…according to an article I found in Diabetes Care. As background, be aware that one theory holds that T2 diabetes is caused primarily by body tissue insulin resistance, separate from what’s going on in the pancreas beta (β) cells that produce insulin to control blood sugar.
Although it has long been assumed that insulin resistance is the leading factor in the pathogenesis of type 2 diabetes, evidence for the importance of the pancreatic β-cells has accumulated over the past decades. In fact, the vast majority of genes associated with type 2 diabetes have been linked to the β-cell, and impairments in β-cell mass and in insulin secretion have been reported in numerous studies in patients with type 2 diabetes.
It has also been suggested that obesity causes type 2 diabetes through impaired insulin action. Undoubtedly, the risk of developing type 2 diabetes increases markedly with BMI. However, if obesity were really the cause of type 2 diabetes, one would expect the vast majority of obese individuals to develop hyperglycemia, whereas in reality ∼80% of obese individuals remain free of diabetes. These findings suggest that obesity and insulin resistance are indeed important cofactors that increase the individual risk of diabetes but that the actual cause of the disease seems to be clearly linked to the β-cells.
The conundrum of whether loss of mass or loss of function underlies the β-cell defects in type 2 diabetes is not likely to be conclusively solved on the basis of the evidence we have reviewed here. Decreased cell mass and acceleration of the biological processes resulting in β-cell loss have been described in type 2 diabetes by a number of laboratories. On the other hand, several lines of evidence suggest that β-cell functional defects may exist in type 2 diabetes.
Both viewpoints tacitly assume that 1) type 2 diabetes is a rather homogeneous entity, at least when it comes to β-cell biology, and 2) overall islet secretory capacity is a linear function of the product between β-cell number and isolated β-cell function. It is possible that neither assumption holds true.
The most likely scenario, indeed, is that a variable combination of the two processes, loss of mass and loss of function, is at work in type 2 diabetes. Indeed, there appears to be a tight relationship between mass of pancreatic β-cells and functional insulin secretion.