Evidence map›Paper›PMID 26993496›Full record

ArticleDiabetes & vascular disease research2016

(-)-Epicatechin-induced recovery of mitochondria from simulated diabetes: Potential role of endothelial nitric oxide synthase.

Israel Ramírez-Sánchez, Alonso Rodríguez, Aldo Moreno-Ulloa, Guillermo Ceballos, Francisco Villarreal

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes & vascular disease research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.7field-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

31 citing papers in PubMed, 55 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

5 authors at 2 institutions in 2 countries.

Israel Ramírez-SánchezSección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, México D.F., Mexico Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
Alonso RodríguezDepartment of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
Aldo Moreno-UlloaSección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, México D.F., Mexico Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
Guillermo CeballosSección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, México D.F., Mexico.
Francisco VillarrealDepartment of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA fvillarr@ucsd.edu.
University of California, San Diego · USInstituto Politécnico Nacional · MX

Funding

Epicatechin and derivatives to preserve muscle structure function in diabetesR01DK098717 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HENRY, ROBERT ROY, VILLARREAL, FRANCISCO J · 2014 to 2017
$1.4M
Targeting cellular bioenergetics for the prevention and treatment of diabetesR24DK092154 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI VILLARREAL, FRANCISCO J · 2011 to 2011
$459k
NIDDK NIH HHS R01 DK098717NIDDK NIH HHS R24 DK092154
6 · The paper itself

Abstract

(-)-Epicatechin increases indicators associated with mitochondrial biogenesis in endothelial cells and myocardium. We investigated endothelial nitric oxide synthase involvement on (-)-epicatechin-induced increases in indicators associated with mitochondrial biogenesis in human coronary artery endothelial cells cultured in normal-glucose and high-glucose media, as well as to restore indicators of cardiac mitochondria from the effects of simulated diabetes. Here, we demonstrate the role of endothelial nitric oxide synthase on (-)-epicatechin-induced increases in mitochondrial proteins, transcription factors and sirtuin 1 under normal-glucose conditions. In simulated diabetes endothelial nitric oxide synthase function, mitochondrial function-associated and biogenesis-associated indicators were adversely impacted by high glucose, effects that were reverted by (-)-epicatechin. As an animal model of type 2 diabetes, 2-month old C57BL/6 mice were fed a high-fat diet for 16 weeks. Fasting and fed blood glucose levels were increased and NO plasma levels decreased. High-fat-diet-fed mice myocardium revealed endothelial nitric oxide synthase dysfunction, reduced mitochondrial activity and markers of mitochondrial biogenesis. The administration of 1 mg/kg (-)-epicatechin for 15 days by oral gavage shifted these endpoints towards control mice values. Results suggest that endothelial nitric oxide synthase mediates (-)-epicatechin-induced increases of indicators associated with mitochondrial biogenesis in endothelial cells. (-)-Epicatechin also counteracts the negative effects that high glucose or simulated type 2 diabetes has on endothelial nitric oxide synthase function.

Indexed as

AnimalsCatechinCells, CulturedDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalEndothelial CellsEnzyme InhibitorsHumansMice, Inbred C57BLMitochondria, HeartMyocardiumNitric OxideNitric Oxide Synthase Type IIIOrganelle BiogenesisPhosphorylationCatechinEnzyme InhibitorsNitric OxideNitric Oxide Synthase Type IIINOS3 protein, humanNos3 protein, mousecardiomyocytesdiabetesendothelial cellsendothelial nitric oxide synthase(-)-Epicatechin

Identifiers

PMID26993496
PMCPMC5107246
OpenAlexW2299224499

What OpenQuestion holds

Textmetadata
LicenceTDM
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.