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- Aug 24, 2017
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Everyone here knows PUFAs are bad, but I just wanted to post this study, which shows some of the mechanisms how PUFAs and SFAs work. In the study the soybean oil increases bodyfat, inflammation, fatty liver, cancer promoting genes, glucose intolerance, diabetes, etc., whereas the coconut oil has the opposite effect. Soybean oil contains a fair bit of γ-tocopherol, but this was not enough to protect against its harmful effects.
Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver
They had 4 groups, and all four ate 40% fat.
Group 1 (HFD): 36% coconut oil + 4% soybean oil
Group 2 (F-HFD): same as group 1 + 25.9 kcal% of energy from added fructose
Group 3 (SO-HFD): 21 kcal% fat calories from coconut oil and 19 kcal% from soybean oil
Group 4 (F-SO-HFD): same as group 3 + 25.9 kcal% of energy from added fructose
All groups ate the same amounts of food.
Core findings:
"Mice fed SO-HFD gained more weight and at a faster rate than mice fed HFD".
"Addition of fructose also increased body weight above HFD (Fig 1A right), although not as much as soybean oil (Fig 1B left). SO-HFD mice gained slightly more weight than F-SO-HFD mice, although this difference was significant only between weeks 8 and 16"
Fructose protects against the obesogenic effect of PUFAs.
"we found that at 20 weeks the F-HFD did not cause diabetes (fasting blood glucose level > 200 mg/dL) whereas the SO-HFD did (Fig 4A). Furthermore, the F-HFD mice were just barely less tolerant to glucose than the Viv mice while the SO-HFD were extremely intolerant. Interestingly, the addition of fructose to SO-HFD (F-SO-HFD) actually slightly ameliorated the glucose intolerance of SO-HFD. Notably, the diet consisting primarily of coconut oil (HFD) did not show any diabetes or glucose intolerance at 20 weeks."
Fructose does not cause diabetes and might actually prevent glucose intolerance caused by PUFAs.
"At 33 weeks, the SO-HFD mice were the most insulin resistant and much more so than F-SO-HFD mice, which were indistinguishable from F-HFD and HFD"
Fructose restored the insulin resistance caused by PUFAs.
"SO-HFD livers had very large lipid droplets that were consistently accompanied by severe hepatocyte ballooning, suggesting potential liver damage"
"the fatty acid translocase Cd36, which aids in free fatty acid (FFAs) uptake and contributes to hepatic steatosis [68] and fatty acid binding protein Fabp4 that helps maintain hepatic metabolic balance and links diet induced obesity to insulin resistance [69,70] was increased in SO-HFD, while fatty acid binding protein 5 (Fabp5), which plays an important role in detoxifying FFAs and preventing lipid dysregulation [71], was decreased three-fold."
Enzymes that increase fatty acid import into cells are significantly increased, and enzymes that detox fatty acids are decreased. Ray mentioned that PUFAs inhibit it's own detoxification, and looks like inhibiting Fabp5 is one mechanism. PUFAs also cause lipid accumulation in muscles and other organs, and it might be by increasing Cd36 and Fabp4.
"Similarly, Igfbp1, an important regulator of insulin like growth factor 1 (IGF1) activity, showed an almost five-fold increase in SO-HFD versus HFD livers: increased hepatic expression of Igfbp1 is associated with diabetes [72]. In the inflammation category, Lgals1 (Galectin-1), an important immune response modulator and biomarker for hepatocellular carcinoma (HCC) [73–75] was also markedly increased in SO-HFD but not HFD"
"The most notable gene was Pdk4, which was elevated four-fold in SO-HFD compared to HFD and encodes a mitochondrial gene that plays an important role in the balance between glucose and fatty acid oxidation [76]. In contrast, Hyou1 and Slc25a30 (KMCP1) were expressed at higher levels in HFD compared to both SO-HFD and Viv. Since these genes are considered to be protective against oxidative damage [77–80], this suggests that coconut oil may be beneficial but that soybean oil diminishes the effect."
Pdk4 inhibits the activity of pyruvate dehydrogase (PDH), which is essential for glucose oxidation. Palmitic acid increases PDH. One important thing about this is that, PUFAs increase uncoupling, which reduce ATP, but then also inhibit PDH, so no glucose is able to make up for the loss of ATP. With SFAs, they also increase uncoupling, but also increase glucose oxidation to make up for the reduction in ATP. With PUFAs that inhibit PDH, most of the glucose is going to lactate and not CO2, as lactate dehydrogenase as also elevated in the PUFA group. PUFAs lead to low ATP production and keeps the cells in a low energy state, by also inhibiting many of the complexes in the mitochondrial membrane that's necessary for ATP production.
"Genes in the cancer category showed a definite predominance of pro-proliferation genes upregulated in SO-HFD while anti-proliferative genes tended to be upregulated in HFD but not SO-HFD."
"Both capric and lauric acid have been shown to cause a decrease in adiposity, increased insulin secretion and improved serum lipid profile"
"Interestingly, the pro-inflammatory eicosanoid 12-HETE (an AA metabolite) and the marker of lipid peroxidation 13-HODE+9-HODE (LA metabolite) [91–93] were significantly decreased in HFD versus Viv at both 16 and 35 weeks, suggesting that coconut oil may be protective against inflammation. The lower levels of these metabolites could be due to decreased expression of Cyp2c54 (Fig 9B), which is known to metabolize AA and LA to HETEs and HODEs"
This is a very good study in my opinion showing how and why coconut oil/saturated fat are good and PUFAs are bad. Longer chain saturated fat, such as stearic acid, will have its own set of benefits not discussed in this study, because coconut oil doesn't have lots of stearic acid.
