I always believed insulin is the right treatment for declining beta cell dysfunction though OHA are used as first line . This review article published in Lancet confirms my view.
The natural history of type 2 diabetes is characterised by worsening hyperglycaemia and progressive deterioration in function of the insulin-secreting pancreatic β cells. Despite intense investigative efforts, the pathophysiological basis underlying β-cell dysfunction (and the concomitant loss of β-cell mass) remains unclearNevertheless, the central importance of declining β-cell function in type 2 diabetes is underscored by its correlation with a progressive loss of glycaemic control, which typically occurs over time. Although β-cell dysfunction contributes to worsening glycaemia, hyperglycaemia itself further undermines β-cell function. This so-called glucotoxicity is apparent in the observation that the first-phase component of normal biphasic insulin secretion is abolished when the blood glucose concentration exceeds 6·4 mmol/L. Accordingly, early in the course of type 2 diabetes (ie, when sufficient residual β-cell mass still exists), the glucose-lowering effect of antidiabetic therapy can be amplified by improved endogenous insulin secretion secondary to the elimination of hyperglycaemia. Unfortunately, however, this effect is ultimately transient, because no oral antidiabetic agent has yet been shown to profoundly change the inexorable β-cell deterioration and worsening glycaemia in type 2 diabetes.
