Evidence map›Paper›PMID 28938414›Full record

ArticleEndocrinology2017

Sex- and Tissue-Specific Role of Estrogen Sulfotransferase in Energy Homeostasis and Insulin Sensitivity.

Wojciech G Garbacz, Mengxi Jiang, Meishu Xu, Jun Yamauchi, H Henry Dong, Wen Xie

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Inhibition of Estrogen Sulfotransferase (Journal of the American Society of Nephrology : JASN · 2020
    Article
  10. Article
  11. Article
  12. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Wojciech G GarbaczCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261.
Mengxi JiangCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261.
Meishu XuCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261.
Jun YamauchiDivision of Endocrinology and Diabetes, Department of Pediatrics, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261.
H Henry DongDivision of Endocrinology and Diabetes, Department of Pediatrics, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261.
Wen XieCenter for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15261.
University of Pittsburgh · USChildren's Hospital of Pittsburgh · USUniversity of Pittsburgh Medical Center · 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
Fox01 in Beta-Cell CompensationR01DK098437 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DONG, HENGJIANG HENRY · 2014 to 2017
$1.4M
NIDDK NIH HHS R01 DK083952NIDDK NIH HHS R01 DK098437NIEHS NIH HHS R01 ES023438
6 · The paper itself

Abstract

Estrogen sulfotransferase catalyzes the sulfoconjugation and deactivation of estrogens. Previously, we showed that loss of Est in male ob/ob mice, but not in female ob/ob mice, exacerbated the diabetic phenotype, but the underlying mechanism was unclear. In this study, we show that transgenic reconstitution of Est in the adipose tissue, but not in the liver, attenuated diabetic phenotype in Est-deficient ob/ob mice (obe mice). Mechanistically, adipose reconstitution of Est in obe mice (oae mice) resulted in reduced local and systemic inflammation, improved insulin sensitivity, and increased energy expenditure. At the molecular level, adipose induction of lipocalin-2 (Lcn2) in oae males may have contributed to the inhibition of inflammation because the level of Lcn2 was negatively associated with tumor necrosis factor (Tnf) α expression, and treatment of differentiated adipocytes with Lcn2 antagonized Tnfα-responsive inhibition of insulin signaling. The metabolic benefit of adipose reconstitution of Est was sex specific, because adipose reconstitution of Est in obe females had little effect. Interestingly, despite their improved metabolic functions, obe male mice with reconstituted Est in their adipose tissue failed to ameliorate the impairment of the structure and function of the pancreatic islets. In summary, our study uncovers a crucial adipose- and male-specific role of Est in maintaining the whole-body energy homeostasis.

Indexed as

3T3-L1 CellsAdipose TissueAdiposityAnimalsCells, CulturedEnergy MetabolismFemaleHomeostasisInsulin ResistanceMaleMiceMice, Inbred C57BLMice, ObeseMice, TransgenicOrgan SpecificitySex Factorsestrone sulfotransferaseSulfotransferases

Identifiers

PMID28938414
PMCPMC5695832
OpenAlexW2751589694

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.