Evidence map›Paper›PMID 24153306›Full record

ArticleNature2013

A diurnal serum lipid integrates hepatic lipogenesis and peripheral fatty acid use.

Sihao Liu, Jonathan D Brown, Kristopher J Stanya, Edwin Homan, Mathias Leidl, Karen Inouye, Prerna Bhargava, Matthew R Gangl, Lingling Dai, Ben Hatano and 4 more

Open access · greenAbstract read
In one paragraph

Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 1 pooled it
12.7field-weighted citation impact, top 1% 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

140 citing papers in PubMed, 1 synthesis or guideline pooled it, 225 citations in OpenAlex.

  1. Pooled it
  2. Oxalic acid and diacylglycerol 36:3 are cross-species markers of sleep debt.Proceedings of the National Academy of Sciences of the United States of America · 2015
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80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 3 countries.

Sihao Liu1] Department of Genetics and Complex Diseases, Division of Biological Sciences, Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115, USA [2].
Jonathan D Brown
Kristopher J Stanya
Edwin Homan
Mathias Leidl
Karen Inouye
Prerna Bhargava
Matthew R Gangl
Lingling Dai
Ben Hatano
Gökhan S Hotamisligil
Alan Saghatelian
Jorge Plutzky
Chih-Hao Lee
Harvard University · USAstraZeneca (Japan) · JPBrigham and Women's Hospital · USCentral South University · CN

Funding

Tissue AnalysesP01HL048743 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 1992 to 2014
$26.3M
Interdisciplinary Training in Genes and the EnvironmentT32ES016645 · NIEHS · HARVARD SCHOOL OF PUBLIC HEALTH · PI LEE, CHIH-HAO · 2008 to 2018
$4.0M
PPAR Delta Functions in LiverR01DK075046 · NIDDK · HARVARD SCHOOL OF PUBLIC HEALTH · PI LEE, CHIH-HAO · 2007 to 2015
$3.0M
Hepatic Lipase, PPAR-delta and Fatty Acid MetabolismK08HL105678 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROWN, JONATHAN DAVID · 2011 to 2015
$678k
NHLBI NIH HHS K08 HL105678NHLBI NIH HHS K08HL105678NHLBI NIH HHS P01 HL048743NHLBI NIH HHS R01HL048743NIDDK NIH HHS R01 DK075046NIDDK NIH HHS R01DK075046NIEHS NIH HHS T32 ES016645
6 · The paper itself

Abstract

Food intake increases the activity of hepatic de novo lipogenesis, which mediates the conversion of glucose to fats for storage or use. In mice, this program follows a circadian rhythm that peaks with nocturnal feeding and is repressed by Rev-erbα/β and an HDAC3-containing complex during the day. The transcriptional activators controlling rhythmic lipid synthesis in the dark cycle remain poorly defined. Disturbances in hepatic lipogenesis are also associated with systemic metabolic phenotypes, suggesting that lipogenesis in the liver communicates with peripheral tissues to control energy substrate homeostasis. Here we identify a PPARδ-dependent de novo lipogenic pathway in the liver that modulates fat use by muscle via a circulating lipid. The nuclear receptor PPARδ controls diurnal expression of lipogenic genes in the dark/feeding cycle. Liver-specific PPARδ activation increases, whereas hepatocyte-Ppard deletion reduces, muscle fatty acid uptake. Unbiased metabolite profiling identifies phosphatidylcholine 18:0/18:1 (PC(18:0/18:1) as a serum lipid regulated by diurnal hepatic PPARδ activity. PC(18:0/18:1) reduces postprandial lipid levels and increases fatty acid use through muscle PPARα. High-fat feeding diminishes rhythmic production of PC(18:0/18:1), whereas PC(18:0/18:1) administration in db/db mice (also known as Lepr(-/-)) improves metabolic homeostasis. These findings reveal an integrated regulatory circuit coupling lipid synthesis in the liver to energy use in muscle by coordinating the activity of two closely related nuclear receptors. These data implicate alterations in diurnal hepatic PPARδ-PC(18:0/18:1) signalling in metabolic disorders, including obesity.

Indexed as

Circadian RhythmLipogenesisAcetyl-CoA CarboxylaseAnimalsDiabetes MellitusFatty AcidsGene Expression RegulationHomeostasisLipidsLiverMaleMiceMice, Inbred C57BLMusclesObesityPhosphatidylcholinesAcetyl-CoA CarboxylaseFatty AcidsLipidsPhosphatidylcholinesPPAR delta

Identifiers

PMID24153306
PMCPMC4141623
OpenAlexW2043425632

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.