schliessen

Filtern

 

Bibliotheken

Higher protein kinase C ζ in fatty rat liver and its effect on insulin actions in primary hepatocytes

We previously showed the impairment of insulin-regulated gene expression in the primary hepatocytes from Zucker fatty (ZF) rats, and its association with alterations of hepatic glucose and lipid metabolism. However, the molecular mechanism is unknown. A preliminary experiment shows that the expressi... Full description

Journal Title: PLoS ONE Vol.10(3), p.e0121890
Main Author: Wei Chen
Other Authors: Matthew Ray Goff , Heqian Kuang , Guoxun Chen
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0121890
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: doaj_soai_doaj_org_article_1b32e4ab1f144cd99f777c42a7d3a7c2
title: Higher protein kinase C ζ in fatty rat liver and its effect on insulin actions in primary hepatocytes
format: Article
creator:
  • Wei Chen
  • Matthew Ray Goff
  • Heqian Kuang
  • Guoxun Chen
subjects:
  • Sciences (General)
ispartof: PLoS ONE, Vol.10(3), p.e0121890
description: We previously showed the impairment of insulin-regulated gene expression in the primary hepatocytes from Zucker fatty (ZF) rats, and its association with alterations of hepatic glucose and lipid metabolism. However, the molecular mechanism is unknown. A preliminary experiment shows that the expression level of protein kinase C ζ (PKCζ), a member of atypical PKC family, is higher in the liver and hepatocytes of ZF rats than that of Zucker lean (ZL) rats. Herein, we intend to investigate the roles of atypical protein kinase C in the regulation of hepatic gene expression. The insulin-regulated hepatic gene expression was evaluated in ZL primary hepatocytes treated with atypical PKC recombinant adenoviruses. Recombinant adenovirus-mediated overexpression of PKCζ, or the other atypical PKC member PKCι/λ, alters the basal and impairs the insulin-regulated expressions of glucokinase, sterol regulatory element-binding protein 1c, the cytosolic form of phosphoenolpyruvate carboxykinase, the catalytic subunit of glucose 6-phosphatase, and insulin like growth factor-binding protein 1 in ZL primary hepatocytes. PKCζ or PKCι/λ overexpression also reduces the protein level of insulin receptor substrate 1, and the insulin-induced phosphorylation of AKT at Ser473 and Thr308. Additionally, PKCι/λ overexpression impairs the insulin-induced Prckz expression, indicating the crosstalk between PKCζ and PKCι/λ. We conclude that the PKCζ expression is elevated in hepatocytes of insulin resistant ZF rats. Overexpressions of aPKCs in primary hepatocytes impair insulin signal transduction, and in turn, the down-stream insulin-regulated gene expression. These data suggest that elevation of aPKC expression may contribute to the hepatic insulin resistance at gene expression level.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0121890
fulltext: fulltext_linktorsrc
issn:
  • 1932-6203
  • 19326203
url: Link


@attributes
ID989081921
RANK0.06999999
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordidoai_doaj_org_article_1b32e4ab1f144cd99f777c42a7d3a7c2
sourceiddoaj_s
recordidTN_doaj_soai_doaj_org_article_1b32e4ab1f144cd99f777c42a7d3a7c2
sourcesystemOther
dbidDOA
pqid1668236838
galeid419036350
display
typearticle
titleHigher protein kinase C ζ in fatty rat liver and its effect on insulin actions in primary hepatocytes
creatorWei Chen ; Matthew Ray Goff ; Heqian Kuang ; Guoxun Chen
ispartofPLoS ONE, Vol.10(3), p.e0121890
identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0121890
subjectSciences (General)
descriptionWe previously showed the impairment of insulin-regulated gene expression in the primary hepatocytes from Zucker fatty (ZF) rats, and its association with alterations of hepatic glucose and lipid metabolism. However, the molecular mechanism is unknown. A preliminary experiment shows that the expression level of protein kinase C ζ (PKCζ), a member of atypical PKC family, is higher in the liver and hepatocytes of ZF rats than that of Zucker lean (ZL) rats. Herein, we intend to investigate the roles of atypical protein kinase C in the regulation of hepatic gene expression. The insulin-regulated hepatic gene expression was evaluated in ZL primary hepatocytes treated with atypical PKC recombinant adenoviruses. Recombinant adenovirus-mediated overexpression of PKCζ, or the other atypical PKC member PKCι/λ, alters the basal and impairs the insulin-regulated expressions of glucokinase, sterol regulatory element-binding protein 1c, the cytosolic form of phosphoenolpyruvate carboxykinase, the catalytic subunit of glucose 6-phosphatase, and insulin like growth factor-binding protein 1 in ZL primary hepatocytes. PKCζ or PKCι/λ overexpression also reduces the protein level of insulin receptor substrate 1, and the insulin-induced phosphorylation of AKT at Ser473 and Thr308. Additionally, PKCι/λ overexpression impairs the insulin-induced Prckz expression, indicating the crosstalk between PKCζ and PKCι/λ. We conclude that the PKCζ expression is elevated in hepatocytes of insulin resistant ZF rats. Overexpressions of aPKCs in primary hepatocytes impair insulin signal transduction, and in turn, the down-stream insulin-regulated gene expression. These data suggest that elevation of aPKC expression may contribute to the hepatic insulin resistance at gene expression level.
languageeng
oafree_for_read
source
version8
lds50peer_reviewed
links
openurl$$Topenurl_article
openurlfulltext$$Topenurlfull_article
linktorsrc$$Uhttps://doaj.org/article/1b32e4ab1f144cd99f777c42a7d3a7c2$$EView_full_text_in_DOAJ
search
creatorcontrib
0Wei Chen
1Matthew Ray Goff
2Heqian Kuang
3Guoxun Chen
titleHigher protein kinase C ζ in fatty rat liver and its effect on insulin actions in primary hepatocytes
description

