Evidence map›Paper›PMID 19751410›Full record

ReviewAnnals of the New York Academy of Sciences2009

From sugar to fat: How the transcription factor XBP1 regulates hepatic lipogenesis.

Laurie H Glimcher, Ann-Hwee Lee

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Characterizing the Ovarian Cytogenetic Dynamics of Sichuan Bream (International journal of molecular sciences · 2025
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  3. RNA-seq analysis reveals transcriptome changes in livers fromBiochemistry and biophysics reports · 2025
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  7. Review
  8. Sterol and lipid metabolism in bees.Metabolomics : Official journal of the Metabolomic Society · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
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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

2 authors at 1 institution in 1 country.

Laurie H GlimcherDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA. lglimche@hsph.harvard.edu
Ann-Hwee Lee
Harvard University · US

Funding

Arming the Immune System Against PathogensP01AI056296 · NIAID · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI GLIMCHER, LAURIE HOLLIS · 2003 to 2007
$20.0M
TRANSCRIPTIONAL REGULATION OF THE IMMUNE RESPONSER01AI032412 · NIAID · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI GLIMCHER, LAURIE HOLLIS · 1991 to 2010
$4.6M
NIAID NIH HHS AI32412NIAID NIH HHS P01 AI056296NIAID NIH HHS P01 AI56296NIAID NIH HHS R01 AI032412
6 · The paper itself

Abstract

Lipogenesis occurs primarily in the liver, where dietary carbohydrates control the expression of key enzymes in glycolytic and lipogenic pathways. We have recently discovered that the transcription factor XBP1, best known as a key regulator of the unfolded protein response (UPR), is required for de novo fatty acid synthesis in the liver, a function unrelated to its role in the UPR.(1) XBP1 protein expression is induced in the liver by a high carbohydrate diet and directly controls the induction of critical genes involved in fatty acid synthesis. Specific deletion of XBP1 in adult liver using an inducible approach results in profound hypocholesterolemia and hypotriglyceridemia, which could be attributed to diminished production of lipids in the liver. Notably, this phenotype is not associated with fatty liver (hepatic steatosis) or significant compromise in protein secretion. XBP1 joins an already rich field of transcriptional regulatory proteins in the control of hepatic lipogenesis. Its function in lipogenesis appears to be highly significant as evidenced by the phenotype of the genetic mutant strain. A more complete understanding of the mechanisms by which XBP1 accelerates de novo fatty acid synthesis in the liver while preserving normal hepatic lipid composition is highly relevant to the treatment of diseases such as atherosclerosis and metabolic syndrome that are associated with dyslipidemia. Since excess fat accumulation in the liver could result from increased hepatic fatty acid synthesis, compounds that inhibit XBP1 activation may also be useful therapeutics for the treatment of human alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD), increasingly common causes of morbidity and mortality in the United States.

Indexed as

AdultCarbohydratesCholesterolDietary CarbohydratesDNA-Binding ProteinsDyslipidemiasFatty AcidsGenes, MHC Class IIHumansInsulin ResistanceLipidsLiverMetabolic DiseasesMetabolic SyndromeObesityRegulatory Factor X Transcription FactorsCarbohydratesCholesterolDietary CarbohydratesDNA-Binding ProteinsFatty AcidsLipidsRegulatory Factor X Transcription FactorsRNA, MessengerTranscription FactorsTriglyceridesX-Box Binding Protein 1XBP1 protein, human

Identifiers

PMID19751410
PMCPMC3096021
OpenAlexW1935526712

What OpenQuestion holds

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LicenceTDM
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.