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BAN ALL RUSTLING FROM JIMMIES | Mark Bell eats Taco Bell | GOSAD (Gallon of Soup a Day) | Yodelling Mode | How can I eat food without food? The sticky doesn't say. | >tfw no gf 2018 | Am I built for blogposting?

File: 266efbaa5b990a8⋯.png (96.09 KB, 622x538, 311:269, The-mechanisms-of-action-o….png)

c8f96c  No.141713

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.”

“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].”

“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].”

“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.”

“overall soybean oil induced more obesity, diabetes, IR and liver injury than either fructose

or saturated fat from coconut oil in mice.”

“Addition of fructose also increased body weight above HFD (Fig 1A right), although not as much as soybean oil (Fig 1B left).”

“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.”

“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.”

“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.”

“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).”

“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).”

“Most, but not all obesity, diabetes and inflammation promoting genes had elevated expression in SO-HFD versus HFD livers, as well as versus Viv”

c8f96c  No.141714

>>141713

“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. This suggests that coconut oil may also be protective against liver cancer, though the protection may be nullified by soybean oil (Fig 8).”

“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 (Fig 11C and 11D).”

“The increase in obesity in the U.S. over the last half-century coincides with a shift in the dietary preference away from saturated fats from animal products and toward plant-based unsaturated fats [16].”

“While this study was in progress, two groups published papers with results similar to ours—namely, that a high fat diet supplemented with oils high in LA leads to obesity and fatty liver [24,53,146]. Other studies have also shown that dietary LA can cause adiposity in humans [165,166] and lead to hyperglycemia as well as obesity in mice [19,167].”

Note: I don’t think the rectal prolapse is inevitable in all high fructose diets, but interestingly, it does remind me of the situation some non-human primates experience. It could be an artifact of the inflexibility of the diet (meaning the mice always ate the same thing), the unique context of the experiment, and/or some interaction with an unidentified negative component. Humans outside of laboratory conditions are generally able to change things on impulse and correct course when an imbalance arises. This is the first mention of an association with fructose and specifically rectal prolapse that I have encountered. Curiously, the state of the rectum was not elaborated on the non-fructose diets. If rectal prolapse occurred on one diet, it would seem prudent to determine the qualities of the other rectums. If not prolapsed, were they suffering a different and/or worse condition? The issue may also be a matter of language. “Prolapse” is alarming, but these intestines were examined after removal from the corpses. They did not clarify if the mice exhibited prolapse on the exterior of their butts while living. Are we simply looking at the difference between a tight-ass and a relaxed ass?


c8f96c  No.141715

>>141714

One more note: the addition of a refined source of carbohydrates is often different than the addition of a whole food containing those same carbohydrates. Meaning that, for example, adding pure sucrose or fructose can speed up the metabolic rate and the usage and disposal of rate limiting nutrients such as vitamins and minerals. On the other hand, whole foods such as fruits are a package that come with vitamins, minerals, proteins, and antioxidants. It is unclear if their experiment encountered unique quirks from the induction of deficiencies that whole foods or diets of a different balance would frequently avoid, and also there is the possibility of an increased metabolic rate achieving the same potential conclusion of a comparable but somewhat different diet and environment at a faster rate. The inflexibility of the diets are probably their most damning feature.


893ba2  No.141733

Ebihara, Ken, et al. Decrease in endogenous brain allopregnanolone induces autism spectrum disorder (ASD)-like behavior in mice: A novel animal model of ASD. Behavioural brain research 334 (2017): 6-15.

https://doi.org/10.1016/j.bbr.2017.07.019


893ba2  No.141736

Alam, Murad, et al. Subcutaneous Infiltration of Carbon Dioxide (Carboxytherapy) for Abdominal Fat Reduction: A Randomized Clinical Trial. Journal of the American Academy of Dermatology (2018).

https://doi.org/10.1016/j.jaad.2018.04.038

>A total of 16 participants completed the study. Ultrasound measurement indicated less fat volume on the side treated with carboxytherapy 1 week after the last treatment (P = .011), but the lower fat volume was not maintained at 28 weeks.


