Type 2 diabetes onset results from chronic low-grade inflammation.
Type 2 diabetes is characterized by insulin resistance. The body is producing enough insulin, but that insulin is less effective than it should be. It is poorly absorbed by the cells – which are said to ‘resist’ the effects of insulin.
In type 2 diabetes the body tries to compensate for this insulin resistance by producing more insulin. So while it may appear as if there is too little insulin (the symptoms of insulin deficiency are present) there may in fact be an actual excess of insulin – especially in the early stages of type 2 diabetes.
Insulin resistance is associated with, or caused by, chronic low-grade inflammation.
There is evidence that insulin resistance in the liver specifically results from over activation of NF-kB. It is likely that insulin resistance in general results from over-activation, though the mechanism remains unclear.
What is clear is that insulin resistance – and therefore diabetes type 2 – results from chronic inflammation.
The implication is that by reducing or eliminating chronic inflammation we will decrease the likelihood of developing diabetes type 2. Further, that reducing or eliminating chronic inflammation would be of benefit in the treatment of diabetes type 2.
The publication:
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Mol Med. 2008 Mar-Apr;14(3-4):222-31.
Inflammatory mechanisms in the regulation of insulin resistance.
Tilg H, Moschen AR.
Department of Gastroenterology and Hepatology, Innsbruck Medical University, Innsbruck, Austria.
Summary of the abstract
Insulin resistance (IR) plays a key role in the pathophysiology of obesity-related diseases such as type 2 diabetes and nonalcoholic fatty liver disease.
It has been demonstrated that IR is associated with a state of chronic low-grade inflammation, and several mediators released from various cell types have been identified as being involved in the development of IR.
Liver cell over activation of NF-kB is associated with IR and can mimic all features of fatty liver disease.
The evidence for an important role of many pro-inflammatory pathways in IR is overwhelming.
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