Insulin resistance and inflammation are close related phenomena.There are several points of interaction like cytokines,oxidative stress, modulation by insulin signaling circuits, interaction with vessels endothelium , LOx-1 in endothelium cells. Each one of the above, among others, deserve long standing basic and clinical studies. This is a multiphactor biological interconnection. Models for study are type 2 diabetes, metabolic syndrome and dyslipidemia.

Regarding the interaction with cytokines Regina mentioned...Fox01 stimulates macrophages, which migrate to the liver and adipose tissue in insulin-resistant states, and increase production of a cytokine called interleukin-1 beta (IL-1B). IL-1B in turn interferes with insulin signaling. Insulin typically inhibits Fox01 but when there is a lack of insulin or when cells such as macrophages are resistant to its presence, there are no brakes on Fox01's stimulation of IL-1B and its further interference with insulin signaling.

Inflammation per se is not obligatory. Insulin itself leads to a insulin resistance; every time a cell is exposed to insulin, the production of GLUT4 (type four glucose receptors) on the cell's membrane decreases somewhat. In the presence of a higher than usual level of insulin, this down-regulation acts as a kind of positive feedback, increasing the need for insulin. Another recently found factor is the lipid raft content of cholesterol. Insulin receptors need for their function high enough cholesterol levels on the cell membrane but at the same time removal of excess cholesterol activates the insulin receptor see :

www.ncbi.nlm.nih.gov/pubmed/15943586

S Vainio - ‎2005 Biochem J. 2005 Nov 1;391(Pt 3):465-72. Defective insulin receptor activation and altered lipid rafts in Niemann-Pick type C disease hepatocytes. And

A Ros-Baro 2001

At the same time we must remember that these disturbances at the cell membrane level will also lead to defective immune reactions and consequently will lead to inflammation. However, in this case insulin resistance is prior to inflammation.

This is a controversial but important question. Insulin resistance is possible prior to insulin resistance when insulin clearance is impaired. See the work of Jarrold Olefsky and Sonia Najjar. However, typically insulin resistance is accompanied by inflammation. See the work of Gerald Shulman, Andrew Greenberg, Gökhan Hotamisligil, and Steven Shoelson. Additionally, treating inflammation reduces insulin resistance (e.g., salicylates).

I agree with Thomas Brown. this remains a controversial question. it seems however that inflammation plays a contributory role in progression rather than causal since inflammation is not seen earlier than say impairment in glycogen synthesis in the muscle.

All answers are possible, as there are always more than meet the eye in physiological or pharmacological or patho-physiological questions. However, the most rationale, speaking from a non-pharmacological angle and easiest to understand is the answer of Anu Makela.

I wrote a paper in 2004, where I reported that carbazole alkaloids of Murrraya koenigii, Curry Leaf tree, act by inhibiting insulin release, and hence useful in managing type 2 diabetes resulting from insulin resistance. The slow acting anti-hyperglycaemic nature of the extract and compounds may be due to the time frame it takes for excess insulin to be mopped up from the system, in this case 3 days. The plant and extract also has anti-inflammatory  and febrifuge properties. 

Could these 2 properties in Curry not be a circumstantial evidence to the link of diabetes and inflammation? If so, there are many more palnts with these 2 activities. Since anti-diabetic studies are very expensive, should we not be thinking in line of inflammation studies as a possible in-vitro preliminary test for diabetic studies?

Nevertheless, I believe se