Evidence map›Paper›PMID 40336478›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2025

Exercise-Stimulated Resolvin Biosynthesis in the Adipose Tissue Is Abrogated by High-Fat Diet-Induced Adrenergic Deficiency.

Ernesto Pena Calderin, Jing-Juan Zheng, Nolan L Boyd, Will Lynch, Brian E Sansbury, Matthew Spite, Bradford G Hill, Jason Hellmann

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Ernesto Pena CalderinCenter for Cardiometabolic Science, Christina Lee Brown Envirome Institute, Division of Environmental Medicine (E.P.C., J.-J.Z., N.L.B., W.L., B.E.S., B.G.H., J.H.), University of Louisville School of Medicine, KY.ORCID 0000-0002-4403-9543
Jing-Juan ZhengCenter for Cardiometabolic Science, Christina Lee Brown Envirome Institute, Division of Environmental Medicine (E.P.C., J.-J.Z., N.L.B., W.L., B.E.S., B.G.H., J.H.), University of Louisville School of Medicine, KY.ORCID 0009-0009-3745-9249
Nolan L BoydCenter for Cardiometabolic Science, Christina Lee Brown Envirome Institute, Division of Environmental Medicine (E.P.C., J.-J.Z., N.L.B., W.L., B.E.S., B.G.H., J.H.), University of Louisville School of Medicine, KY.ORCID 0000-0001-9537-6040
Will LynchCenter for Cardiometabolic Science, Christina Lee Brown Envirome Institute, Division of Environmental Medicine (E.P.C., J.-J.Z., N.L.B., W.L., B.E.S., B.G.H., J.H.), University of Louisville School of Medicine, KY.ORCID 0009-0004-2127-6564
Brian E SansburyCenter for Cardiometabolic Science, Christina Lee Brown Envirome Institute, Division of Environmental Medicine (E.P.C., J.-J.Z., N.L.B., W.L., B.E.S., B.G.H., J.H.), University of Louisville School of Medicine, KY.ORCID 0000-0002-6339-2940
Matthew SpiteCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (M.S.).ORCID 0000-0002-8868-3648
Bradford G HillCenter for Cardiometabolic Science, Christina Lee Brown Envirome Institute, Division of Environmental Medicine (E.P.C., J.-J.Z., N.L.B., W.L., B.E.S., B.G.H., J.H.), University of Louisville School of Medicine, KY.ORCID 0000-0001-5332-8286
Jason HellmannCenter for Cardiometabolic Science, Christina Lee Brown Envirome Institute, Division of Environmental Medicine (E.P.C., J.-J.Z., N.L.B., W.L., B.E.S., B.G.H., J.H.), University of Louisville School of Medicine, KY.ORCID 0000-0001-9573-6843

Funding

TBDP30GM127607 · NIGMS · UNIVERSITY OF LOUISVILLE · PI JONES, STEVEN P · 2018 to 2022
$6.3M
Role of Inflammation-Resolving Lipid Mediators In Ischemic RevascularizationR01HL106173 · NHLBI · UNIVERSITY OF LOUISVILLE · PI SPITE, MATTHEW R · 2011 to 2023
$5.7M
Exercise-enhanced resolution of inflammationR01GM127495 · NIGMS · UNIVERSITY OF LOUISVILLE · PI HELLMANN, JASON L · 2018 to 2022
$2.5M
Effects of Air Pollution on Stem Cell HealthR01ES028268 · NIEHS · UNIVERSITY OF LOUISVILLE · PI HABERZETTL, PETRA, HILL, BRADFORD GUY · 2018 to 2022
$2.2M
Metabolic optimization of cell therapyR01HL130174 · NHLBI · UNIVERSITY OF LOUISVILLE · PI HILL, BRADFORD GUY · 2016 to 2020
$1.9M
High fat diet-induced adrenergic dysfunction and resolution of adipose inflammationF31DK131920 · NIDDK · UNIVERSITY OF LOUISVILLE · PI PENA CALDERIN, ERNESTO HECTOR · 2022 to 2024
$84k
NHLBI NIH HHS R01 HL106173NHLBI NIH HHS R01 HL130174NIDDK NIH HHS F31 DK131920NIEHS NIH HHS R01 ES028268NIGMS NIH HHS P30 GM127607NIGMS NIH HHS R01 GM127495
6 · The paper itself

Abstract

backgroundDiet-induced white adipose tissue inflammation is associated with insulin resistance and metabolic perturbations. Conversely, exercise protects against the development of diet-induced chronic inflammation and insulin resistance independent of weight loss; however, the mechanisms remain largely unknown. We have recently shown that through adrenergic stimulation of macrophages, exercise promotes resolution of acute peritoneal inflammation by enhancing the biosynthesis of specialized proresolving lipid mediators. In this study, we sought to determine whether exercise stimulates proresolving pathways in adipose tissue and whether this response is modified by diet. Specifically, we hypothesized that exercise stimulates proresolving pathways by adrenergic signaling, which is inhibited by high-fat diet, priming the development of chronic inflammation in the adipose tissue.

methodsTo explore the dietary dependence of the proresolving effects of exercise, mice were fed either a control or high-fat diet for 2 weeks before, and throughout, a 4-week period of daily treadmill running. Glucose handling, body weight and composition, lipemia, and exercise performance were evaluated at the end of the feeding and exercise interventions. Likewise, changes in catecholamines and their biosynthetic enzymes were measured along with adipose tissue specialized proresolving lipid mediator levels and macrophage phenotype and abundance.

resultsWhen compared with sedentary controls, macrophages isolated from mice exposed to 4 weeks of exercise display elevated expression of the specialized proresolving lipid mediator biosynthetic enzyme

conclusionsTaken together, these results suggest that a diet high in fat diminishes the proresolving effects of exercise in the adipose tissue via decreasing the biosynthesis of catecholamines.

Indexed as

Adipose TissueAdipose Tissue, WhiteDiet, High-FatEicosapentaenoic AcidPanniculitisPhysical Conditioning, AnimalAnimalsArachidonate 12-LipoxygenaseArachidonate 15-LipoxygenaseDisease Models, AnimalMacrophagesMaleMiceMice, Inbred C57BLSignal TransductionTime FactorsAlox15 protein, mouseArachidonate 12-LipoxygenaseArachidonate 15-LipoxygenaseEicosapentaenoic Acidadipose tissueadrenal glandsdiet, high fatexercisemacrophagesmicespecialized pro-resolving mediators

Identifiers

PMID40336478
PMCPMC12188829

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Registered trials

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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.