Journal of Diabetes and Its Complications
Volume 19, Issue 3 , Pages 178-181 , May 2005

Should minimal blood glucose variability become the gold standard of glycemic control?

  • Irl B. Hirsch

      Affiliations

    • University of Washington Medical Center, Box 356176, 1959 NE Pacific Street, PO Seattle, WA 98105-6176, United States
    • Corresponding Author InformationCorresponding author. Tel.: +1 206 598 4882; fax: +1 206 598 4976.
    • ,
  • Michael Brownlee

      Affiliations

    • Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, United States
    • Department Pathology, Albert Einstein College of Medicine, Bronx, NY, United States

Received 30 September 2004 ,Accepted 19 October 2004.

References 

  1. American Diabetes Association. Standards of medical care in diabetes. Diabetes Care. 2004;27:S15–S35
  2. Betteridge DJ. What is oxidative stress?. Metabolism. 2000;49(Suppl. 1):3–8
  3. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001;414:813–820
  4. Ceriello A, Quagliaro L, Catone B, et al. Role of hyperglycemia in nitrotyrosine postprandial generation. Diabetes Care. 2002;25:1439–1443
  5. Du X, Matsumura T, Edelstein D, et al. Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. Journal of Clinical Investigation. 2003;112:1049–1057
  6. Hirsch IB. Blood glucose monitoring technology: translating data into practice. Endocrine Practice. 2004;10:67–76
  7. Jones SC, Saunders HJ, Qi W, Pollock CA. Intermittent high glucose enhances cell growth and collagen synthesis in cultured human tubulointerstitial cells. Diabetologia. 1999;42:1113–1119
  8. Quagliaro L, Piconi L, Assalone R, Martinelli L, Motz E, Ceriello A. Intermittent high glucose enhances apoptosis related to oxidative stress in human umbilical vein endothelial cells: The role of protein kinase C and NAD(P)H-Oxidase activation. Diabetes. 2003;52:2795–2804
  9. Risso A, Mercuri F, Quagliaro L, Damante G, Ceriello A. Intermitten high glucose enhances apoptosis in human umbilical vein endothelial cells in culture. American Journal of Physiology Endocrinology and Metabolism. 2001;281:E924–E930
  10. Schiekofer S, Andrassy M, Chen J, Rudofsky G, Schneider J, Wendt T, et al. Acute hyperglycemia causes intracellular formation of CML and activation of ras, p42/44 MAPK, and nuclear factor κB in PBMCs. Diabetes. 2003;52:621–633
  11. The Diabetes Control and Complications Trial (DCCT) Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. New England Journal of Medicine. 1993;329:977–986
  12. The Diabetes Control and Complications Trial (DCCT) Research Group. The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the Diabetes Control and Complications Trial. Diabetes. 1995;44:968–983
  13. The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. Effect of intensive therapy on the microvascular complications of type 1 diabetes mellitus. JAMA. 2002;287:2563–2569
  14. The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. Intensive diabetes therapy and carotid intima-media thickness in type 1 diabetes mellitus. New England Journal of Medicine. 2003;348:2294–2303

PII: S1056-8727(04)00114-X

doi: 10.1016/j.jdiacomp.2004.10.001

Journal of Diabetes and Its Complications
Volume 19, Issue 3 , Pages 178-181 , May 2005

Article Tools

* Image Usage & Resolution