Evidence map›Paper›PMID 31188872›Full record

ArticlePloS one2019

Obesity-associated, but not obesity-independent, tumors respond to insulin by increasing mitochondrial glucose oxidation.

Aviva Rabin-Court, Marcos R Rodrigues, Xian-Man Zhang, Rachel J Perry

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
1.6field-weighted citation impact, top 16% 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, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Mechanism and recent updates on insulin-related disorders.World journal of clinical cases · 2023
    Review
  4. Article
  5. Obesity: a perfect storm for carcinogenesis.Cancer metastasis reviews · 2022
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Current mechanisms in obesity and tumor progression.Current opinion in clinical nutrition and metabolic care · 2020
    Review
  13. Review
  14. Article
  15. Article
  16. 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

4 authors at 1 institution in 1 country.

Aviva Rabin-CourtDepartment of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Marcos R RodriguesDepartment of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, United States of America.ORCID 0000-0002-3530-7083
Xian-Man ZhangDepartment of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Rachel J PerryDepartment of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, United States of America.ORCID 0000-0003-0748-8064
Yale University · US

Funding

Regulation of tumor growth and metabolism by hyperinsulinemiaR00CA215315 · NCI · YALE UNIVERSITY · PI PERRY, RACHEL JAMISON · 2018 to 2020
$689k
Regulation of tumor growth and metabolism by hyperinsulinemiaK99CA215315 · NCI · YALE UNIVERSITY · PI PERRY, RACHEL JAMISON · 2017 to 2018
$297k
NCI NIH HHS K99 CA215315NCI NIH HHS R00 CA215315
6 · The paper itself

Abstract

Obesity is associated with increased incidence and worse prognosis of more than one dozen tumor types; however, the molecular mechanisms for this association remain under debate. We hypothesized that insulin, which is elevated in obesity-driven insulin resistance, would increase tumor glucose oxidation in obesity-associated tumors. To test this hypothesis, we applied and validated a stable isotope method to measure the ratio of pyruvate dehydrogenase flux to citrate synthase flux (VPDH/VCS, i.e. the percent of total mitochondrial oxidation fueled by glucose) in tumor cells. Using this method, we found that three tumor cell lines associated with obesity (colon cancer [MC38], breast cancer [4T1], and prostate cancer [TRAMP-C3] cells) increase VPDH/VCS in response to physiologic concentrations of insulin. In contrast, three tumor cell lines that are not associated with obesity (melanoma [YUMM1.7], B cell lymphoma [BCL1 clone 5B1b], and small cell lung cancer [NCI-H69] cells) exhibited no oxidative response to insulin. The observed increase in glucose oxidation in response to insulin correlated with a dose-dependent increase in cell division in obesity-associated tumor cell lines when grown in insulin, whereas no alteration in cell division was seen in tumor types not associated with obesity. These data reveal that a shift in substrate preference in the setting of physiologic insulin may comprise a metabolic signature of obesity-associated tumors that differs from that of those not associated with obesity.

Indexed as

AlanineBreast NeoplasmsCell Line, TumorCitrate (si)-SynthaseColonic NeoplasmsFemaleGene Expression RegulationGlucoseGlutamic AcidHumansInsulinIsotope LabelingKetone OxidoreductasesLymphoma, B-CellMaleMelanomaAlanineCitrate (si)-SynthaseGlucoseGlutamic AcidInsulinKetone Oxidoreductasespyruvate dehydrogenase (NADP+)Receptor, Insulin

Identifiers

PMID31188872
PMCPMC6561592
OpenAlexW2952167479

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.