Evidence map›Paper›PMID 29032027›Full record

ArticleEBioMedicine2017

Peripheral Neuropathy and Hindlimb Paralysis in a Mouse Model of Adipocyte-Specific Knockout of Lkb1.

Yan Xiong, Jessica C Page, Naagarajan Narayanan, Chao Wang, Zhihao Jia, Feng Yue, Xine Shi, Wen Jin, Keping Hu, Meng Deng and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Sex-specific role of sensory neuron LKB1 on metabolic stress-induced mechanical hypersensitivity and mitochondrial respiration.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
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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

14 authors at 4 institutions in 2 countries.

Yan XiongLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling 712100, China; Department of Animal Sciences, Purdue University, West Lafayette, IN 47906, USA; Joint Laboratory of Lipid Metabolism, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Beijing 100193, China.
Jessica C PageDepartment of Basic Medical Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, IN 47906, USA.
Naagarajan NarayananDepartment of Agricultural and Biological Engineering, Purdue University, West Lafayette, IN 47906, USA; Bindley Bioscience Center, Purdue University, West Lafayette, IN 47906, USA.
Chao WangDepartment of Animal Sciences, Purdue University, West Lafayette, IN 47906, USA.
Zhihao JiaDepartment of Animal Sciences, Purdue University, West Lafayette, IN 47906, USA.
Feng YueDepartment of Animal Sciences, Purdue University, West Lafayette, IN 47906, USA.
Xine ShiLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling 712100, China.
Wen JinJoint Laboratory of Lipid Metabolism, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Beijing 100193, China.
Keping HuJoint Laboratory of Lipid Metabolism, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Beijing 100193, China.
Meng DengDepartment of Agricultural and Biological Engineering, Purdue University, West Lafayette, IN 47906, USA; Bindley Bioscience Center, Purdue University, West Lafayette, IN 47906, USA; Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47906, USA; School of Materials Engineering(,) Purdue University, West Lafayette, IN 47907, USA.
Riyi ShiDepartment of Basic Medical Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, IN 47906, USA; Department of Agricultural and Biological Engineering, Purdue University, West Lafayette, IN 47906, USA; Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47906, USA.
Tizhong ShanDepartment of Animal Sciences, Purdue University, West Lafayette, IN 47906, USA.
Gongshe YangLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling 712100, China. Electronic address: gsyang@nwsuaf.edu.cn.
Shihuan KuangDepartment of Animal Sciences, Purdue University, West Lafayette, IN 47906, USA; Joint Laboratory of Lipid Metabolism, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Beijing 100193, China. Electronic address: skuang@purdue.edu.
Purdue University West Lafayette · USChinese Academy of Medical Sciences & Peking Union Medical College · CNNorthwest A&F University · CNNorth West Agriculture and Forestry University · CN

Funding

Transgenic Mouse Core Facility Shared Resource (TMCF-SR)P30CA023168 · NCI · PURDUE UNIVERSITY WEST LAFAYETTE · PI John Tesmer · 1985 to 2026
$43.4M
Notch signaling in liposarcomaR01CA212609 · NCI · PURDUE UNIVERSITY · PI KUANG, SHIHUAN · 2017 to 2021
$1.8M
6 · The paper itself

Abstract

Brown adipose tissues (BAT) burn lipids to generate heat through uncoupled respiration, thus representing a powerful target to counteract lipid accumulation and obesity. The tumor suppressor liver kinase b1 (Lkb1) is a key regulator of cellular energy metabolism; and adipocyte-specific knockout of Lkb1 (Ad-Lkb1 KO) leads to the expansion of BAT, improvements in systemic metabolism and resistance to obesity in young mice. Here we report the unexpected finding that the Ad-Lkb1 KO mice develop hindlimb paralysis at mid-age. Gene expression analyses indicate that Lkb1 KO upregulates the expression of inflammatory cytokines in interscapular BAT and epineurial brown adipocytes surrounding the sciatic nerve. This is followed by peripheral neuropathy characterized by infiltration of macrophages into the sciatic nerve, axon degeneration, reduced nerve conductance, and hindlimb paralysis. Mechanistically, Lkb1 KO reduces AMPK phosphorylation and amplifies mammalian target-of-rapamycin (mTOR)-dependent inflammatory signaling specifically in BAT but not WAT. Importantly, pharmacological or genetic inhibition of mTOR ameliorates inflammation and prevents paralysis. These results demonstrate that BAT inflammation is linked to peripheral neuropathy.

Indexed as

Adenylate KinaseAdipose Tissue, BrownAMP-Activated Protein Kinase KinasesAnimalsCytokinesDisease Models, AnimalHumansMacrophagesMiceMice, KnockoutParaplegiaPeripheral Nervous System DiseasesPhosphorylationProtein Serine-Threonine KinasesSciatic NerveUp-RegulationAdenylate KinaseAMP-Activated Protein Kinase KinasesCytokinesProtein Serine-Threonine KinasesSTK11 protein, humanBrown adipocyteInflammationLiver kinase b1 (serine/threonine kinase 11)mTORParalysisSciatic nerve

Identifiers

PMID29032027
PMCPMC5652135
OpenAlexW2759816807

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.