THESIS

ecause of an absolute decrease in the amount of insulin produced by the pancreas
(type 1 diabetes) or because of a relative deficiency of insulin in patients whose
tissues are resistant to the hormone (type 2 diabetes). Insulin resistance is an
impairment of insulin action, especially in the insulin-stimulated uptake of glucose by
the tissue and the inhibition of glucose output by the liver and of fat breakdown
(lipolysis). Insulin resistance is often associated with aberrations in other aspects of
metabolism, especially of lipids, as well as obesity. The hallmark of untreated
diabetes mellitus is elevated blood glucose concentration. It is estimated that 114
million people re suffering from diabetes. By the year 2010, this figure may reach 333
million worldwide. Among the numerous environmental factors that may interact with
genetic potential to develop insulin resistance and type 2-diabetes, the role of dietary
carbohydrate and fiber intake has been investigated. There is evidence that rapidly
digested starches increase the risk of type 2 diabetes. However, there is support for the
contention those eating foods that are rich in slowly digested starch (low GI) and
resistant starch or starch high in soluble fiber, as well as the avoidance of excess
weight and physical inactivity, reduces the risk of developing type 2-diabetes
(Salmeron et al. 1997)
6.4.1 Low GI diet and diabetes mellitus
The trivial effects of low GI foods observed in diabetic subjects over
the short and long terms comprise reduction of post-orandial blood glucose response
(Miller et al. 2003). The majority of studies suggest that foods and diets with low GI
offer greater benefits for diabetes mellitus patients than foods with a high GI (Willet
et al. 2002). A recent meta-analysis (Miller et al. 2003) based on the results of 14
short- and medium-term clinical studies has shown that low GI diet is liked to a
reduction in the concentration of glycosylated haemoglobin and fructisamine, two
major markers that reflect glycaemia control and are linked to potential complications
of diabetes. Furthermore, many animal and human studies demonstrate greater
sensitivity to insulin after a low GI diet than after a high GI diet (Ludwig, 2002).
70