Evidence map›Paper›PMID 26983960›Full record

ArticleDiabetes2016

Exercise Prevents Diet-Induced Cellular Senescence in Adipose Tissue.

Marissa J Schafer, Thomas A White, Glenda Evans, Jason M Tonne, Grace C Verzosa, Michael B Stout, Daniel L Mazula, Allyson K Palmer, Darren J Baker, Michael D Jensen and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 1 pooled it
13.2field-weighted citation impact, top 1% 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

162 citing papers in PubMed, 1 synthesis or guideline pooled it, 255 citations in OpenAlex.

  1. Pooled it
  2. Biomarkers of Cellular Senescence Predict the Onset of Mobility Disability and Are Reduced by Physical Activity in Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
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  13. Exercise benefits in metabolism on cardiovascular disease.Frontiers in cardiovascular medicine · 2026
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102 more citing papers are in PubMed but not listed here.

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

17 authors at 2 institutions in 1 country.

Marissa J SchaferRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN.
Thomas A WhiteRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN.
Glenda EvansRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN.
Jason M TonneDepartment of Molecular Medicine, Mayo Clinic, Rochester, MN.
Grace C VerzosaDepartment of Surgery, Mayo Clinic, Rochester, MN.
Michael B StoutRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Department of Internal Medicine, Mayo Clinic, Rochester, MN.
Daniel L MazulaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN.
Allyson K PalmerRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN.
Darren J BakerRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, MN.
Michael D JensenDivision of Endocrinology, Department of Medicine, Mayo Clinic, Rochester, MN.
Michael S TorbensonDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN.
Jordan D MillerRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Department of Surgery, Mayo Clinic, Rochester, MN.
Yasuhiro IkedaDepartment of Molecular Medicine, Mayo Clinic, Rochester, MN.
Tamara TchkoniaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN.
Jan M van DeursenRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN.
James L KirklandRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Department of Internal Medicine, Mayo Clinic, Rochester, MN.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN lebrasseur.nathan@mayo.edu.
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

Obesity and Energy Metabolism CoreP30DK050456 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BERNLOHR, DAVID A · 1995 to 2015
$17.0M
Systems Biology and Bioinformatics CoreP01AG041122 · NIA · MAYO CLINIC ROCHESTER · PI CAMPISI, JUDITH · 2012 to 2016
$9.8M
TECHNOLOGY NMR SPECTROSCOPYU24DK100469 · NIDDK · MAYO CLINIC ROCHESTER · PI NAIR, K SREEKUMARAN · 2013 to 2017
$9.0M
BUBRI in Normal and Neoplastic GrowthR01CA096985 · NCI · MAYO CLINIC ROCHESTER · PI BAKER, DARREN · 2002 to 2022
$6.2M
Role of SIRT6 in calcific aortic valve diseaseR01HL111121 · NHLBI · MAYO CLINIC ROCHESTER · PI MILLER, JORDAN D · 2013 to 2017
$2.0M
Removal of Senescent Cells for Adipose-derived Stem Cell TransplantsF30AG046061 · NIA · MAYO CLINIC ROCHESTER · PI PALMER, ALLYSON K · 2013 to 2017
$204k
NCI NIH HHS R01 CA096985NHLBI NIH HHS R01 HL111121NIA NIH HHS F30 AG046061NIA NIH HHS P01 AG041122NIDDK NIH HHS P30 DK050456NIDDK NIH HHS U24 DK100469
6 · The paper itself

Abstract

Considerable evidence implicates cellular senescence in the biology of aging and chronic disease. Diet and exercise are determinants of healthy aging; however, the extent to which they affect the behavior and accretion of senescent cells within distinct tissues is not clear. Here we tested the hypothesis that exercise prevents premature senescent cell accumulation and systemic metabolic dysfunction induced by a fast-food diet (FFD). Using transgenic mice that express EGFP in response to activation of the senescence-associated p16(INK4a) promoter, we demonstrate that FFD consumption causes deleterious changes in body weight and composition as well as in measures of physical, cardiac, and metabolic health. The harmful effects of the FFD were associated with dramatic increases in several markers of senescence, including p16, EGFP, senescence-associated β-galactosidase, and the senescence-associated secretory phenotype (SASP) specifically in visceral adipose tissue. We show that exercise prevents the accumulation of senescent cells and the expression of the SASP while nullifying the damaging effects of the FFD on parameters of health. We also demonstrate that exercise initiated after long-term FFD feeding reduces senescent phenotype markers in visceral adipose tissue while attenuating physical impairments, suggesting that exercise may provide restorative benefit by mitigating accrued senescent burden. These findings highlight a novel mechanism by which exercise mediates its beneficial effects and reinforces the effect of modifiable lifestyle choices on health span.

Indexed as

Adipose TissueAgingAnimalsbeta-GalactosidaseBody CompositionBody WeightCellular SenescenceCyclin-Dependent Kinase Inhibitor p16DietFast FoodsGreen Fluorescent ProteinsMaleMiceMice, TransgenicPhysical Conditioning, Animalbeta-GalactosidaseCyclin-Dependent Kinase Inhibitor p16enhanced green fluorescent proteinGreen Fluorescent Proteins

Identifiers

PMID26983960
PMCPMC4878429
OpenAlexW2304048947

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.