ABSTRACT
Type 2 diabetes mellitus is defined by hyperglycemia, which is the result of an inability of the pancreas to make enough insulin for an individual’s insulin resistance. Once this relative deficiency in insulin develops, the ability to produce insulin is no longer balanced with the insulin resistance and hepatic glucose production, thus the sugar begins to rise (1). When this mismatch is present, it is a progressive disease with a relentless decline in insulin secretion (2). The therapeutic armamentarium for the management of type 2 diabetes has widely expanded with the introduction of new oral and injectable agents, but their individual blood glucoselowering potency is limited (3). In contrast, the blood glucose-lowering potential of insulin is only limited by the dose that one is willing to take. Insulin therapy should no longer be viewed as a “last resort” to be used after long-term oral agent combinations have failed, but, rather, as a therapeutic tool for earlier use in achieving glycemic targets. Simple strategies for starting insulin therapy with low doses in combination with oral agents have been shown to be effective (4-7). Once patients on combination oral therapy are started on insulin replacement, a structured titration regimen may suffice to accomplish glycemic targets. Many people will require an insulin regimen that will include prandial insulin to address postprandial hyperglycemia and to achieve and maintain target A1c levels.
