Evidence map›Paper›PMID 29924632›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2018

Heat shock protein 72 regulates hepatic lipid accumulation.

Ashley E Archer, Robert S Rogers, Alex T Von Schulze, Joshua L Wheatley, E Matthew Morris, Colin S McCoin, John P Thyfault, Paige C Geiger

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-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

22 citing papers in PubMed, 58 citations in OpenAlex.

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  12. Endothelial HSP72 is not reduced in type 2 diabetes nor is it a key determinant of endothelial insulin sensitivity.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
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  20. Heat therapy: possible benefits for cognitive function and the aging brain.Journal of applied physiology (Bethesda, Md. : 1985) · 2020
    Review
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

8 authors at 2 institutions in 1 country.

Ashley E ArcherDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, Kansas.
Robert S RogersDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, Kansas.
Alex T Von SchulzeDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, Kansas.
Joshua L WheatleyDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, Kansas.
E Matthew MorrisDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, Kansas.
Colin S McCoinDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, Kansas.
John P ThyfaultDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, Kansas.
Paige C GeigerDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, Kansas.
University of Kansas Medical Center · USVeterans Health Administration · US

Funding

Nuclear Receptors in Liver Health and DiseaseP20GM103549 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2012 to 2015
$8.1M
Molecular Regulation of Cell Development and Differentiation Phase III COBREP30GM122731 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI VIVIAN, JAY L · 2017 to 2021
$5.6M
Pilot Grants ProgramP30GM118247 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI WEINMAN, STEVEN A · 2016 to 2020
$5.5M
Targeting stress-mediated pathways in the treatment of muscle insulin resistanceR01AG031575 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GEIGER, PAIGE C · 2010 to 2014
$1.2M
Hepatic mitochondrial function control of high-fat diet-induced weight gainK01DK112967 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI MORRIS, E MATTHEW · 2017 to 2021
$872k
JEOL JEM-1400 Transmission Electron Microscope with AMT-XR611M Digital Camera SysS10RR027564 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ABRAHAMSON, DALE R · 2010 to 2010
$418k
NCRR NIH HHS S10 RR027564NIA NIH HHS R01 AG031575NIDDK NIH HHS K01 DK112967NIGMS NIH HHS P20 GM103549NIGMS NIH HHS P30 GM118247NIGMS NIH HHS P30 GM122731
6 · The paper itself

Abstract

Induction of the chaperone heat shock protein 72 (HSP72) through heat treatment (HT), exercise, or overexpression improves glucose tolerance and mitochondrial function in skeletal muscle. Less is known about HSP72 function in the liver where lipid accumulation can result in insulin resistance and nonalcoholic fatty liver disease (NAFLD). The purpose of this study was 1) to determine whether weekly in vivo HT induces hepatic HSP72 and improves glucose tolerance in rats fed a high-fat diet (HFD) and 2) to determine the ability of HSP72 to protect against lipid accumulation and mitochondrial dysfunction in primary hepatocytes. Male Wistar rats were fed an HFD for 15 wk and were given weekly HT (41°C, 20 min) or sham treatments (37°C, 20 min) for the final 7 wk. Glucose tolerance and insulin sensitivity were assessed, along with HSP72 induction and triglyceride storage, in the skeletal muscle and liver. The effect of an acute loss of HSP72 in primary hepatocytes was examined via siRNA. Weekly in vivo HT improved glucose tolerance, elevated muscle and hepatic HSP72 protein content, and reduced muscle triglyceride storage. In primary hepatocytes, mitochondrial morphology was changed, and fatty acid oxidation was reduced in small interfering HSP72 (siHSP72)-treated hepatocytes. Lipid accumulation following palmitate treatment was increased in siHSP72-treated hepatocytes. These data suggest that HT may improve systemic metabolism via induction of hepatic HSP72. Additionally, acute loss of HSP72 in primary hepatocytes impacts mitochondrial health as well as fat oxidation and storage. These findings suggest therapies targeting HSP72 in the liver may prevent NAFLD.

Indexed as

Hyperthermia, InducedAnimalsBlood GlucoseCells, CulturedDiet, High-FatDisease Models, AnimalFatty AcidsHepatocytesHSP72 Heat-Shock ProteinsInsulin ResistanceLiverMaleMice, Inbred C57BLMitochondria, LiverMuscle, SkeletalNon-alcoholic Fatty Liver DiseaseBlood GlucoseFatty AcidsHSP72 Heat-Shock Proteinsheat shock proteinsliver metabolismmitochondrianonalcoholic fatty liver diseasesteatosis

Identifiers

PMID29924632
PMCPMC6230886
OpenAlexW2809488478

What OpenQuestion holds

Textmetadata
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.