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Is the Future Bright for Diabetes?

Michael M. Bond, DO, Scott W. Yates, MD, MBA, FACP,FACPE
Volume: 97 Issue: 11 November, 2004

Abstract:

There is no doubt that there is an epidemic of diabetes raging in the United States. Type 2 diabetes is characterized by decreased sensitivity to insulin action in muscle, liver, and fat cells, as well as a progressive decline in pancreatic insulin production. The precise causes of insulin resistance and eventual β cell failure remain unclear, however it appears that both genetic predisposition and environmental factors interact.1–3 In particular, obesity and sedentary lifestyle are closely linked to the onset and progression of type 2 diabetes mellitus. Recent trials have confirmed conventional wisdom that weight loss, exercise, and some medications can delay or prevent the onset of diabetes.4,5

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References:

1. Eriksson J, Franssila-Kallunki A, Ekstrand A, et al. Early metabolic defects in persons at increased risk for non-insulin dependent diabetes mellitus. New Engl J Med 1989;321:337–341.
 
2. Matthaei S, Stumvoll M, Kellerer M, et al. Pathophysiology and pharmacological treatment of insulin resistance. Endocr Rev 2000;21:585–618.
 
3. Ferrannini, E. Insulin resistance versus insulin deficiency in non-insulin-dependent diabetes mellitus: problems and prospects. Endocr Rev 1998;19:477–490.
 
4. Hu G, Lindstrom M, Valle T, et al. Physical activity, body mass index, and risk of type 2 diabetes in patients with normal or impaired glucose regulation. Arch Intern Med 2004;164:892–896.
 
5. Diabetes Prevention Research Group. Reduction in the evidence of type 2 diabetes with life-style intervention or metformin. N Engl J Med 2002;346:393–403.
 
6. Despres JP, Lamarche B, Mauriege P, et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med 1996;334:952–957.
 
7. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet1998;352:854–865.
 
8. Putzer G, Ramirez A, Sneed K, et al. Prevalence of patients with type 2 diabetes mellitus reaching the American Diabetes Association’s target guidelines in a university primary care setting. South Med J2004;97:145–148.
 
9. Rizvi AA. Type 2 diabetes: epidemiologic trends, evolving pathogenic concepts, and recent changes in therapeutic approach. South Med J 2004;11:1079–1087.
 
10. Anonymous. New chemical entities and line extensions [AstraZeneca International Web site]. Available at http://www.astrazeneca.com/article/501216.aspx.
 
11. Anonymous. Symlin (pramlintide acetate) [Amylin Pharmaceuticals Web site]. Available athttp://www.amylin.com/Pipeline/Symlin.cfm.
 
12. Anonymous. Exenatide (synthetic exendin-4) [Amylin Pharmaceuticals Web site]. Available athttp://www.amylin.com/Pipeline/AC2993.cfm.
 
13. Zander M, Madsbad S, Madsen JL and Holst JJ. Effect of 6-week course of glucagon-like peptide-1 on glycaemic control, insulin sensitivity, and beta-cell function in type 2 diabetes: a parallel-group study.Lancet 9 March 2002;359:9309.
 
14. Ahren B, Landin-Olsson M, Jansson PA, Svensson M, Holmes D, Schwiezer A. Inhibition of dipeptidyl peptidase-4 reduces glycemia, sustains insulin levels, and reduces glucaton levels in type 2 diabetes. J Clin Endocrinol Metab May 2004;89(5):2078–84.
 
15. Anonymous. Product candidates: oral insulin [Emisphere Technologies, Inc. Web site]. Available athttp://www.emisphere.com/pc_oi.asp.
 
16. Anonymous. Aradigm and Novo Nordisk release interim analysis of initial pulmonary insulin phase 3 trial. Available at http://ir.thomsonfn.com/InvestorRelations/PubNewsStory.aspx?partner=7677&storyId=113007.
 

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