The increasing inactivity and high density diets consumed by people in developing and developed countries makes them particularly vulnerable to developing type II (formerly called "adult onset") Diabetes Mellitus (non-insulin dependent DM or NIDDM). How the the phenotype interacts with the environment (in its broadest sense) determines most chronic disease (see Barker's hypothesis). A calorie-dense particularly high fat, high refined carbohydrate diet, together with low levels of activity leads to fat accumulation, which in turn is associated with dyslipidaemia, insulin resistance, vascular occlusion and eventual necrotic and other outcomes, (AMI, PVD retinopathy, nephropathy, stroke). The initial manifestation of these problems is called Syndrome X or Metabolic Syndrome.

The common pathway of these complications is through the production of diffuse vascular damage, by way of both the rapid development of vascular atheroma and fluctuating serum glucose levels. In DM, fluctuating blood glucose is a marker for damage to the basement membrane of the micro-circulation, but not the larger vessels, where atheroma is a more frequent problem. Obviously then, small blood vessels will be affected first, followed by larger vessels, and so tissues reliant on micro-vascular support might be expected to be affected first.

Can you think what tissues are likely to be affected first?