Evidence map›Paper›PMID 34157297›Full record

ArticleBiochemical pharmacology2021

Sex-specific expression mechanism of hepatic estrogen inactivating enzyme and transporters in diabetic women.

Muluneh Fashe, MyeongJin Yi, Tatsuya Sueyoshi, Masahiko Negishi

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

Article in Biochemical pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Metabolic Messengers: oestradiol.Nature metabolism · 2025
    Review
  4. Mechanisms of altered hepatic drug disposition during pregnancy: small molecules.Expert opinion on drug metabolism & toxicology · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
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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

4 authors at 1 institution in 1 country.

Muluneh FashePharmacogenetics Section, Reproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: muluneh@email.unc.edu.
MyeongJin YiPharmacogenetics Section, Reproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Tatsuya SueyoshiPharmacogenetics Section, Reproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Masahiko NegishiPharmacogenetics Section, Reproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: negishi@niehs.nih.gov.
National Institutes of Health · US

Funding

Structural Study Of SulfotransferasesZ01ES071005 · NIEHS · ENVIRONMENTAL HEALTH SCIENCES · PI NEGISHI, MASAHIKO · 1999 to 2007
$388k
Intramural NIH HHS Z01 ES071005
6 · The paper itself

Abstract

Circulating estrogens levels significantly decrease in menopause and levels off in postmenopausal women. Accordingly, the liver represses levels of enzymes and membrane transporters, thereby decreasing capability of inactivating and excreting estrogens. Women increasingly develop type 2 diabetes during or after menopause. Estrogens are known to promote liver diseases in these women. Here, we have found that the estrogen inactivating sulfotransferase (SULT1E1) and an ATP-binding cassette subfamily G member 2 (ABCG2), a gene encoding breast cancer resistance protein that exports sulfated estrogens, increased their expression levels in diabetic women but not men. For the sulfotransferase gene, phosphorylated nuclear receptors ERα and RORα, at Ser212 and Ser100, respectively, bind their response elements to activate the SULT1E1 promoter in women. This coordinated increase in estrogen inactivation and excretion, and the phosphorylated nuclear receptor-mediated gene activation could be a defense mechanism against toxicities of estrogens through inactivation and excretion in the livers of women.

Indexed as

AdultAgedAnimalsATP Binding Cassette Transporter, Subfamily G, Member 2Chlorocebus aethiopsCOS CellsDiabetes Mellitus, Type 2Estrogen Receptor alphaFemaleGene Expression RegulationHumansLiverMaleMiddle AgedNeoplasm ProteinsNuclear Receptor Subfamily 1, Group F, Member 1ABCG2 protein, humanATP Binding Cassette Transporter, Subfamily G, Member 2Estrogen Receptor alphaestrone sulfotransferaseNeoplasm ProteinsNuclear Receptor Subfamily 1, Group F, Member 1RORA protein, humanSulfotransferasesDiabetesEstrogensEstrogen sulfotransferaseGenderGene expressionHuman liver

Identifiers

PMID34157297
PMCPMC8344073
OpenAlexW3173923847

What OpenQuestion holds

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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.