Comparison of glucose-induced changes in electrical activity, insulin release, lactate output and potassium permeability between normal and ob/ob mouse islets: effects of cooling

Author:

Scott A. M.,Dawson C. M.,Gonçalves A. A.

Abstract

ABSTRACT A comparison has been made between the glucose-induced changes in electrical activity, insulin release, lactate output and potassium permeability in normal and ob/ob obese (Norwich strain) mice. The electrical response of the islet membrane to high glucose (22·2 mmol/l) stimulation was different in the two types of mice, generating continuous spike activity in normal but producing bursts of activity in ob/ob mouse islets. The absolute amounts of insulin and lactate produced by ob/ob islets in response to both basal and high glucose concentrations were greater than the absolute amounts produced by normal islets, though the ratio of the amount produced in high glucose concentrations to the amount produced in basal glucose concentrations was not significantly different between normal and ob/ob islets for both parameters. Glucose-induced changes in potassium permeability were smaller in ob/ob than in normal mice. Cooling from 37 to 27 °C, during steady-state glucose stimulation, reduced both lactate output and insulin release, the temperature coefficients being similar in both types of mice. The effect of temperature reduction on electrical activity was more marked in the islets of ob/ob mice than in those of normal mice; spike frequency was unaffected in normal but reduced in ob/ob mice, whereas spike amplitude was decreased in both. Cooling-induced inhibition of potassium permeability was greater in the islets of ob/ob mice than in those of normal mice. These results show that this new colony of ob/ob mice (Norwich strain) is comparable to normal mice in terms of the dynamics of insulin release and lactate output in response to glucose, but that the response of the β-cell membrane electrical activity and potassium permeability to glucose is different. J. Endocr. (1985) 107, 265–273

Publisher

Bioscientifica

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism

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