Evidence map›Paper›PMID 23639358›Full record

ArticleJournal of molecular biology2013

Regulation of lipoprotein assembly, secretion and fatty acid β-oxidation by Krüppel-like transcription factor, klf-3.

Jun Zhang, Sanya Hashmi, Fatima Cheema, Nafla Al-Nasser, Razan Bakheet, Ranjit S Parhar, Futwan Al-Mohanna, Randy Gaugler, M Mahmood Hussain, Sarwar Hashmi

Abstract read
In one paragraph

Article in Journal of molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  9. From worms to humans: Understanding intestinal lipid metabolism via model organisms.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023
    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

10 authors at 3 institutions in 2 countries.

Jun ZhangDevelopmental Biology, New York Blood Center, New York, NY 10065, USA.
Sanya Hashmi
Fatima Cheema
Nafla Al-Nasser
Razan Bakheet
Ranjit S Parhar
Futwan Al-Mohanna
Randy Gaugler
M Mahmood Hussain
Sarwar Hashmi
Rutgers, The State University of New Jersey · USKing Faisal Specialist Hospital & Research Centre · SANew York Blood Center · US

Funding

MOLECULAR MECHANISMS OF CHYLOMICRON ASSEMBLYR01DK046900 · NIDDK · SUNY DOWNSTATE MEDICAL CENTER · PI HUSSAIN, M MAHMOOD · 2001 to 2011
$3.0M
Avoiding toxicity associated with MTP ablationR01HL095924 · NHLBI · SUNY DOWNSTATE MEDICAL CENTER · PI HUSSAIN, M MAHMOOD · 2010 to 2013
$1.9M
NHLBI NIH HHS R01 HL095924NIDDK NIH HHS R01 DK046900
6 · The paper itself

Abstract

Lipid metabolism is coordinately regulated through signaling networks that integrate biochemical pathways of fat assimilation, mobilization and utilization. Excessive diversion of fat for storage is a key risk factor for many fat-related human diseases. Dietary lipids are absorbed from the intestines and transported to various organs and tissues to provide energy and maintain lipid homeostasis. In humans, disparity between triglycerides (TG) synthesis and removal, via mitochondrial β-oxidation and VLDL (very low density lipoprotein) secretion, causes excessive TG accumulation in the liver. The mutation in Caenorhabditis elegans KLF-3 leads to high TG accumulation in the worm's intestine. Our previous data suggested that klf-3 regulates lipid metabolism by promoting fatty acid β-oxidation. Depletion of cholesterol in the diet has no effect on fat deposition in klf-3 (ok1975) mutants. Addition of vitamin D in the diet, however, increases fat levels in klf-3 worms. This suggests that excess vitamin D may be lowering the rate of fatty acid β-oxidation, with the eventual increase in fat accumulation. We also demonstrate that mutation in klf-3 reduces expression of C. elegans dsc-4 and/or vit genes, the orthologs of mammalian microsomal triglyceride transfer protein and apolipoprotein B, respectively. Both microsomal triglyceride transfer protein and apolipoprotein B are essential for mammalian lipoprotein assembly and transport, and mutation in both dsc-4 (qm182) and vit-5 (ok3239) results in high fat accumulation in worm intestine. Genetic interactions between klf-3 and dsc-4, as well as vit-5 genes, suggest that klf-3 may have an important role in regulating lipid assembly and secretion.

Indexed as

Gene Expression RegulationAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsFatty AcidsKruppel-Like Transcription FactorsLipoproteinsMutant ProteinsOxidation-ReductionTranscription FactorsCaenorhabditis elegans ProteinsFatty AcidsKLF-3 protein, C elegansKruppel-Like Transcription FactorsLipoproteinsMutant ProteinsTranscription Factors4′,6-diamidino-2-phenylindoleapoBapolipoprotein BC. elegansDAPIFAfatty acidfatty acid β-oxidationIFAimmunofluorescence assayklflipoprotein assembly and secretionmicrosomal triglyceride transfer proteinMTPnematode growth mediumNGMPBSphosphate-buffered salinepolyunsaturated fatty acidPUFAreal-time PCRRT-PCR

Identifiers

PMID23639358
PMCPMC4371790
OpenAlexW2080904805

What Socratic holds

Textmetadata
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 Socratic graph.