I hope by now you, my gentle reader(s), are familiar with the story of diabetes, insulin resistance and their link with chronic inflammation. Let me emphasize once more. Inflammation per se is not a bad thing; it is an essential process in the immune defence of the body. Whenever there is an invasion of a tissue, internal or external, by a foreign substance – such as a pathogen, the inflammatory process, initiated by signals from the primary defence cells in the tissue (such as Macrophages), calls in reinforcements from bone marrow derived immune cells, the secondary defence system of the body – in form of leukocytes (a.k.a. White Blood Cells/WBCs; e.g. neutrophils, T- and B-lymphocytes, monocytes, and sometimes basophils and eosinophils) and/or mast cells, from blood into the tissue. These defence cells communicate with each other and perform their action by releasing chemical substances known as cytokines and chemokines, that act as messengers.
In the FIRST POST of this two part series, I laid out some facts about Type 2 diabetes which results from insulin resistance, and indicated how non-esterified (‘Free’) Fatty Acids (FFAs) induce chronic inflammation via engagement of TLR4 and the NF-κB pathway, eventually leading to Insulin resistance – and yet, since FFA doesn’t bind TLR4, it’s not known how the twain meets. The elegant set of studies described in the Pal at al. paper in the July 29, 2012 issue of Nature Medicine  provides evidence for a mechanism hypothesized to be active in lipid-induced insulin resistance, i.e., one that can connect the dots.
Nature Medicine has recently featured studies dealing with obesity-related insulin resistance which leads to a type of diabetes, called Type 2 diabetes. Of these papers, one by Pal et al. (Nature Medicine, 18(8):1284, August 2012) highlights some specific aspects of the disease, including prospects for future therapeutics. I found it interesting – for various reasons* – enough to spur me to write about diabetes in the context of their observations. I shall make it a 2-part series; in the first post, I would talk a bit about diabetes in general, and follow it up with a review of the main findings of their elegant studies. (Full disclosure: I have parents and grandparents who are/were diabetic.)