Evidence map›Paper›PMID 27694529›Full record

ArticlePhysiological reports2016

Reduced mitochondrial mass and function add to age-related susceptibility toward diet-induced fatty liver in C57BL/6J mice.

Kerstin Lohr, Fiona Pachl, Amin Moghaddas Gholami, Kerstin E Geillinger, Hannelore Daniel, Bernhard Kuster, Martin Klingenspor

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 33 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

7 authors at 2 institutions in 1 country.

Kerstin LohrChair of Molecular Nutritional Medicine, Technische Universität München, Else Kröner Fresenius Center for Nutritional Medicine, Freising-Weihenstephan, Germany Z I E L - Research Center for Nutrition and Food Sciences, Technische Universität München, Freising-Weihenstephan, Germany.
Fiona PachlChair of Proteomics and Bioanalytics, Technische Universität München Bavarian Biomolecular Mass Spectrometry Center, Freising-Weihenstephan, Germany.
Amin Moghaddas GholamiChair of Proteomics and Bioanalytics, Technische Universität München Bavarian Biomolecular Mass Spectrometry Center, Freising-Weihenstephan, Germany.
Kerstin E GeillingerZ I E L - Research Center for Nutrition and Food Sciences, Technische Universität München, Freising-Weihenstephan, Germany Nutritional Physiology, Technische Universität München, Freising-Weihenstephan, Germany.
Hannelore DanielZ I E L - Research Center for Nutrition and Food Sciences, Technische Universität München, Freising-Weihenstephan, Germany Nutritional Physiology, Technische Universität München, Freising-Weihenstephan, Germany.
Bernhard KusterChair of Proteomics and Bioanalytics, Technische Universität München Bavarian Biomolecular Mass Spectrometry Center, Freising-Weihenstephan, Germany.
Martin KlingensporChair of Molecular Nutritional Medicine, Technische Universität München, Else Kröner Fresenius Center for Nutritional Medicine, Freising-Weihenstephan, Germany Z I E L - Research Center for Nutrition and Food Sciences, Technische Universität München, Freising-Weihenstephan, Germany mk@tum.de.
Technical University of Munich · DEFresenius (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a major health burden in the aging society with an urging medical need for a better understanding of the underlying mechanisms. Mitochondrial fatty acid oxidation and mitochondrial-derived reactive oxygen species (ROS) are considered critical in the development of hepatic steatosis, the hallmark of NAFLD. Our study addressed in C57BL/6J mice the effect of high fat diet feeding and age on liver mitochondria at an early stage of NAFLD development. We therefore analyzed functional characteristics of hepatic mitochondria and associated alterations in the mitochondrial proteome in response to high fat feeding in adolescent, young adult, and middle-aged mice. Susceptibility to diet-induced obesity increased with age. Young adult and middle-aged mice developed fatty liver, but not adolescent mice. Fat accumulation was negatively correlated with an age-related reduction in mitochondrial mass and aggravated by a reduced capacity of fatty acid oxidation in high fat-fed mice. Irrespective of age, high fat diet increased ROS production in hepatic mitochondria associated with a balanced nuclear factor erythroid-derived 2 like 2 (NFE2L2) dependent antioxidative response, most likely triggered by reduced tethering of NFE2L2 to mitochondrial phosphoglycerate mutase 5. Age indirectly influenced mitochondrial function by reducing mitochondrial mass, thus exacerbating diet-induced fat accumulation. Therefore, consideration of age in metabolic studies must be emphasized.

Indexed as

Age FactorsAnimalsCross-Sectional StudiesDiet, High-FatEnergy IntakeFatty AcidsFatty LiverLipid MetabolismLiverMaleMiceMice, Inbred C57BLMitochondriaNF-E2-Related Factor 2Non-alcoholic Fatty Liver DiseaseOxidation-ReductionFatty AcidsNfe2l2 protein, mouseNF-E2-Related Factor 2PGAM5 protein, mousePhosphoprotein PhosphatasesReactive Oxygen SpeciesAgediet‐induced obesityfatty acid oxidationmitochondrianonalcoholic fatty liver diseaseproteomics

Identifiers

PMID27694529
PMCPMC5064140
OpenAlexW2527472313

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.