Omega 3 Depletion In Liver Promotes Fatty Liver

[Nigel Forester]

Hepatic n-3 Polyunsaturated Fatty Acid Depletion Promotes Steatosis and Insulin Resistance in Mice: Genomic Analysis of Cellular Targets

 

[Hugh Johnson]

N-3 depletion diet also had less saturated fat. So it was just replacing n-3 with n-6, and we know n-6 is inflammatory while n-3 is immunosuppressive and thus anti-inflammatory. Pretty predictable result.

 

[methylenewhite]

Table S6: Composition of control (CT) and n-3 PUFA depleted (DEF) diet. Formulated by Research Diets. Parenthetical numbers indicate the manufacturer's diet number.
pone.0023365.s006.doc

Table S7: Fatty acid composition of soybean and sunflower oil. Fatty acid composition of soybean and sunflower oil used for the CT and DEF diet respectively.
pone.0023365.s007.doc


It's a junk science. Real title for the study is sunflower oil leads to steatosis faster than soybean oil.
The authors also state: "We have reproduced a drastic drop in n-3 PUFA among hepatic phospholipids by feeding C57Bl/6J mice for 3 months with an n-3 PUFA depleted diet (DEF) versus a control diet (CT), which only differed in the PUFA content." They lie not only PUFA content is different.

Table S7. Fatty acid composition of soybean and sunflower oil

Composition g/100g of oil

soybean sunflower
C16:0 10.4 6.6

C18:0 3.8 5.1

C20:0 0 0.5

C16:1 0 0.5

C18:1 24.4 23.1

C18:2 n-6 53.6 63.7

C18:3 n-3 7.8 0.5

This is scientific misconduct.

 

[gaze]

how research likes this gets published is beyond me. it’s as if there’s 0 critical thinking going on.

 

[Nigel Forester]

Thanks intelligent posters!!

 

[Tristan Loscha]

Discussion
Several papers suggest that decreased n-3/n-6 PUFA ratio in the diet is associated with changes in n-3/n-6 PUFA ratio in hepatic membrane phospholipids, on the one hand, and on the development of hepatic steatosis in humans, on the other hand [14]-[16]. Even if we can not exclude that metabolic changes of the liver (such as oxidative stress) may contribute to changes in hepatic fatty acid profile [15], it is conceivable that the imbalance dietary intake of PUFA plays a crucial role in the appearance of steatosis [14].

In a previous study, we have reported toxic steatosis in female mice fed with n-3 PUFA depleted- sucrose rich diet for two generations [18]. In this case, the hepatic morphological alterations were associated with a low expression of factors and enzymes involved in lipogenesis and an increase in the expression of those involved in fatty acid oxidation [18]. In the present study, we have created a model of nutritional n-3 PUFA depletion which did not provide any signs of hepatic toxicity that could compromise the interpretation of the metabolic data.

PUFA excess is an issue,but what should take its place,MONO didnt cut it in this study,there is still desire for viscosity params of membranes which have to be abided?

Further:

A targeted change in the lipid source of the diet allowed us to create a mouse model to explore the biochemical mechanisms underlying hepatic lipid accumulation under n-3 PUFA depletion. As previously shown in rats [23], 3 months of dietary n-3 PUFA depletion were sufficient to induce an altered fatty acid pattern in hepatic PLs, characterised by a large decrease in n-3 PUFA and a parallel increase in MUFA, without changing the total n-6 PUFA and saturated fatty acid levels. These changes were associated with hepatic accumulation of TG and esterified cholesterol, leading to a mixed macro- and microvesicular steatosis.