_lppaiva
Member
- Joined
- Jul 30, 2019
- Messages
- 116
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.
[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.
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