What is type 2 diabetes?

Abstract

Type 2 diabetes is a common metabolic disorder characterized by chronic hyperglycaemia. It is associated with a reduced life expectancy owing to a greater risk of heart disease, stroke, peripheral neuropathy, renal disease, blindness and amputation. At present, the best predictors of increased diabetes risk and progression to diabetes are an elevated fasting plasma glucose, an abnormal glucose tolerance test, obesity and evidence of impaired insulin action. However, the mechanisms by which people with impaired fasting glucose and/or abnormal glucose tolerance `progress' to overt type 2 diabetes are not completely understood. Moreover, type 2 diabetes is defined in a `negative' sense (hyperglycaemia occurring in the absence of evidence of autoimmune destruction of islet cells). This has two consequences - one is the heterogeneity of the disease, the other is that the disease is identified purely in terms of hyperglycaemia, to a certain extent ignoring the underlying mechanisms that lead to the disease. In this review, we explore some of these mechanisms in an attempt to remind readers that hyperglycaemia is one of many abnormalities in type 2 diabetes.

Figure 1

Cumulative incidence of diabetes according to initial fasting plasma glucose Reproduced with permission of the American Diabetes Association from Dinnen SF, et al. Diabet Car 1998; 21: 1408–13.

Figure 2

a. Plasma glucose concentrations observed on glucagon-suppressed vs. non-suppressed study days b. By design, insulin concentrations did not differ on both days of the experiment. However, on one day, glucagon concentrations were suppressed to mimic the postprandial suppression of glucagon seen in non-diabetic individuals Reproduced with permission of the Endocrine Society from Shah P, et al. J Clin Endocrinol Metab 2000; 85: 4053–9.

Figure 2

a. Plasma glucose concentrations observed on glucagon-suppressed vs. non-suppressed study days b. By design, insulin concentrations did not differ on both days of the experiment. However, on one day, glucagon concentrations were suppressed to mimic the postprandial suppression of glucagon seen in non-diabetic individuals Reproduced with permission of the Endocrine Society from Shah P, et al. J Clin Endocrinol Metab 2000; 85: 4053–9.