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Research Article Free access | 10.1172/JCI118688

Alterations in basal and glucose-stimulated voltage-dependent Ca2+ channel activities in pancreatic beta cells of non-insulin-dependent diabetes mellitus GK rats.

S Kato, H Ishida, Y Tsuura, K Tsuji, M Nishimura, M Horie, T Taminato, S Ikehara, H Odaka, I Ikeda, Y Okada, and Y Seino

Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Department of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.

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Published June 1, 1996 - More info

Published in Volume 97, Issue 11 on June 1, 1996
J Clin Invest. 1996;97(11):2417–2425. https://doi.org/10.1172/JCI118688.
© 1996 The American Society for Clinical Investigation
Published June 1, 1996 - Version history
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Abstract

In genetically occurring non-insulin-dependent diabetes mellitus (NIDDM) model rats (GK rats), the activities of L- and T-type Ca2+ channels in pancreatic beta cells are found to be augmented, by measuring the Ba2+ currents via these channels using whole-cell patch-clamp technique, while the patterns of the current-voltage curves are indistinguishable. The hyper-responsiveness of insulin secretion to nonglucose depolarizing stimuli observed in NIDDM beta cells could be the result, therefore, of increased voltage-dependent Ca2+ channel activity. Perforated patch-clamp recordings reveal that the augmentation of L-type Ca2+ channel activity by glucose is markedly less pronounced in GK beta cells than in control beta cells, while glucose-induced augmentation of T-type Ca2+ channel activity is observed neither in the control nor in the GK beta cells. This lack of glucose-induced augmentation of L-type Ca2+ channel activity in GK beta cells might be causatively related to the selective impairment of glucose-induced insulin secretion in NIDDM beta cells, in conjunction with an insufficient plasma membrane depolarization due to impaired closure of the ATP-sensitive K+ channels caused by the disturbed intracellular glucose metabolism in NIDDM beta cells.

Version history
  • Version 1 (June 1, 1996): No description
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