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Q&A:
Beyond Glycemic Control: Managing Obesity and Cardiovascular Disease Risk for Patients With Type 2 Diabetes in the Primary Care Setting
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Steven V. Edelman, MD
University of California, San Diego
Veterans Affairs Medical Center
San Diego, California
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Dr. Edelman provides expert feedback to questions submitted by health care professionals on this topic. These questions were submitted by participants in a CME/CE-certified multimedia activity.
Go online now to participate in this activity:
www.peerviewpress.com/n186
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- Can you add basal insulin such as insulin glargine to a patient already receiving exenatide?
- Will all patients with type 2 diabetes eventually need insulin?
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Can you add basal insulin such as insulin glargine to a patient already receiving exenatide? |
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Although this is an “off-label” approach, many providers are using these agents together, and physiologically the combination makes a lot of sense. Exenatide works mainly on the postprandial glucose levels, whereas basal insulin primarily reduces the fasting glucose levels. There are no safety issues except for a potential of insulin- or sulfonylurea- (if the patient is on one) induced hypoglycemia as the blood glucose levels are lowered. I have used this combination myself at my university clinic with tremendous success in terms of glycemic control and weight maintenance or weight loss. |
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Will all patients with type 2 diabetes eventually need insulin? |
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Type 2 diabetes is at one end of the continuum, represented by the fully compensated insulin-resistant state to impaired glucose tolerance (IGT) to overt type 2 diabetes. A triad of metabolic defects characterizes type 2 diabetes: insulin resistance, nonautoimmune β-cell dysfunction, and inappropriately increased hepatic glucose production. The natural history of type 2 diabetes directly reflects the interrelationships among these 3 defects (Edelman SV, Henry RR. Diagnosis and Management of Type 2 Diabetes. 8th ed. West Islip, NY: Professional Communications, Inc; 2008). The primary and earliest pathogenic lesion is insulin resistance, with the β-cell able to compensate for a variable length of time by secreting supraphysiologic amounts of insulin. Insulin resistance, compensatory hyperinsulinemia, and mild postprandial hyperglycemia characterize IGT. Over time, however, the β-cell begins to fail and as relative insulin deficiency occurs, fasting hyperglycemia and full-blown type 2 diabetes develops. In addition, as insulin levels fall, the inhibitory effect of insulin on hepatic glucose production decreases and significant fasting hyperglycemia develops. Further progression of the disease is marked by an absolute insulin deficiency. Obesity, aging, weight gain in adulthood, and physical inactivity are some of the environmental factors that impact the natural history of diabetes, affecting its progression at all points in the continuum.
We do have some evidence that we can prevent the development of type 2 diabetes in patients with prediabetes via lifestyle changes and use of insulin sensitizers, metformin, and alpha-glucosidase inhibitors; however we do not have long-term studies looking at their effectiveness in altering the natural history of type 2 diabetes to the degree of avoiding insulin therapy (Edelman SV, Henry RR. Diagnosis and Management of Type 2 Diabetes. 8th ed. West Islip, NY: Professional Communications, Inc; 2008). If we can prevent β-cell failure by early diagnosis and aggressive therapy with agents that preserve β-cell function, it is possible that insulin therapy might not be necessary. The ultimate goal is not to avoid insulin therapy but to control glycemia and other cardiovascular risk factors. |
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| This CME/CE activity is jointly sponsored by the University of Florida College of Medicine, Amedco, LLC, and PVI, PeerView Institute for Medical Education. |
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US Physicians – 0.5 AMA PRA Category 1 Credit(s)TM.
US Nurses – 0.5 contact hour(s). |
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| This activity is supported by an educational grant from Amylin Pharmaceuticals, Inc. and Eli Lilly and Company. |
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