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August 1, 1991British Journal of PharmacologyOpen Access

Barbiturates inhibit ATP‐K+channels and voltage‐activated currents in CRI‐G1 insulin‐secreting cells

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Population

CRI-G1 insulin-secreting cells

Design

Preclinical

Authors

RKRoland Z. KozlowskiMansfield UniversityMAMichael L.J. AshfordUniversity of Dundee

Discussion

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Overview

Certain barbiturates may impair beta-cell insulin release via KATP blockade; leaves open in vivo relevance and clinical glucose effects.

Structured PICO

P
Population
CRI-G1 insulin-secreting cells
I
Intervention
Barbiturates (thiopentone, secobarbitone, pentobarbitone, phenobarbitone) and alloxan
O
Outcome
Inhibition of ATP-K+ channel activity and voltage-activated whole-cell currentssurrogate

Barbiturates inhibit ATP-K+ channels in insulin-secreting cells, likely through a membrane-mediated mechanism driven by hydrophobicity.

Cite This Study

Kozlowski et al. (1991) studied this question.

synapsesocial.com/papers/6a855dd9f047f857d83d9f50https://doi.org/10.1111/j.1476-5381.1991.tb12370.x
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Also Consider

Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Effects of sulphonylureas and diazoxide on insulin secretion and nucleotide‐sensitive channels in an insulin‐secreting cell line1988 · 170 citations
  2. 2Barbiturates Block Sodium and Potassium Conductance Increases in Voltage-Clamped Lobster Axons1968 · 109 citations
  3. 3Regulation of the Voltage Gated K<sup>+</sup> Channel K<sub>v1.3</sub> by Recombinant Human Klotho Protein2014 · 5,603 citations