893ba2  No.141739

Edinburgh, Robert, et al. Pre-Exercise Breakfast Ingestion versus Extended Overnight Fasting Increases Postprandial Glucose Flux after Exercise in Healthy Men: Pre-exercise feeding and postprandial glucose flux. American Journal of Physiology: Endocrinology and Metabolism (2018).

https://doi.org/10.1152/ajpendo.00163.2018

>In a randomized order, twelve men underwent breakfast-rest (BR; 3 h semi-recumbent), breakfast-exercise (BE; 2 h semi-recumbent before 60-min of cycling (50% peak power output) and overnight fasted-exercise (FE; as per BE omitting breakfast) trials. […] Plasma intestinal fatty acid binding (I-FABP) concentrations were determined as a marker of intestinal damage. Results: Breakfast before exercise increased post-exercise plasma glucose disposal rates […] Plasma I-FABP concentrations during exercise were 264 pg•mL-1 [196 to 332 pg•mL-1] lower in BE versus FE (p = 0.01). Conclusion: Breakfast before exercise increases post-exercise postprandial plasma glucose disposal, which is offset (primarily) by increased appearance rates of orally-ingested glucose.


893ba2  No.141779

Massiera, Florence, et al. A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations. Journal of lipid research (2010) : jlr-M006866.

https://dx.doi.org/10.1194%2Fjlr.M006866

>The prevalence of obesity has steadily increased over the last few decades. During this time, populations of industrialized countries have been exposed to diets rich in fat with a high content of linoleic acid and a low content of α-linolenic acid compared with recommended intake. To assess the contribution of dietary fatty acids, male and female mice fed a high-fat diet (35% energy as fat, linoleic acid:α-linolenic acid ratio of 28) were mated randomly and maintained after breeding on the same diet for successive generations. Offspring showed, over four generations, a gradual enhancement in fat mass due to combined hyperplasia and hypertrophy with no change in food intake. Transgenerational alterations in adipokine levels were accompanied by hyperinsulinemia. Gene expression analyses of the stromal vascular fraction of adipose tissue, over generations, revealed discrete and steady changes in certain important players, such as CSF3 and Nocturnin. Thus, under conditions of genome stability and with no change in the regimen over four generations, we show that a Western-like fat diet induces a gradual fat mass enhancement, in accordance with the increasing prevalence of obesity observed in humans.


64fbb3  No.141805

File: 96be30ddfe503ee⋯.jpg (50.38 KB, 450x513, 50:57, 1438170680094.jpg)

Only you care, so bag up your shit and toss it so we don't have to step in it.


893ba2  No.141808

>>141805

>Only you care

he says while demonstrating just how much he doesn't care by posting in my blog thread, lol. Anything else you wanna be transparent about?


893ba2  No.141816

>>141733

Liang, Tehming, and Shutsung Liao. Inhibition of steroid 5α-reductase by specific aliphatic unsaturated fatty acids. Biochemical Journal 285.2 (1992): 557-562.

https://doi.org/10.1042/bj2850557

>Human or rat microsomal 5 alpha-reductase activity, as measured by enzymic conversion of testosterone into 5 alpha-dihydrotestosterone or by binding of a competitive inhibitor, [3H]17 beta-NN-diethulcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one ([3H]4-MA) to the reductase, is inhibited by low concentrations (less than 10 microM) of certain polyunsaturated fatty acids. The relative inhibitory potencies of unsaturated fatty acids are, in decreasing order: gamma-linolenic acid greater than cis-4,7,10,13,16,19-docosahexaenoic acid = cis-6,9,12,15-octatetraenoic acid = arachidonic acid = alpha-linolenic acid greater than linoleic acid greater than palmitoleic acid greater than oleic acid greater than myristoleic acid. […] The methyl esters and alcohol analogues of these compounds, glycerols, phospholipids, saturated fatty acids, retinoids and carotenes were inactive even at 0.2 mM. […] gamma-Linolenic acid, but not the corresponding saturated fatty acid (stearic acid), inhibited the 5 alpha-reductase activity, but not the 17 beta-dehydrogenase activity, of human prostate cancer cells in culture.




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