Evidence map›Paper›PMID 25093462›Full record

ArticleEndocrinology2014

Molecular mechanisms underlying fasting modulated liver insulin sensitivity and metabolism in male lipodystrophic Bscl2/Seipin-deficient mice.

Weiqin Chen, Hongyi Zhou, Pradip Saha, Luge Li, Lawrence Chan

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Ablation ofDisease models & mechanisms · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Exploring Seipin: From Biochemistry to Bioinformatics Predictions.International journal of cell biology · 2018
    Review
  18. Article
  19. Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Weiqin ChenDepartment of Physiology (W.C., H.Z.), Medical College of Georgia at Georgia Regents University, Augusta, Georgia 30912; and Diabetes and Endocrinology Research Center, Division of Diabetes, Endocrinology and Metabolism, Departments of Medicine (P.S., L.L., L.C.), Molecular and Cellular Biology (L.C.), and Biochemistry, Baylor College of Medicine (L.C.), and St. Luke's Medical Center (L.C.), Houston, Texas 77030.
Hongyi Zhou
Pradip Saha
Luge Li
Lawrence Chan
Augusta University · USSt. Luke's Hospital · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
THE ROLE OF LACTOSYLCERAMIDE IN RENAL AGING AND DISEASEP20RR017677 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MAO, CUNGUI · 2002 to 2011
$23.4M
Diabetes Endocrinology Research CenterP30DK079638 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 2008 to 2012
$6.4M
MODELS FOR ATHEROSCLEROSIS RESEARCHR01HL051586 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 1994 to 2014
$5.5M
NCI NIH HHS P30 CA138313NCRR NIH HHS P20 RR017677NHLBI NIH HHS HL-51586NHLBI NIH HHS R01 HL051586NIDDK NIH HHS P30 DK079638NIDDK NIH HHS P30DK079638
6 · The paper itself

Abstract

Bscl2(-/-) mice recapitulate many of the major metabolic manifestations in Berardinelli-Seip congenital lipodystrophy type 2 (BSCL2) individuals, including lipodystrophy, hepatomegly, hepatic steatosis, and insulin resistance. The mechanisms that underlie hepatic steatosis and insulin resistance in Bscl2(-/-) mice are poorly understood. To address this issue, we performed hyperinsulinemic-euglycemic clamp on Bscl2(-/-) and wild-type mice after an overnight (16-h) fast, and found that Bscl2(-/-) actually displayed increased hepatic insulin sensitivity. Interestingly, liver in Bscl2(-/-) mice after a short term (4-h) fast had impaired acute insulin signaling, a defect that disappeared after a 16-hour fast. Notably, fasting-dependent hepatic insulin signaling in Bscl2(-/-) mice was not associated with liver diacylglyceride and ceramide contents, but could be attributable in part to the expression of hepatic insulin signaling receptor and substrates. Meanwhile, increased de novo lipogenesis and decreased β-oxidation led to severe hepatic steatosis in fed or short-fasted Bscl2(-/-) mice whereas liver lipid accumulation and metabolism in Bscl2(-/-) mice was markedly affected by prolonged fasting. Furthermore, mice with liver-specific inactivation of Bscl2 manifested no hepatic steatosis even under high-fat diet, suggesting Bscl2 does not play a cell autonomous role in regulating liver lipid homeostasis. Overall, our results offered new insights into the metabolic adaptations of liver in response to fasting and uncovered a novel fasting-dependent regulation of hepatic insulin signaling in a mouse model of human BSCL2.

Indexed as

AnimalsDisease Models, AnimalFastingGTP-Binding Protein gamma SubunitsHeterotrimeric GTP-Binding ProteinsHumansInsulin ResistanceLipodystrophy, Congenital GeneralizedLiverMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionBscl2 protein, mouseGTP-Binding Protein gamma SubunitsHeterotrimeric GTP-Binding Proteins

Identifiers

PMID25093462
PMCPMC4197977
OpenAlexW2014932253

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.