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Statements

Subject Item
n2:RIV%2F60461373%3A22330%2F12%3A43894330%21RIV13-MSM-22330___
rdf:type
n8:Vysledek skos:Concept
dcterms:description
Background: Resident macrophages (Kupffer cells, KCs) in the liver can undergo both pro- or anti-inflammatory activation pathway and exert either beneficiary or detrimental effects on liver metabolism. Until now, their role in the metabolically dysfunctional state of steatosis remains enigmatic. Aim of our study was to characterize the role of KCs in relation to the onset of hepatic insulin resistance induced by a high-fat (HF) diet rich in monounsaturated fatty acids. Methods: Male Wistar rats were fed either standard (SD) or high-fat (HF) diet for 4 weeks. Half of the animals were subjected to the acute GdCl3 treatment 24 and 72 hrs prior to the end of the experiment in order to induce the reduction of KCs population. We determined the effect of HF diet on activation status of liver macrophages and on the changes in hepatic insulin sensitivity and triacylglycerol metabolism imposed by acute KCs depletion by GdCl3. Results: We found that a HF diet rich in MUFA itself triggers an alternative but not the classical activation program in KCs. In a steatotic, but not in normal liver, a reduction of the KCs population was associated with a decrease of alternative activation and with a shift towards the expression of pro- inflammatory activation markers, with the increased autophagy, elevated lysosomal lipolysis, increased formation of DAG, PKC epsilon activation and marked exacerbation of HF diet-induced hepatic insulin resistance. Conclusions: We propose that in the presence of a high MUFA content the population of alternatively activated resident liver macrophages may mediate beneficial effects on liver insulin sensitivity and alleviate the metabolic disturbances imposed by HF diet feeding and steatosis. Our data indicate that macrophage polarization towards an alternative state might be a useful strategy for treating type 2 diabetes. Background: Resident macrophages (Kupffer cells, KCs) in the liver can undergo both pro- or anti-inflammatory activation pathway and exert either beneficiary or detrimental effects on liver metabolism. Until now, their role in the metabolically dysfunctional state of steatosis remains enigmatic. Aim of our study was to characterize the role of KCs in relation to the onset of hepatic insulin resistance induced by a high-fat (HF) diet rich in monounsaturated fatty acids. Methods: Male Wistar rats were fed either standard (SD) or high-fat (HF) diet for 4 weeks. Half of the animals were subjected to the acute GdCl3 treatment 24 and 72 hrs prior to the end of the experiment in order to induce the reduction of KCs population. We determined the effect of HF diet on activation status of liver macrophages and on the changes in hepatic insulin sensitivity and triacylglycerol metabolism imposed by acute KCs depletion by GdCl3. Results: We found that a HF diet rich in MUFA itself triggers an alternative but not the classical activation program in KCs. In a steatotic, but not in normal liver, a reduction of the KCs population was associated with a decrease of alternative activation and with a shift towards the expression of pro- inflammatory activation markers, with the increased autophagy, elevated lysosomal lipolysis, increased formation of DAG, PKC epsilon activation and marked exacerbation of HF diet-induced hepatic insulin resistance. Conclusions: We propose that in the presence of a high MUFA content the population of alternatively activated resident liver macrophages may mediate beneficial effects on liver insulin sensitivity and alleviate the metabolic disturbances imposed by HF diet feeding and steatosis. Our data indicate that macrophage polarization towards an alternative state might be a useful strategy for treating type 2 diabetes.
dcterms:title
Kupffer cells ameliorate hepatic insulin resistance induced by high-fat diet rich in monounsaturated fatty acids: the evidence for the involvement of alternatively activated macrophages Kupffer cells ameliorate hepatic insulin resistance induced by high-fat diet rich in monounsaturated fatty acids: the evidence for the involvement of alternatively activated macrophages
skos:prefLabel
Kupffer cells ameliorate hepatic insulin resistance induced by high-fat diet rich in monounsaturated fatty acids: the evidence for the involvement of alternatively activated macrophages Kupffer cells ameliorate hepatic insulin resistance induced by high-fat diet rich in monounsaturated fatty acids: the evidence for the involvement of alternatively activated macrophages
skos:notation
RIV/60461373:22330/12:43894330!RIV13-MSM-22330___
n8:predkladatel
n12:orjk%3A22330
n3:aktivita
n17:S n17:P
n3:aktivity
P(GAP301/11/2418), P(NS9696), S
n3:cisloPeriodika
Article Number: 22
n3:dodaniDat
n6:2013
n3:domaciTvurceVysledku
n16:3931390
n3:druhVysledku
n18:J
n3:duvernostUdaju
n11:S
n3:entitaPredkladatele
n13:predkladatel
n3:idSjednocenehoVysledku
146045
n3:idVysledku
RIV/60461373:22330/12:43894330
n3:jazykVysledku
n20:eng
n3:klicovaSlova
PREVENTS; STEATOSIS; DEPLETION; AUTOPHAGY; EXPRESSION; RAT-LIVER; METABOLIC SYNDROME; LIVER-DISEASE; NECROSIS-FACTOR-ALPHA; PROTEIN-KINASE-C
n3:klicoveSlovo
n4:LIVER-DISEASE n4:EXPRESSION n4:STEATOSIS n4:DEPLETION n4:PREVENTS n4:RAT-LIVER n4:METABOLIC%20SYNDROME n4:AUTOPHAGY n4:NECROSIS-FACTOR-ALPHA n4:PROTEIN-KINASE-C
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[A30604956F2B]
n3:nazevZdroje
Nutrition & metabolism
n3:obor
n19:ED
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
7
n3:projekt
n9:GAP301%2F11%2F2418 n9:NS9696
n3:rokUplatneniVysledku
n6:2012
n3:svazekPeriodika
9
n3:tvurceVysledku
Papáčková, Zuzana Kazdová, Ludmila Daňková, Helena Páleníčková, Eliška Cahová, Monika Škop, Vojtěch Ždychová, Jana
n3:wos
000303875700001
s:issn
1743-7075
s:numberOfPages
15
n14:doi
10.1186/1743-7075-9-22
n10:organizacniJednotka
22330