Evidence map›Paper›PMID 22890841›Full record

ArticleMolecular and cellular biology2012

Disruption of the selenocysteine lyase-mediated selenium recycling pathway leads to metabolic syndrome in mice.

Lucia A Seale, Ann C Hashimoto, Suguru Kurokawa, Christy L Gilman, Ali Seyedali, Frederick P Bellinger, Arjun V Raman, Marla J Berry

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Global loss of selenocysteine lyase in mice drives lipid accumulation in brown adipocytes.American journal of physiology. Endocrinology and metabolism · 2026
    Article
  6. Article
  7. Review
  8. Cardiac redox imbalance upon disruption of selenocysteine decomposition in mice.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  9. A selenomethionine deficient, high-fructose diet does not lead to cardiometabolic disorder in the selenocysteine lyase knockout mice.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Selenium and selenoproteins in thermogenic adipocytes.Archives of biochemistry and biophysics · 2022
    Review
  16. Selenium status and type 2 diabetes risk.Archives of biochemistry and biophysics · 2022
    Review
  17. Review
  18. Review
  19. Review
  20. Review

7 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Lucia A SealeDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii, USA.
Ann C Hashimoto
Suguru Kurokawa
Christy L Gilman
Ali Seyedali
Frederick P Bellinger
Arjun V Raman
Marla J Berry
University of Hawaiʻi at Mānoa · US

Funding

WORLDWIDE EPIDEMIOLOGY &EPIZOOTIOLOGY OF HANTAVIRUSG12RR003061 · NCRR · UNIVERSITY OF HAWAII AT MANOA · PI ALLEN, JOHN A · 1986 to 2011
$32.3M
RESEARCH DESIGN, BIOSTATISTICS AND RESEARCH ETHICS COREG12MD007601 · NIMHD · UNIVERSITY OF HAWAII AT MANOA · PI BERRY, MARLA J · 2012 to 2016
$13.0M
MECHANISM OF SELENOPROTEIN SYNTHESIS IN EUKARYOTESR01DK047320 · NIDDK · UNIVERSITY OF HAWAII AT MANOA · PI BERRY, MARLA J · 1994 to 2020
$5.8M
NCRR NIH HHS G12 RR003061NCRR NIH HHS G12-RR003061NIDDK NIH HHS R01 DK047320NIDDK NIH HHS R01-DK47320NIMHD NIH HHS G12 MD007601NIMHD NIH HHS G12-MD007601
6 · The paper itself

Abstract

Selenium (Se) is an essential trace element used for biosynthesis of selenoproteins and is acquired either through diet or cellular recycling mechanisms. Selenocysteine lyase (Scly) is the enzyme that supplies Se for selenoprotein biosynthesis via decomposition of the amino acid selenocysteine (Sec). Knockout (KO) of Scly in a mouse affected hepatic glucose and lipid homeostasis. Mice lacking Scly and raised on an Se-adequate diet exhibit hyperinsulinemia, hyperleptinemia, glucose intolerance, and hepatic steatosis, with increased hepatic oxidative stress, but maintain selenoprotein levels and circulating Se status. Insulin challenge of Scly KO mice results in attenuated Akt phosphorylation but does not decrease phosphorylation levels of AMP kinase alpha (AMPKα). Upon dietary Se restriction, Scly KO animals develop several characteristics of metabolic syndrome, such as obesity, fatty liver, and hypercholesterolemia, with aggravated hyperleptinemia, hyperinsulinemia, and glucose intolerance. Hepatic glutathione peroxidase 1 (GPx1) and selenoprotein S (SelS) production and circulating selenoprotein P (Sepp1) levels are significantly diminished. Scly disruption increases the levels of insulin-signaling inhibitor PTP1B. Our results suggest a dependence of glucose and lipid homeostasis on Scly activity. These findings connect Se and energy metabolism and demonstrate for the first time a unique physiological role of Scly in an animal model.

Indexed as

AMP-Activated Protein KinasesAnimalsFatty LiverGlucose IntoleranceGlutathione PeroxidaseGlutathione Peroxidase GPX1HypercholesterolemiaHyperinsulinismLeptinLyasesMaleMetabolic SyndromeMiceMice, Inbred C57BLMice, KnockoutObesityAMP-Activated Protein KinasesGlutathione PeroxidaseGlutathione Peroxidase GPX1Gpx1 protein, mouseLeptinLyasesPrkaa1 protein, mouseProtein Tyrosine Phosphatase, Non-Receptor Type 1Proto-Oncogene Proteins c-aktPtpn1 protein, mouseSeleniumselenocysteine lyaseSelenoproteins

Identifiers

PMID22890841
PMCPMC3457337
OpenAlexW1997472526

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.