Electrophysiological Measurements Show Marked Differences in the Properties of the Pancreatic β-Cell K-Channels from Albino Mice and a Strain of ob/ob (Obese) Mice

  • L. M. Rosario
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 211)


Several mouse mutants exhibiting obesity or diabetes-like syndromes (e.g. yellow obese, obese, diabetes, KK, New Zealand obese) have been used as animal models of diabetes mellitus11,12,28. They all have hyperglycemia, hyperinsulinemia, and obesity as common metabolic characteristics28. Among these mouse mutants, particular attention has been paid to the homozygous diabetes mouse carrying the diabetes gene (commonly known as the db/db mouse), and the homozygous obese mouse carrying the obese gene (the ob/ob mouse). Besides the metabolic disorders and the insulin receptor defects characteristic of the diabetes-like syndromes, little is known about the possible malfunction of the pancreatic β-cell. In this context, the earlier membrane potential measurements carried out by Meissner and Schmidt in pancreatic β-cells from C57BL/KsJ db/db-mouse islets33 assume a special significance. These authors have shown that the db/db β-cells exhibit a pattern of bursting or continuous electrical activity which is virtually insensitive to the concentration of the natural secretagogue D-glucose, thus suggesting an impairment of the db/db β-cell K+-permeability9. In pancreatic β-cells from normal mouse islets, K+-permeability is now known to play a key role in both the generation and regulation of the glucose-induced bursts of electrical activity3–5,7.


Electrical Activity Mouse Islet Increase Glucose Concentration Potassium Permeability Normal Adult Mouse 


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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • L. M. Rosario
    • 1
  1. 1.Laboratory of Cell Biology and Genetics, NIDDKNational Institutes of HealthBethesdaUSA

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