Evidence map›Paper›PMID 1644911›Full record

ArticleThe Journal of clinical investigation1992

Preservation of insulin mRNA levels and insulin secretion in HIT cells by avoidance of chronic exposure to high glucose concentrations.

R P Robertson, H J Zhang, K L Pyzdrowski, T F Walseth

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 7% 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

67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 233 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Nrf2 and Antioxidant Response in Animal Models of Type 2 Diabetes.International journal of molecular sciences · 2023
    Review
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  15. β-Cell dysfunction in diabetes: a crisis of identity?Diabetes, obesity & metabolism · 2016
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

7 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

R P RobertsonDiabetes Center, University of Minnesota Medical School, Minneapolis 55455.
H J Zhang
K L Pyzdrowski
T F Walseth
University of Minnesota · USDiabetes Australia · AU

Funding

PGE RECEPTOR - LIVER AND FAT METABOLISMR01DK038325 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ROBERTSON, RODERICK PAUL · 1986 to 2010
$3.6M
NIDDK NIH HHS R01-DK 38325
6 · The paper itself

Abstract

Glucose toxicity of the pancreatic beta cell is considered to play a secondary role in the pathogenesis of type II diabetes mellitus. To gain insights into possible mechanisms of action of glucose toxicity, we designed studies to assess whether the loss of insulin secretion associated with serial passages of HIT-T15 cells might be caused by chronic exposure to high glucose levels since these cells are routinely cultured in media containing supramaximal stimulatory concentrations of glucose. We found that late passages of HIT cells serially cultured in media containing 11.1 mM glucose lost insulin responsivity and had greatly diminished levels of insulin content and insulin mRNA. In marked contrast, late passages of HIT cells cultured serially in media containing 0.8 mM glucose retained insulin mRNA, insulin content, and insulin responsivity to glucose in static incubations and during perifusion with glucose. No insulin gene mutation or alteration of levels of GLUT-2 were found in late passages of HIT cells cultured with media containing 11.1 mM glucose. These data uniquely indicate that loss of beta cell function in HIT cells passed serially under high glucose conditions is caused by loss of insulin mRNA, insulin content, and insulin secretion and is preventable by culturing HIT cells under low glucose conditions. This strongly suggests potential genetic mechanisms of action for glucose toxicity of beta cells.

Indexed as

AnimalsCell DivisionCell LineCricetinaeCulture MediaGene ExpressionGenesGlucoseInsulinInsulin SecretionIn Vitro TechniquesIslets of LangerhansMesocricetusMonosaccharide Transport ProteinsRNA, MessengerCulture MediaGlucoseInsulinMonosaccharide Transport ProteinsRNA, Messenger

Identifiers

PMID1644911
PMCPMC443105
OpenAlexW2033763256

What OpenQuestion holds

Textmetadata
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.