The article confounded me about the start of increased ROS production: I understood that this overproduction is the core event in the oxidative stress, that is the object of possible inhibitory treatments.
I understood better the role of MPO (mieloperoxidasis). It looks like the operative weapon of leucocytes and monocytes.
These inflammatory cells are increased in many tissues (EG: fat tissues) during insulin resistance. Both are involved in the overall inflammation promoted by insulin resistance.
Inhibition of MPO looks like a castraction of the overall inflammation. At my opinion, the winning choice is prevention of the overall inflammation and not the sterilization of the inflammation.
I have to think to the meaning of this choice of mine: is it scientific or an opinion?
I sincerely ask for comments!
I think macrophage polarization to M1 profile in adipose tissue is also an important hallmark of chronic low grade inflammation, e.g. obesity, type 2 diabetes.
By adding more omega-3 PUFAs as resolvin precursors, much could be done to achieve a more anti-inflammatory millieu.
The details are presented in the attached article.
Sorry I ddidn't answer the question directly, but merely added some info I find interesting and complementary for a possible discussion.
Regrads,
Karlo
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