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Am J Physiol Endocrinol Metab (July 31, 2007). doi:10.1152/ajpendo.00359.2007
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Submitted on June 11, 2007
Accepted on July 29, 2007

Metabolic and Electrical Oscillations: Partners in Controlling Pulsatile Insulin Secretion

Richard Bertram1, Arthur Sherman2, and Leslie S. Satin3*

1 Department of Mathematics and Programs in Neuroscience and Molecular Biophysics, Florida State University, Tallahassee, Florida, United States
2 Laboratory of Biological Modeling, National Institutes of Health, NIDDK, Bethesda,, Maryland, United States
3 Department of Pharmacology and Toxicology, Virginia Commonwealth University, Medical College of Virginia Campus, Richmond, Virginia, United States

* To whom correspondence should be addressed. E-mail: lsatin{at}vcu.edu.

Impairment of insulin secretion from the {beta}-cells of the pancreatic islets of Langerhans is central to the development of type 2 diabetes mellitus and has therefore been the subject of much investigation. Great advances have been made in this area, but the mechanisms underlying the pulsatility of insulin secretion remain controversial. The period of these pulses is 4 to 6 minutes, and reflects oscillations in islet membrane potential and intracellular free Ca2+. Pulsatile blood insulin levels appear to play an important physiological role in insulin action, and are lost in patients with type 2 diabetes and their near relatives. We present evidence for a recently developed {beta}-cell model, the "Dual Oscillator Model", in which oscillations in activity are due to both electrical and metabolic mechanisms. This model is capable of explaining much of the available data on islet activity and offers possible resolutions of a number of longstanding issues. The model, however, still lacks direct confirmation and raises new issues. In this article, we highlight both the successes of the model and the challenges that it poses for the field.




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