They also show that fructose protects against the harm of PUFAs.
But this is just a rat study, so should be carefully extrapolated to humans, but still it shows some good points. I advise to read to whole study.
Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver
They had 4 groups, and all four ate 40% fat.
Group 1 (HFD): 36% coconut oil + 4% soybean oil
Group 2 (F-HFD): same as group 1 + 25.9 kcal% of energy from added fructose
Group 3 (SO-HFD): 21 kcal% fat calories from coconut oil and 19 kcal% from soybean oil
Group 4 (F-SO-HFD): same as group 3 + 25.9 kcal% of energy from added fructose
All groups ate the same amounts of food.
Core findings:
"Mice fed SO-HFD gained more weight and at a faster rate than mice fed HFD".
"Addition of fructose also increased body weight above HFD (Fig 1A right), although not as much as soybean oil (Fig 1B left). SO-HFD mice gained slightly more weight than F-SO-HFD mice, although this difference was significant only between weeks 8 and 16"
Fructose protects against the obesogenic effect of PUFAs.
"we found that at 20 weeks the F-HFD did not cause diabetes (fasting blood glucose level > 200 mg/dL) whereas the SO-HFD did (Fig 4A). Furthermore, the F-HFD mice were just barely less tolerant to glucose than the Viv mice while the SO-HFD were extremely intolerant. Interestingly, the addition of fructose to SO-HFD (F-SO-HFD) actually slightly ameliorated the glucose intolerance of SO-HFD. Notably, the diet consisting primarily of coconut oil (HFD) did not show any diabetes or glucose intolerance at 20 weeks."
Fructose does not cause diabetes and might actually prevent glucose intolerance caused by PUFAs.
"At 33 weeks, the SO-HFD mice were the most insulin resistant and much more so than F-SO-HFD mice, which were indistinguishable from F-HFD and HFD"
Fructose restored the insulin resistance caused by PUFAs.
"SO-HFD livers had very large lipid droplets that were consistently accompanied by severe hepatocyte ballooning, suggesting potential liver damage"
"the fatty acid translocase Cd36, which aids in free fatty acid (FFAs) uptake and contributes to hepatic steatosis [68] and fatty acid binding protein Fabp4 that helps maintain hepatic metabolic balance and links diet induced obesity to insulin resistance [69,70] was increased in SO-HFD, while fatty acid binding protein 5 (Fabp5), which plays an important role in detoxifying FFAs and preventing lipid dysregulation [71], was decreased three-fold."
Enzymes that increase fatty acid import into cells are significantly increased, and enzymes that detox fatty acids are decreased. Ray mentioned that PUFAs inhibit it's own detoxification, and looks like inhibiting Fabp5 is one mechanism. PUFAs also cause lipid accumulation in muscles and other organs, and it might be by increasing Cd36 and Fabp4.
"Similarly, Igfbp1, an important regulator of insulin like growth factor 1 (IGF1) activity, showed an almost five-fold increase in SO-HFD versus HFD livers: increased hepatic expression of Igfbp1 is associated with diabetes [72]. In the inflammation category, Lgals1 (Galectin-1), an important immune response modulator and biomarker for hepatocellular carcinoma (HCC) [73–75] was also markedly increased in SO-HFD but not HFD"
"The most notable gene was Pdk4, which was elevated four-fold in SO-HFD compared to HFD and encodes a mitochondrial gene that plays an important role in the balance between glucose and fatty acid oxidation [76]. In contrast, Hyou1 and Slc25a30 (KMCP1) were expressed at higher levels in HFD compared to both SO-HFD and Viv. Since these genes are considered to be protective against oxidative damage [77–80], this suggests that coconut oil may be beneficial but that soybean oil diminishes the effect."
Pdk4 inhibits the activity of pyruvate dehydrogase (PDH), which is essential for glucose oxidation. Palmitic acid increases PDH. One important thing about this is that, PUFAs increase uncoupling, which reduce ATP, but then also inhibit PDH, so no glucose is able to make up for the loss of ATP. With SFAs, they also increase uncoupling, but also increase glucose oxidation to make up for the reduction in ATP. With PUFAs that inhibit PDH, most of the glucose is going to lactate and not CO2, as lactate dehydrogenase as also elevated in the PUFA group. PUFAs lead to low ATP production and keeps the cells in a low energy state, by also inhibiting many of the complexes in the mitochondrial membrane that's necessary for ATP production.
"Genes in the cancer category showed a definite predominance of pro-proliferation genes upregulated in SO-HFD while anti-proliferative genes tended to be upregulated in HFD but not SO-HFD."
"Both capric and lauric acid have been shown to cause a decrease in adiposity, increased insulin secretion and improved serum lipid profile"
"Interestingly, the pro-inflammatory eicosanoid 12-HETE (an AA metabolite) and the marker of lipid peroxidation 13-HODE+9-HODE (LA metabolite) [91–93] were significantly decreased in HFD versus Viv at both 16 and 35 weeks, suggesting that coconut oil may be protective against inflammation. The lower levels of these metabolites could be due to decreased expression of Cyp2c54 (Fig 9B), which is known to metabolize AA and LA to HETEs and HODEs"
This is a very good study in my opinion showing how and why coconut oil/saturated fat are good and PUFAs are bad. Longer chain saturated fat, such as stearic acid, will have its own set of benefits not discussed in this study, because coconut oil doesn't have lots of stearic acid.
They also show that fructose protects against the harm of PUFAs.
But this is just a rat study, so should be carefully extrapolated to humans, but still it shows some good points. I advise to read to whole study.