Failure of glucose to elicit a normal secretory response in fetal pancreatic beta cells results from glucose insensitivity of the ATP-regulated K+ channels.

Journal article

Fetal pancreatic beta cells demonstrate a deficient insulin release in response to glucose, but the underlying mechanism at the cellular level is unknown. By using beta cells from 21-day fetal rats we made an attempt to clarify the mechanism(s) behind this reduced glucose response. In addition to measuring insulin release, glucose metabolism, and cellular ATP content, ATP-regulated K+ channels (G channels) and voltage-activated Ca2+ currents were investigated with the patch-clamp technique. I...

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Authors: Rorsman, P; Arkhammar, P; Bokvist, K; Hellerström, C; Nilsson, T

• Publication status: Published
• Journal: Proceedings of the National Academy of Sciences of the United States of America
• Volume: 86
• Issue: 12
• Pages: 4505-4509
• Publication date: 1989-06-01
• DOI: 10.1073/pnas.86.12.4505
• EISSN: 1091-6490
• ISSN: 0027-8424
• Language: English
• Keywords: Cell Aggregation; Fetus; Islets of Langerhans; Rats; Insulin; Electric Conductivity; Glucose; Kinetics; Animals; Adenosine Triphosphate; Calcium Channels; Potassium Channels; Tolbutamide