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Nutrition in Clinical Practice
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Pancreatic Islet Cell Transplantation: A Treatment Strategy for Type I Diabetes Mellitus

Nicholas Onaca, MD
Goran B. Klintmalm, MD, PhD
Marlon F. Levy, MD

Transplant Services, Baylor University Medical Center, Dallas, Texas

Correspondence: Correspondence: Nicholas Onaca, MD, Transplant Services, Baylor University Medical Center, 3500 Gaston Avenue, Dallas, TX 75246. Electronic mail may be sent to nicholao{at}baylorhealth.edu.

Type I diabetes mellitus continues to be a serious disease with long-term morbidity from complications of the disease, despite better knowledge of physiology and better patient care. Pancreatic islet cell transplantation, still experimental, is gaining acceptance as a treatment strategy for individuals with type 1 diabetes who have poor glucose control and frequent hypoglycemic episodes despite maximal care. The procedure can improve glucose control, avoiding further hypoglycemic episodes, and can achieve insulin-independence at the expense of immunosuppression treatment. Islet cell transplantation does not correct all the metabolic abnormalities seen in type 1 diabetes, and glucose tolerance can remain abnormal. The dietary management of the patients still needs to be defined. Further research is focused at improvement in islet isolation and the refinement of immunosuppression strategies aiming toward immune tolerance, bringing hope for a cure of diabetes.

Nutrition in Clinical Practice, Vol. 19, No. 2, 154-164 (2004)
DOI: 10.1177/0115426504019002154
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This article has been cited by other articles:


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 Nutr Clin PractHome page
N. Onaca, B. Naziruddin, S. Matsumoto, H. Noguchi, G. B. Klintmalm, and M. F. Levy
Pancreatic Islet Cell Transplantation: Update and New Developments
Nutr Clin Pract, October 1, 2007; 22(5): 485 - 493.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
T. B. Gibson, M. C. Lawrence, C. J. Gibson, C. A. Vanderbilt, K. McGlynn, D. Arnette, W. Chen, J. Collins, B. Naziruddin, M. F. Levy, et al.
Inhibition of Glucose-Stimulated Activation of Extracellular Signal-Regulated Protein Kinases 1 and 2 by Epinephrine in Pancreatic {beta}-Cells.
Diabetes, April 1, 2006; 55(4): 1066 - 1073.
[Abstract] [Full Text] [PDF]