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  #1   ^
Old Fri, Apr-27-18, 04:47
teaser's Avatar
teaser teaser is offline
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Default Oxidative stress makes difference between metabolically abnormal and healthy obesitie

Scientists at Osaka University clarified that deletion of adipose oxidative stress (Fat ROS) decreased lipid accumulation in the liver, clinically improving insulin resistance and inducing metabolically healthy obesity. In fact, Fat ROS suppressed lipid accumulation and increased ectopic lipid accumulation in the liver, worsening insulin resistance. Their research results were published in Diabetes on Wednesday, April 4, 2018.

In most people, obesity is caused by eating too much and moving too little. There are two types of obesity: metabolically abnormal obesity associated with insulin resistance and metabolic disorder and metabolically healthy obesity without these complicating disorders; however, the molecular mechanism behind this difference was unknown.

In 2004, a group of researchers led by Atsunori Fukuhara reported that oxidative stress increased in the obese adipose tissues. However, it was difficult to create a mouse model in which oxidative stress was manipulated to target adipocytes. So, the causal role of Fat ROS in obesity in vivo still remained unclear.

In their research, this group clarified the following: Fat ROS-eliminated mice, in which two antioxidant enzymes (Catalase and Sod1) were overexpressed in adipocytes using an adipocyte-specific aP2 promoter cassette, exhibited adipose expansion with decreased ectopic lipid accumulation and improved insulin sensitivity. Conversely, Fat ROS-augmented, Adipoq promoter-driven Cre transgenic mice, in which antioxidant substance glutathione was depleted specifically in adipocytes, exhibited restricted adipose expansion associated with increased ectopic lipid accumulation and deteriorated insulin sensitivity.

SREBF1 transcriptional activities were suppressed by oxidative stress, suppressing expression of lipogenic genes in adipocytes, which was found to be the underlying mechanism for suppression of de novo lipogenesis by oxidative stress.

It is expected that the results of this study will lead to the development of drugs targeting Fat ROS to induce healthy adipose expansion, which will lead to treatment of obese type 2 diabetes.

In most people, obesity is caused by eating too much and moving too little.

No article looking at those things that limit body fat accumulation besides "eating too much and moving too little" is complete without this mantra. Wouldn't want anybody to get the wrong idea. Even if this statement were true, beginning every press release or research article with a statement of faith is still questionable.

Legitimate area of research, but most people aren't looking for a way to make themselves fatter. Skinny fat? Maybe we can fix that. Maybe not the way you'd like. We maybe have enough ways to treat diabetes that increase obesity.
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  #2   ^
Old Fri, Apr-27-18, 10:09
M Levac M Levac is offline
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The eating too much and growing fat part, and the adipose expansion and ectopic lipid accumulation part, are not the same phenomenon.

Adipose expansion is fat tissue growth. Ectopic lipid accumulation is accumulation of lipid outside of adipose tissue, i.e. in muscle tissue for example.

Anyways, the mouse experiment with overexpression of antioxidants actually shows greater fat tissue growth, i.e. the mice grew fatter.

We have two obvious examples of this difference with the Jersey cows which are typically lean (little or no marbling), and the Angus cows which are typically fat (lots of marbling). When these two species are fattened before slaughter, marbling doesn't change, instead the degree of fat accumulation where there is already fat tissue increases. So, in the Jersey cows, most excess fat accumulation occurs outside muscles with muscles remaining relatively lean, in the Angus cows marbling becomes thicker and there's more fat outside muscles as well just like in the Jersey cows.

So how are they fattened? We force them to sit on the couch and watch TV all day and night, right? Har har. But seriously, we feed them grains, mostly corn and wheat. We don't force-feed them (i.e. eat too much), we just change their diet.

How it applies to humans, because it does apply to humans at least conceptually. Our fat tissue grows bigger from excess antioxidants, but at least ectopic lipid accumulation isn't a problem, so we're healthy-obese (as absurd as that sounds). Or, our fat tissue doesn't grow (cuz we breathe in lots and lots of oxygen with our lungs, cuz that's what they're there for, ya?), instead ectopic lipid accumulation spreads (cuz breathing in lots and lots of oxygen with our lungs is a bad thing apparently, that's how we get punished for it, doh!).

What they actually meant to say:
It is expected that the results of this study will lead to the development of drugs targeting Fat ROS to induce healthy adipose expansion make people fatter, which will lead to treatment of obese type 2 diabetes.
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