Evidence map›Paper›PMID 37735685›Full record

ArticleMicrobiome2023

Reducing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome.

N K Newman, Y Zhang, J Padiadpu, C L Miranda, A A Magana, C P Wong, K A Hioki, J W Pederson, Z Li, M Gurung and 9 more

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Microbiome, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
8.4field-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

29 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Cxcl9 as a Marker of Adipose Tissue Changes Caused by Bariatric Surgery and Psoriasis.Clinical, cosmetic and investigational dermatology · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Gut-Adipose Tissue Axis and Metabolic Health.Current issues in molecular biology · 2025
    Review
  18. Article
  19. Article
  20. 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

19 authors at 3 institutions in 1 country.

N K Newman *Department of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, Corvallis, OR, USA.
Y Zhang *School of Biological and Population Health Sciences, Nutrition Program, Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
J Padiadpu *Department of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, Corvallis, OR, USA.
C L MirandaDepartment of Pharmaceutical Sciences, Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
A A MaganaDepartment of Chemistry, Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
C P WongSchool of Biological and Population Health Sciences, Nutrition Program, Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
K A HiokiDepartment of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, Corvallis, OR, USA.
J W PedersonDepartment of Biomedical Sciences, Carlson College of Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
Z LiDepartment of Biomedical Sciences, Carlson College of Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
M GurungDepartment of Biomedical Sciences, Carlson College of Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
A M BruceDepartment of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, Corvallis, OR, USA.
K BrownDepartment of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, Corvallis, OR, USA.
G BobeDepartment of Animal Sciences, Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
T J SharptonDepartment of Microbiology, Department of Statistics, Oregon State University, Corvallis, OR, USA.
N ShulzhenkoDepartment of Biomedical Sciences, Carlson College of Veterinary Medicine, Oregon State University, Corvallis, OR, USA. Natalia.Shulzhenko@oregonstate.edu.
C S MaierDepartment of Chemistry, Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
J F StevensDepartment of Pharmaceutical Sciences, Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
A F Gombart *Department of Biochemistry and Biophysics, Linus Pauling Institute, Corvallis, OR, USA. adrian.gombart@oregonstate.edu.
A Morgun *Department of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, Corvallis, OR, USA. morguna@oregonstate.edu.
Oregon State University · USArkansas Children's Nutrition Center · USOregon Health & Science University · US

Funding

Vitamin D, Xanthohumol and Nuclear Receptors: Targeting Immunity, Microbiota andR01AT009168 · NCCIH · OREGON STATE UNIVERSITY · PI GOMBART, ADRIAN FRIEDRICH, MAIER, CLAUDIA S · 2015 to 2019
$3.0M
Gut microbiota mediates the interplay between immunity and glucose metabolismR01DK103761 · NIDDK · OREGON STATE UNIVERSITY · PI SHULZHENKO, NATALIA · 2015 to 2019
$1.7M
Triple Quadrupole/Linear Ion Trap LC-MS/MS for LPIS10RR027878 · NCRR · OREGON STATE UNIVERSITY · PI STEVENS, JAN FREDERIK · 2010 to 2010
$484k
NCCIH NIH HHS R01 AT009168NCRR NIH HHS S10 RR027878NIDDK NIH HHS DK103761NIDDK NIH HHS R01 DK103761NIH HHS 5R01AT009168
6 · The paper itself

Abstract

backgroundThe gut microbiota contributes to macrophage-mediated inflammation in adipose tissue with consumption of an obesogenic diet, thus driving the development of metabolic syndrome. There is a need to identify and develop interventions that abrogate this condition. The hops-derived prenylated flavonoid xanthohumol (XN) and its semi-synthetic derivative tetrahydroxanthohumol (TXN) attenuate high-fat diet-induced obesity, hepatosteatosis, and metabolic syndrome in C57Bl/6J mice. This coincides with a decrease in pro-inflammatory gene expression in the gut and adipose tissue, together with alterations in the gut microbiota and bile acid composition.

resultsIn this study, we integrated and interrogated multi-omics data from different organs with fecal 16S rRNA sequences and systemic metabolic phenotypic data using a Transkingdom Network Analysis. By incorporating cell type information from single-cell RNA-seq data, we discovered TXN attenuates macrophage inflammatory processes in adipose tissue. TXN treatment also reduced levels of inflammation-inducing microbes, such as Oscillibacter valericigenes, that lead to adverse metabolic phenotypes. Furthermore, in vitro validation in macrophage cell lines and in vivo mouse supplementation showed addition of O. valericigenes supernatant induced the expression of metabolic macrophage signature genes that are downregulated by TXN in vivo.

conclusionsOur findings establish an important mechanism by which TXN mitigates adverse phenotypic outcomes of diet-induced obesity and metabolic syndrome. TXN primarily reduces the abundance of pro-inflammatory gut microbes that can otherwise promote macrophage-associated inflammation in white adipose tissue. Video Abstract.

Indexed as

Gastrointestinal MicrobiomeMetabolic SyndromeAdipose TissueAnimalsInflammationMiceObesityRNA, Ribosomal, 16SRNA, Ribosomal, 16S

Identifiers

PMID37735685
PMCPMC10512512
OpenAlexW4386932174

What Socratic 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 Socratic graph.