We previously showed the impairment of insulin-regulated gene expression in the primary hepatocytes from Zucker fatty (ZF) rats, and its association with alterations of hepatic glucose and lipid metabolism. However, the molecular mechanism is unknown. A preliminary experiment shows that the expression level of protein kinase C ζ (PKCζ), a member of atypical PKC family, is higher in the liver and hepatocytes of ZF rats than that of Zucker lean (ZL) rats. Herein, we intend to investigate the roles of atypical protein kinase C in the regulation of hepatic gene expression. The insulin-regulated hepatic gene expression was evaluated in ZL primary hepatocytes treated with atypical PKC recombinant adenoviruses. Recombinant adenovirus-mediated overexpression of PKCζ, or the other atypical PKC member PKCι/λ, alters the basal and impairs the insulin-regulated expressions of glucokinase, sterol regulatory element-binding protein 1c, the cytosolic form of phosphoenolpyruvate carboxykinase, the catalytic subunit of glucose 6-phosphatase, and insulin like growth factor-binding protein 1 in ZL primary hepatocytes. PKCζ or PKCι/λ overexpression also reduces the protein level of insulin receptor substrate 1, and the insulin-induced phosphorylation of AKT at Ser473 and Thr308. Additionally, PKCι/λ overexpression impairs the insulin-induced Prckz expression, indicating the crosstalk between PKCζ and PKCι/λ. We conclude that the PKCζ expression is elevated in hepatocytes of insulin resistant ZF rats. Overexpressions of aPKCs in primary hepatocytes impair insulin signal transduction, and in turn, the down-stream insulin-regulated gene expression. These data suggest that elevation of aPKC expression may contribute to the hepatic insulin resistance at gene expression level.

subjectSciences (General)
general
0English
1Public Library of Science (PLoS)
210.1371/journal.pone.0121890
3Directory of Open Access Journals (DOAJ)
sourceiddoaj_s
recordiddoaj_soai_doaj_org_article_1b32e4ab1f144cd99f777c42a7d3a7c2
issn
01932-6203
119326203
rsrctypearticle
addtitlePLoS ONE
searchscope
0doaj_full
1doaj1
scope
0doaj_full
1doaj1
lsr45$$EView_full_text_in_DOAJ
tmp01Directory of Open Access Journals (DOAJ)
tmp02DOA
lsr40PLoS ONE, Vol.10 (3), p.e0121890
doi10.1371/journal.pone.0121890
citationpf e0121890 vol 10 issue 3
lsr30VSR-Enriched:[pqid, pages, date, galeid]
sort
titleHigher protein kinase C ζ in fatty rat liver and its effect on insulin actions in primary hepatocytes
authorWei Chen ; Matthew Ray Goff ; Heqian Kuang ; Guoxun Chen
facets
frbrgroupid3463260932887450474
frbrtype5
newrecords20190714
languageeng
topicSciences (General)
collectionDirectory of Open Access Journals (DOAJ)
prefilterarticles
rsrctypearticles
creatorcontrib
0Wei Chen
1Matthew Ray Goff
2Heqian Kuang
3Guoxun Chen
jtitlePLoS ONE
toplevelpeer_reviewed
delivery
delcategoryRemote Search Resource
fulltextfulltext_linktorsrc
addata
au
0Wei Chen
1Matthew Ray Goff
2Heqian Kuang
3Guoxun Chen
atitleHigher protein kinase C ζ in fatty rat liver and its effect on insulin actions in primary hepatocytes
jtitlePLoS ONE
volume10
issue3
spagee0121890
eissn1932-6203
formatjournal
genrearticle
ristypeJOUR
abstract

We previously showed the impairment of insulin-regulated gene expression in the primary hepatocytes from Zucker fatty (ZF) rats, and its association with alterations of hepatic glucose and lipid metabolism. However, the molecular mechanism is unknown. A preliminary experiment shows that the expression level of protein kinase C ζ (PKCζ), a member of atypical PKC family, is higher in the liver and hepatocytes of ZF rats than that of Zucker lean (ZL) rats. Herein, we intend to investigate the roles of atypical protein kinase C in the regulation of hepatic gene expression. The insulin-regulated hepatic gene expression was evaluated in ZL primary hepatocytes treated with atypical PKC recombinant adenoviruses. Recombinant adenovirus-mediated overexpression of PKCζ, or the other atypical PKC member PKCι/λ, alters the basal and impairs the insulin-regulated expressions of glucokinase, sterol regulatory element-binding protein 1c, the cytosolic form of phosphoenolpyruvate carboxykinase, the catalytic subunit of glucose 6-phosphatase, and insulin like growth factor-binding protein 1 in ZL primary hepatocytes. PKCζ or PKCι/λ overexpression also reduces the protein level of insulin receptor substrate 1, and the insulin-induced phosphorylation of AKT at Ser473 and Thr308. Additionally, PKCι/λ overexpression impairs the insulin-induced Prckz expression, indicating the crosstalk between PKCζ and PKCι/λ. We conclude that the PKCζ expression is elevated in hepatocytes of insulin resistant ZF rats. Overexpressions of aPKCs in primary hepatocytes impair insulin signal transduction, and in turn, the down-stream insulin-regulated gene expression. These data suggest that elevation of aPKC expression may contribute to the hepatic insulin resistance at gene expression level.

pubPublic Library of Science (PLoS)
doi10.1371/journal.pone.0121890
oafree_for_read
pagese0121890
date2015-03-30