Evidence map›Paper›PMID 30060148›Full record

ArticleEndocrinology2018

Sex-Dimorphic and Sex Hormone-Dependent Role of Steroid Sulfatase in Adipose Inflammation and Energy Homeostasis.

Yuhan Bi, Mengxi Jiang, Weiwei Guo, Xiudong Guan, Meishu Xu, Songrong Ren, Da Yang, Nilesh W Gaikwad, Kyle W Selcer, Wen Xie

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Adipose Tissue and Endocrine-Disrupting Chemicals: Does Sex Matter?International journal of environmental research and public health · 2020
    Review
  8. Article
  9. Review
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

10 authors at 3 institutions in 2 countries.

Yuhan BiCenter for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Mengxi JiangCenter for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Weiwei GuoCenter for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Xiudong GuanDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Meishu XuCenter for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Songrong RenCenter for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Da YangCenter for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Nilesh W GaikwadGaikwad Steroidomics Laboratory, Davis, California.
Kyle W SelcerDepartment of Biological Sciences, Duquesne University, Pittsburgh, Pennsylvania.
Wen XieCenter for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
University of Pittsburgh · USBeijing Tian Tan Hospital · CNDuquesne University · US

Funding

The AHR-FGF221 Axis in Hepatic Steatosis and Metobolic SyndromeR01DK083952 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIE, WEN · 2010 to 2019
$3.0M
A Novel Regulation of the Phase II Enzyme Estrogen SulfotransferaseR01ES023438 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIE, WEN · 2014 to 2018
$1.7M
NIDDK NIH HHS R01 DK083952NIEHS NIH HHS R01 ES023438
6 · The paper itself

Abstract

Steroid sulfatase (STS), a desulfating enzyme that converts steroid sulfates to hormonally active steroids, plays an important role in the homeostasis of sex hormones. STS is expressed in the adipose tissue of both male and female mice, but the role of STS in the development and function of adipose tissue remains largely unknown. In this report, we show that the adipose expression of Sts was induced in the high-fat diet (HFD) and ob/ob models of obesity and type 2 diabetes. Transgenic overexpression of the human STS in the adipose tissue of male mice exacerbated the HFD-induced metabolic phenotypes, including increased body weight gain and fat mass, and worsened insulin sensitivity, glucose tolerance, and energy expenditure, which were accounted for by adipocyte hypertrophy, increased adipose inflammation, and dysregulation of adipogenesis. The metabolic harm of the STS transgene appeared to have resulted from increased androgen activity in the adipose tissue, and castration abolished most of the phenotypes. Interestingly, the transgenic effects were sex specific, because the HFD-fed female STS transgenic mice exhibited improved metabolic functions, which were associated with attenuated adipose inflammation. The metabolic benefit of the STS transgene in female mice was accounted for by increased estrogenic activity in the adipose tissue, whereas such benefit was abolished upon ovariectomy. Our results revealed an essential role of the adipose STS in energy homeostasis in sex- and sex hormone-dependent manner. The adipose STS may represent a therapeutic target for the management of obesity and type 2 diabetes.

Indexed as

Sex CharacteristicsAdipogenesisAdipose TissueAndrogensAnimalsBody WeightDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalEnergy MetabolismEstrogensFemaleGlucose Tolerance TestGonadal Steroid HormonesHumansInflammationAndrogensEstrogensGonadal Steroid HormonesSteryl-Sulfatase

Identifiers

PMID30060148
PMCPMC6112598
OpenAlexW2884264451

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.