Evidence map›Paper›PMID 31824770›Full record

ArticlePeerJ2019

Propofol inhibits stromatoxin-1-sensitive voltage-dependent K

Munenori Kusunoki, Mikio Hayashi, Tomohiro Shoji, Takeo Uba, Hiromasa Tanaka, Chisato Sumi, Yoshiyuki Matsuo, Kiichi Hirota

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. HCV affects KEndocrine · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Munenori KusunokiDepartment of Anesthesiology, Kansai Medical University, Hirakata, Japan.
Mikio HayashiDepartment of Cell Physiology, Institute of Biomedical Science, Kansai Medical University, Hirakata, Japan.
Tomohiro ShojiDepartment of Anesthesiology, Kansai Medical University, Hirakata, Japan.
Takeo UbaDepartment of Anesthesiology, Kansai Medical University, Hirakata, Japan.
Hiromasa TanakaDepartment of Human Stress Response Science, Institute of Biomedical Science, Kansai Medical University, Hirakata, Japan.
Chisato SumiDepartment of Anesthesiology, Kansai Medical University, Hirakata, Japan.
Yoshiyuki MatsuoDepartment of Human Stress Response Science, Institute of Biomedical Science, Kansai Medical University, Hirakata, Japan.
Kiichi HirotaDepartment of Human Stress Response Science, Institute of Biomedical Science, Kansai Medical University, Hirakata, Japan.
Kansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProper glycemic control is an important goal of critical care medicine, including perioperative patient care that can influence patients' prognosis. Insulin secretion from pancreatic β-cells is generally assumed to play a critical role in glycemic control in response to an elevated blood glucose concentration. Many animal and human studies have demonstrated that perioperative drugs, including volatile anesthetics, have an impact on glucose-stimulated insulin secretion (GSIS). However, the effects of the intravenous anesthetic propofol on glucose metabolism and insulin sensitivity are largely unknown at present.

methodsThe effect of propofol on insulin secretion under low glucose or high glucose was examined in mouse MIN6 cells, rat INS-1 cells, and mouse pancreatic β-cells/islets. Cellular oxygen or energy metabolism was measured by Extracellular Flux Analyzer. Expression of glucose transporter 2 (GLUT2), potassium channels, and insulin mRNA was assessed by

resultsWe showed that propofol, at clinically relevant doses, facilitates insulin secretion under low glucose conditions and GSIS in MIN6, INS-1 cells, and pancreatic β-cells/islets. Propofol did not affect intracellular ATP or ADP concentrations and cellular oxygen or energy metabolism. The mRNA expression of GLUT2 and channels including the voltage-dependent calcium channels Cav1.2, Kir6.2, and SUR1 subunit of K

conclusionsOur data support the hypothesis that glucose induces membrane depolarization at the distal site, leading to K

Indexed as

AnestheticGlucoseInsulinKv channelPancreatic β-cellsPropofolStromatoxin-1

Identifiers

PMID31824770
PMCPMC6894434
OpenAlexW2989698605

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.