Deol, Poonamjot, et al. Soybean oil is more obesogenic and diabetogenic than coconut oil and fructose in mouse: potential role for the liver. PloS one 10.7 (2015): e0132672.
https://doi.org/10.1371/journal.pone.0132672
“The obesity epidemic in the U.S. has led to extensive research into potential contributing dietary factors, especially fat and fructose. Recently, increased consumption of soybean oil, which is rich in polyunsaturated fatty acids (PUFAs), has been proposed to play a causal role in the epidemic. […] C57/BL6 male mice fed a diet moderately high in fat from coconut oil and soybean oil (SO-HFD, 40% kcal total fat) showed statistically significant increases in weight gain, adiposity, diabetes, glucose intolerance and insulin resistance compared to mice on a diet consisting primarily of coconut oil (HFD). […] While the high fructose diet (F-HFD) did not cause as much obesity or diabetes as SO-HFD, it did cause rectal prolapse and a very fatty liver, but no balloon injury. The coconut oil diet (with or without fructose) increased spleen weight while fructose in the presence of soybean oil increased kidney weight. Metabolomics analysis of the liver showed an increased accumulation of PUFAs and their metabolites as well as γ-tocopherol, but a decrease in cholesterol in SO-HFD.”
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“there is a growing body of evidence that suggests that saturated fat from sources such as coconut and palm oil, which are rich in medium chain triglycerides (MCTs), may actually be beneficial for the prevention and treatment of the Metabolic Syndrome [13–15].”
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“Approximately 40 million tons of soybean oil were produced worldwide in 2007, which is about one half of all the edible vegetable oil and one-third of all fats and seed oils produced [17].”
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“Fructose in the diet (F-HFD and F-SO-HFD) had less severe metabolic effects than soybean oil but caused rectal prolapse and seemed to synergize with soybean oil to increase kidney weight.”
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“overall soybean oil induced more obesity, diabetes, IR and liver injury than either fructose
or saturated fat from coconut oil in mice.”
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“Addition of fructose also increased body weight above HFD (Fig 1A right), although not as much as soybean oil (Fig 1B left).”
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“The amount of mesenteric and subcutaneous white adipose tissue (WAT) was significantly greater in SO-HFD than HFD mice; the amount of peri-renal fat was trending in the same direction. Fructose-fed mice (F-HFD and F-SO-HFD) had similar amounts of mesenteric fat and peri-renal fat as SO-HFD mice but lower amounts of subcutaneous WAT.”
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“To our surprise, 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.”
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“Even more striking were the results of the insulin tolerance test. 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 (Fig 4B). All told, these results indicate that a moderately high fat diet of coconut oil, either in the presence or absence of fructose, does not induce significant diabetic symptoms (elevated fasting blood glucose and glucose intolerance) while isocaloric diets with soybean oil (either with or without fructose) do. Counter intuitively, our results also suggest that the addition of fructose to the diet may even protect against the IR caused by soybean oil.”
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“While fructose caused excessive but typically fairly uniform fat deposition (Fig 5C and 5D), as has been observed previously [64,65], the SO-HFD livers had very large lipid droplets that were consistently accompanied by severe hepatocyte ballooning, suggesting potential liver damage (Fig 5E).”
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“Cidea (cell death-inducing DFFA-like effector a) was the most upregulated gene in SO-HFD (~120-fold versus Viv) and barely detectable in Viv and HFD livers (Fig 6D).”
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“Most, but not all obesity, diabetes and inflammation promoting genes had elevated expression in SO-HFD versus HFD livers, as well as versus Viv”
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