Evidence map›Paper›PMID 32212194›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Metabolic-sensing of the skeletal muscle clock coordinates fuel oxidation.

Hongshan Yin, Weini Li, Somik Chatterjee, Xuekai Xiong, Pradip Saha, Vijay Yechoor, Ke Ma

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-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

20 citing papers in PubMed, 28 citations in OpenAlex.

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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

7 authors at 5 institutions in 2 countries.

Hongshan YinDepartment of Cardiology, Third Affiliated Hospital of Hebei Medical University, Shijiazhuang, China.
Weini LiDepartment of Diabetes Complications & Metabolism, Beckman Research Institute of City of Hope, Duarte, CA, USA.
Somik ChatterjeeDepartment of Medicine, Baylor College of Medicine, Houston, TX, USA.
Xuekai XiongDepartment of Diabetes Complications & Metabolism, Beckman Research Institute of City of Hope, Duarte, CA, USA.
Pradip SahaDepartment of Medicine, Baylor College of Medicine, Houston, TX, USA.
Vijay YechoorDiabetes and Beta Cell Biology Center, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Ke MaDepartment of Diabetes Complications & Metabolism, Beckman Research Institute of City of Hope, Duarte, CA, USA.
Baylor College of Medicine · USBeckman Research InstituteCity of Hope · USThird Hospital of Hebei Medical University · CNUniversity of Pittsburgh · US

Funding

Circadian Clock Control of Adipose Depot Development and FunctionR01DK112794 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI MA, KE · 2018 to 2021
$1.7M
Circadian Clock and Beta Cell Stress AdaptationR01DK097160 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI YECHOOR, VIJAY K · 2014 to 2018
$1.7M
NIDDK NIH HHS R01 DK097160NIDDK NIH HHS R01 DK112794
6 · The paper itself

Abstract

Circadian clock confers temporal control in metabolism, with its disruption leading to the development of insulin resistance. Metabolic substrate utilization in skeletal muscle is coordinated with diurnal nutrient cycles. However, whether the molecular clock is involved in this coordination is largely unknown. Using a myocyte-selective genetic ablation mouse model of the essential clock activator Bmal1, here we identify muscle-intrinsic clock as a sensor of feeding cues to orchestrate skeletal muscle oxidation required for global nutrient flux. Bmal1 in skeletal muscle responds robustly to feeding in vivo and insulin induces its expression. Muscle Bmal1 deficiency impaired the transcriptional control of glucose metabolic pathway, resulting in markedly attenuated glucose utilization and fasting hyperglycemia. Notably, the loss of Bmal1 response to feeding abolished fasting-to-feeding metabolic fuel switch from fatty acids to glucose in skeletal muscle, leading to the activation of energy-sensing pathways for fatty acid oxidation. These altered metabolic substrate oxidations in Bmal1-deficient muscle ultimately depleted circulating lipid levels that prevented hepatic steatosis. Collectively, our findings highlight the key role of the metabolic-sensing function of skeletal muscle clock in partitioning nutrient flux between muscle and liver to maintain whole-body lipid and glucose homeostasis.

Indexed as

Circadian ClocksHomeostasisAnimalsARNTL Transcription FactorsFatty AcidsGene Expression RegulationGlucoseLiverMiceMice, TransgenicMuscle, SkeletalARNTL Transcription FactorsFatty AcidsGlucosecircadian clockfatty acid metabolismglucose metabolismhepatic steatosisskeletal muscle

Identifiers

PMID32212194
PMCPMC7597556
OpenAlexW3013575207

What OpenQuestion 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 OpenQuestion graph.