohydrates increased intrahepatic triglycerides (+33%) by stimulating de novo lipogenesis (+98%). Saturated fats significantly increased while unsaturated fats decreased lipolysis. Saturated fats induce insulin resistance and endotoxemia and significantly increased multiple plasma ceramides. The diets had distinct effects on adipose tissue gene expression."

Now, I'm no expert, and this is my first post (Hey guys), but I would like to see if my line of reasoning would be correct.

Studying RP's work for a while, and seeing haidut's post, I've learned to not take these studies at face value and actually try to apply my knowledge to it.

So they got a bunch of overweight individuals, loaded with PUFA, and increased their Saturated fat intake, that most likely started to displace the PUFA, liberating then into the bloodstream, which they themselves state is the major contributer to intrahepatic triglycerides. "Fatty acids in intrahepatic triglycerides can originate from adipose tissue lipolysis, hepatic de novo lipogenesis, and dietary fat (4). Lipolysis provides most of the FAs used for synthesis of intrahepatic triglycerides.". And stated that the major cause of it was saturated fats.

The fact that unsaturated fat increase DIDN'T induce intrahepatic triglycerides due to the downregulating the metabolism, not allowing for the release of more PUFA while continuing to store it. "Saturated fats significantly increased while unsaturated fats decreased lipolysis", this can be further proved by the point that the amount of weight gain in both groups is the same, but one induces intrahepatic triglycerides. "Saturated but not polyunsaturated fat has been reported to increase intrahepatic triglycerides (IHTGs) in young nonobese adults, despite similar weight gain (2). "

There are still, however, some flaws to my theory, as Sugar also increased intrahepatic triglycerides even though de novo lipogenesis only provides SFA (perhaps the SFA provided by sugar can also displace PUFA?). And the ceramides part that I don't know much about:
"Ceramides are synthesized de novo from SFAs, such as palmitate, and interfere with glucose metabolism by inhibiting insulin signaling". Are ceramides made from SFA really? In this case SFA would induce Insulin resistance right?

Anyway,
What do you guys think? Anything to add? Any hasty conclusions I made? Otherwise this study really is a bummer.
 
Last edited:

haidut

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Mar 18, 2013
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Saturated Fat Is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars

[JUST SAW THAT THIS STUDY WAS ALREADY POSTED IN MAY 2018 MY BAD]

"We overfed 38 overweight subjects (age 48 ± 2 years, BMI 31 ± 1 kg/m2, liver fat 4.7 ± 0.9%) 1,000 extra kcal/day of saturated, unsaturated fat or simple sugars for 3 weeks. We measured intrahepatic triglycerides (1H-MRS), pathways contributing to it (lipolysis ([2H5]glycerol) and de novo lipogenesis (2H2O) basally and during euglycemic hyperinsulinemia), insulin resistance, endotoxemia, plasma ceramides, and adipose tissue gene expression at 0 and 3 weeks.

Overfeeding saturated fats increased intrahepatic triglycerides more (+55%) than unsaturated fats (+15%, P < 0.05). Carbohydrates increased intrahepatic triglycerides (+33%) by stimulating de novo lipogenesis (+98%). Saturated fats significantly increased while unsaturated fats decreased lipolysis. Saturated fats induce insulin resistance and endotoxemia and significantly increased multiple plasma ceramides. The diets had distinct effects on adipose tissue gene expression."

Now, I'm no expert, and this is my first post (Hey guys), but I would like to see if my line of reasoning would be correct.

Studying RP's work for a while, and seeing haidut's post, I've learned to not take these studies at face value and actually try to apply my knowledge to it.

So they got a bunch of overweight individuals, loaded with PUFA, and increased their Saturated fat intake, that most likely started to displace the PUFA, liberating then into the bloodstream, which they themselves state is the major contributer to intrahepatic triglycerides. "Fatty acids in intrahepatic triglycerides can originate from adipose tissue lipolysis, hepatic de novo lipogenesis, and dietary fat (4). Lipolysis provides most of the FAs used for synthesis of intrahepatic triglycerides.". And stated that the major cause of it was saturated fats.

The fact that unsaturated fat increase DIDN'T induce intrahepatic triglycerides due to the downregulating the metabolism, not allowing for the release of more PUFA while continuing to store it. "Saturated fats significantly increased while unsaturated fats decreased lipolysis", this can be further proved by the point that the amount of weight gain in both groups is the same, but one induces intrahepatic triglycerides. "Saturated but not polyunsaturated fat has been reported to increase intrahepatic triglycerides (IHTGs) in young nonobese adults, despite similar weight gain (2). "

There are still, however, some flaws to my theory, as Sugar also increased intrahepatic triglycerides even though de novo lipogenesis only provides SFA (perhaps the SFA provided by sugar can also displace PUFA?). And the ceramides part that I don't know much about:
"Ceramides are synthesized de novo from SFAs, such as palmitate, and interfere with glucose metabolism by inhibiting insulin signaling". Are ceramides made from SFA really? In this case SFA would induce Insulin resistance right?

Anyway,
What do you guys think? Anything to add? Any hasty conclusions I made? Otherwise this study really is a bummer.

It is not a bummer at all. Two reasons: (1) This study is about overfeeding. As such, not really sure what its point is. Clearly if there is an overfeeding you'd expect suboptimal results. (2) It is not a study where you had group of people eating entirely one or other type of fat. It simply added the various types of fat on top of a diet that was already high in PUFA. The same trick done in virtually every other "Look! SFA is bad" study.
A legit study would have fed the typical amount of calories these people consumed in order to maintain stable weight and then ensure that each group eats ONLY a specific type of fat (MUFA, PUFA, SFA), not a mix of all of them where one of the types is slightly more abundant.
 
Last edited:
Joined
Aug 18, 2015
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1,815
if u are overweight as is, you have a messed up metabolism, so this is essentially throwing gasoline into a fire anyway, lets give 10 overweight people a ton of sugar everyday, lets watch what happens, shocking they will gain weight, so sugar must be bad right
 

paymanz

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Jan 6, 2015
Messages
2,702
over feeding anything is bad. and fats in general should not make a large percent of diet. its not natural.

but i expected SFA decrease lipolysis compared to USFA
 

rei

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Joined
Aug 6, 2017
Messages
1,607
Why? The increased 'insulin resistance' and 'increased lipolysis' with SFA is completely expected and in line with previous research. When quality fat comes in the body spares glucose and moves over to oxidize fat. PUFA is such a burden that the body does not switch away from glucose oxidation and mainly stuffs the fat into storage.
 

Peater Piper

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Joined
Mar 18, 2016
Messages
806
One thing I'll point out, and I don't know if the study took it into account, is that SFA requires more nutrients to be exported from the liver than PUFA, namely choline and betaine, but glycine and b-vitamins should help as well. It's probably not a great idea to eat a lot of refined SFA since you're not getting the co-factors with it.
 

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