Evidence map›Paper›PMID 30518550›Full record

ArticleThe Journal of biological chemistry2019

Oleate disrupts cAMP signaling, contributing to potent stimulation of pancreatic β-cell autophagy.

Kwan Yi Chu, Liam O'Reilly, Natalie Mellet, Peter J Meikle, Clarissa Bartley, Trevor J Biden

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

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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

6 authors at 3 institutions in 1 country.

Kwan Yi ChuDivision of Diabetes and Metabolism, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010; St. Vincent's Clinical School, Faculty of Medicine, UNSW Sydney, NSW 2052.
Liam O'ReillyDivision of Diabetes and Metabolism, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010.
Natalie MelletBaker IDI Heart and Diabetes Institute, Prahran, Victoria 3004, Australia.
Peter J MeikleBaker IDI Heart and Diabetes Institute, Prahran, Victoria 3004, Australia.
Clarissa BartleyDivision of Diabetes and Metabolism, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010.
Trevor J BidenDivision of Diabetes and Metabolism, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010; St. Vincent's Clinical School, Faculty of Medicine, UNSW Sydney, NSW 2052. Electronic address: t.biden@garvan.org.au.
Baker Heart and Diabetes Institute · AUGarvan Institute of Medical Research · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is critical for maintaining cellular function via clearance of excess nutrients and damaged organelles. In pancreatic β-cells, it helps counter the endoplasmic reticulum (ER) stress that impairs insulin secretory capacity during Type 2 diabetes. Chronic exposure of β-cells to saturated fatty acids (FAs) such as palmitate stimulates ER stress and modulates autophagy, but the effects of unsaturated FAs such as oleate, which are also elevated during obesity, are less well understood. We therefore treated MIN6 cells and mouse islets for 8-48 h with either palmitate or oleate, and then monitored autophagic flux, signaling pathways, lysosomal biology, and phospholipid profiles. Compared with palmitate, oleate more effectively stimulated both autophagic flux and clearance of autophagosomes. The flux stimulation occurred independently of ER stress, nutrient-sensing (mTOR) and signaling pathways (protein kinases A, C, and D). Instead the mechanism involved the exchange factor directly activated by cAMP 2 (EPAC2). Oleate reduced cellular cAMP, and its effects on autophagic flux were reproduced or inhibited, respectively, by

Indexed as

AnimalsApoptosisCyclic AMPGuanine Nucleotide Exchange FactorsInsulin-Secreting CellsMiceMice, Inbred C57BLOleic AcidSignal TransductionTumor Cells, CulturedCyclic AMPGuanine Nucleotide Exchange FactorsOleic AcidRapgef4 protein, mouseautophagybeta cell (B-cell)cyclic AMP (cAMP)lipidpancreatic islet

Identifiers

PMID30518550
PMCPMC6349129
OpenAlexW2902038857

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.