Evidence map›Paper›PMID 28894292›Full record

ArticleInternational journal of obesity (2005)2018

Partitioning of adipose lipid metabolism by altered expression and function of PPAR isoforms after bariatric surgery.

C Jahansouz, H Xu, A V Hertzel, S Kizy, K A Steen, R Foncea, F J Serrot, N Kvalheim, G Luthra, K Ewing and 3 more

RetractedErratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of obesity (2005), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Influence of Weight Loss and Weight Regain on Adipose Tissue Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  4. Article
  5. Review
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  9. Review
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  11. Slc43a3 is a regulator of free fatty acid flux.Journal of lipid research · 2020
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

C JahansouzDepartment of Surgery, University of Minnesota, Minneapolis, MN, USA.
H XuDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA.
A V HertzelDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA.
S KizyDepartment of Surgery, University of Minnesota, Minneapolis, MN, USA.
K A SteenDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA.
R FonceaDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA.
F J SerrotDepartment of Surgery, University of Minnesota, Minneapolis, MN, USA.
N KvalheimDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA.
G LuthraPark Nicollet Bariatric Surgery Center, St. Louis Park, MN, USA.
K EwingCentraCare Bariatric Center, St. Cloud, MN, USA.
D B LeslieDepartment of Surgery, University of Minnesota, Minneapolis, MN, USA.
S IkramuddinDepartment of Surgery, University of Minnesota, Minneapolis, MN, USA.
D A BernlohrDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA.
University of Minnesota · USCentraCare Health System · USPark Nicollet Clinic · US

Funding

Obesity and Energy Metabolism CoreP30DK050456 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BERNLOHR, DAVID A · 1995 to 2015
$17.0M
LIPID BINDING PROTEINS IN OBESITY/DIABETES SYNDROMESR01DK053189 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BERNLOHR, DAVID A · 1998 to 2020
$5.6M
Lipid Binding Proteins in Obesity and Diabetes SyndromesR56DK053189 · NIDDK · UNIVERSITY OF MINNESOTA · PI BERNLOHR, DAVID A · 2011 to 2017
$300k
NIDDK NIH HHS P30 DK050456NIDDK NIH HHS R01 DK053189NIDDK NIH HHS R56 DK053189
6 · The paper itself

Abstract

backgroundBariatric surgery remains the most effective treatment for reducing adiposity and eliminating type 2 diabetes; however, the mechanism(s) responsible have remained elusive. Peroxisome proliferator-activated receptors (PPAR) encompass a family of nuclear hormone receptors that upon activation exert control of lipid metabolism, glucose regulation and inflammation. Their role in adipose tissue following bariatric surgery remains undefined. MATERIALS AND

methodsSubcutaneous adipose tissue biopsies and serum were obtained and evaluated from time of surgery and on postoperative day 7 in patients randomized to Roux-en-Y gastric bypass (n=13) or matched caloric restriction (n=14), as well as patients undergoing vertical sleeve gastrectomy (n=33). Fat samples were evaluated for changes in gene expression, protein levels, β-oxidation, lipolysis and cysteine oxidation.

resultsWithin 7 days, bariatric surgery acutely drives a change in the activity and expression of PPARγ and PPARδ in subcutaneous adipose tissue thereby attenuating lipid storage, increasing lipolysis and potentiating lipid oxidation. This unique metabolic alteration leads to changes in downstream PPARγ/δ targets including decreased expression of fatty acid binding protein (FABP) 4 and stearoyl-CoA desaturase-1 (SCD1) with increased expression of carnitine palmitoyl transferase 1 (CPT1) and uncoupling protein 2 (UCP2). Increased expression of UCP2 not only facilitated fatty acid oxidation (increased 15-fold following surgery) but also regulated the subcutaneous adipose tissue redoxome by attenuating protein cysteine oxidation and reducing oxidative stress. The expression of UCP1, a mitochondrial protein responsible for the regulation of fatty acid oxidation and thermogenesis in beige and brown fat, was unaltered following surgery.

conclusionsThese results suggest that bariatric surgery initiates a novel metabolic shift in subcutaneous adipose tissue to oxidize fatty acids independently from the beiging process through regulation of PPAR isoforms. Further studies are required to understand the contribution of this shift in expression of PPAR isoforms to weight loss following bariatric surgery.

Indexed as

Bariatric SurgeryAdultDiabetes Mellitus, Type 2Fatty Acid-Binding ProteinsFemaleGene Expression RegulationHumansImmunoblottingLipid MetabolismLipolysisMaleObesity, MorbidPPAR deltaSubcutaneous FatTreatment OutcomeUncoupling Protein 2FABP4 protein, humanFatty Acid-Binding ProteinsPPAR deltaUCP2 protein, humanUncoupling Protein 2

Identifiers

PMID28894292
PMCPMC5803459
OpenAlexW2747870087

What OpenQuestion holds

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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.