Reactive oxygen species created by fats and their affect on insulin signalling

Does fat make you fat? And if the answer is yes then which type of fat is the guilty one?

Fat mass expansion in obesity occurs via adipocyte hyperplasia (increased adipocyte number) and/or adipocyte hypertrophy (increased size of adipocytes). The latter is often associated with adipose dysfunction and inflammation.

Increased adipocyte size correlates with serum insulin concentrations, insulin resistance, and increased risk of developing type 2 diabetes. (1) Adipocyte hypertrophy may impair adipose tissue function by inducing local inflammation, mechanical stress, and altered metabolism.

This study (2) explains that:

“the deposition of triglycerides in insulin-sensitive tissues other than adipocytes causes insulin resistance.”

And another (3) says:

“a higher fat mass without increased circulating FFAs does not lead to insulin resistance or type 2 diabetes in mice.”

So clearly, getting fat isn’t necessarily bad for your health, but it’s when your adipose tissue becomes too distended (or the existing fat cells cannot take up anymore and cannot produce new fat cells), which is the problem. In such a situation you’ll have fats floating around that cannot enter adipose tissue, which is then deposited into other tissue (other than adipose tissue), and that’s when you get in trouble.

The type of fat you consume actually has an effect on whether or not you gain healthy weight, and if the fat will start to leak out (out of the adipose tissue) or not…

Adipose hyperplasia (the formation of new fat cells) occurs when reactive oxygen species (ROS) are made in the cells that signal the production of new fat cells; ROS is the base signaler. So how is ROS created? 90% of ROS is created inside cells, with the major contributor being the electron transport chain in the mitochondria. A few other contributors are xanthine oxidase, peroxisomal β-oxidation and NADPH oxidase, but I’m not going to focus on them in this article.


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