Evidence map›Paper›PMID 26658502›Full record

ArticleInvestigative ophthalmology & visual science2015

Effects of Insulin and High Glucose on Human Meibomian Gland Epithelial Cells.

Juan Ding, Yang Liu, David A Sullivan

Open access · hybridAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Immune Fingerprint in Diabetes: Ocular Surface and Retinal Inflammation.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Insulin and the sebaceous gland function.Frontiers in physiology · 2023
    Review
  14. Article
  15. Hyperglycemia Induces Meibomian Gland Dysfunction.Investigative ophthalmology & visual science · 2022
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Corneal alteration and pathogenesis in diabetes mellitus.International journal of ophthalmology · 2019
    Review
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

3 authors at 2 institutions in 1 country.

Juan Ding
Yang Liu
David A Sullivan
Smith-Kettlewell Eye Research Institute · USMassachusetts Eye and Ear Infirmary · US

Funding

Sex, sex steroids and dry eye syndromesR01EY005612 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI SULLIVAN, DAVID A. · 1985 to 2014
$9.0M
The regulation of meibomian gland dysfunction by growth hormone and insulin-likeK99EY023536 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI DING, JUAN · 2014 to 2014
$89k
NEI NIH HHS 1K99EY023536-01A1NEI NIH HHS EY05612NEI NIH HHS K99 EY023536NEI NIH HHS R01 EY005612
6 · The paper itself

Abstract

purposeType 2 diabetes is a risk factor for meibomian gland dysfunction (MGD). We hypothesize that this diabetic impact is due, at least in part, to the effects of insulin resistance/deficiency and hyperglycemia on human meibomian gland epithelial cells (HMGECs). To begin to test this hypothesis, we examined whether insulin and high glucose influence immortalized (I) HMGECs.

methodsImmortalized HMGECs were cultured in serum-containing or -free media and treated with insulin, insulin-like growth factor-1 (IGF-1), IGF-1 receptor (R) blocking antibody, and glucose or mannitol for varying time periods. Specific proteins were detected by Western blots, cell proliferation was evaluated by manual cell counting and lipids were assessed with LipidTOX and high performance thin layer chromatography.

resultsWe found that insulin induces a dose-dependent increase in phosphatidylinositide 3-kinase/Akt (AKT) signaling in IHMGECs. This effect involves the IGF-1R, but not the insulin receptor (IR), and is associated with a stimulation of cell proliferation and neutral lipid accumulation. In contrast, high glucose exposure alters cell morphology, causes a progressive cell loss, and significantly reduces the levels of IGF-1R, phospho (p)-AKT, Foxhead box protein O1 (FOXO1), and sterol-regulatory element binding protein (SREBP-1) in IHMGECs.

conclusionsOur data show that insulin stimulates, and that high glucose is toxic for, IHMGECs. These results support our hypothesis that insulin resistance/deficiency and hyperglycemia are deleterious for HMGECs and may help explain why type II diabetes is a risk factor for MGD.

Indexed as

Blotting, WesternCell CountCell DifferentiationCell ProliferationCells, CulturedDiabetes Mellitus, Type 2Dose-Response Relationship, DrugDry Eye SyndromesEpithelial CellsGlucoseHumansHypoglycemic AgentsInsulinLipid MetabolismLysosomesMeibomian GlandsGlucoseHypoglycemic AgentsInsulin

Identifiers

PMID26658502
PMCPMC4682487
OpenAlexW755322116

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.