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Updated: Jul 3, 2026

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets
Published on: May 11, 2015
Initiating insulin in patients with type 2 diabetes
Thomas J Aoki1, Russell D White
1University of California, Davis Health System, Davis, CA; Aoki Diabetes Research Institute, Sacramento, CA USA.
Abstract:
Overall, 7% of the US population has type 2 diabetes mellitus (T2DM), and among people aged 60 years or older, approximately 20% have T2DM, representing a significant health burden in this age group. Furthermore, the incidence of T2DM is increasing as the obesity epidemic increases and more patients are presenting with T2DM at a younger age. Insulin resistance, which is characterized by impaired glucose tolerance, begins years before the onset of T2DM. In response to impaired glucose tolerance, beta-cell function initially increases (manifested as hyperinsulinemia) to compensate for the increased insulin resistance. Subsequently, a progressive loss of first-phase insulin response occurs, which is manifested by progressively increasing postprandial glucose (PPG) levels. Fasting plasma glucose (FPG) levels eventually rise above 126 mg/dL, a level defined as clinical diabetes. As T2DM progresses, beta-cell function deteriorates further and the patient requires progressively more aggressive therapeutic interventions to achieve glycemic control. It is important for family physicians (FPs) to convey this concept of disease progression to patients at the time of diagnosis. Patients should understand that although they can slow disease progression with long-term lifestyle modifications, they will eventually need to change or add medications as the function of the pancreas continues to decline. FPs should also emphasize that disease progression can be limited but not stopped, and thus, patients should not blame themselves, particularly when they follow management recommendations.
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