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Statements

Subject Item
n2:RIV%2F00064165%3A_____%2F09%3A4717%21RIV10-MZ0-00064165
rdf:type
n4:Vysledek skos:Concept
dcterms:description
We investigated the role of LMNA in adipose tissue by developing a novel mouse model of lipodystrophy. Transgenic mice were generated that express the LMNA mutation that causes familial partial lipodystrophy of the Dunnigan type (FPLD2). The phenotype observed in FPLD-transgenic mice resembles many of the features of human FPLD2, including lack of fat accumulation, insulin resistance, and enlarged, fatty liver. Similar to the human disease, FPLD-transgenic mice appear to develop normally, but after several weeks they are unable to accumulate fat to the same extent as their wild-type littermates. One poorly understood aspect of lipodystrophies is the mechanism of fat loss. To this end, we have examined the effects of the FPLD2 mutation on fat cell function. Contrary to the current literature, which suggests FPLD2 results in a loss of fat, we found that the key mechanism contributing to the lack of fat accumulation involves not a loss, but an apparent inability of the adipose tissue to renew itself. We investigated the role of LMNA in adipose tissue by developing a novel mouse model of lipodystrophy. Transgenic mice were generated that express the LMNA mutation that causes familial partial lipodystrophy of the Dunnigan type (FPLD2). The phenotype observed in FPLD-transgenic mice resembles many of the features of human FPLD2, including lack of fat accumulation, insulin resistance, and enlarged, fatty liver. Similar to the human disease, FPLD-transgenic mice appear to develop normally, but after several weeks they are unable to accumulate fat to the same extent as their wild-type littermates. One poorly understood aspect of lipodystrophies is the mechanism of fat loss. To this end, we have examined the effects of the FPLD2 mutation on fat cell function. Contrary to the current literature, which suggests FPLD2 results in a loss of fat, we found that the key mechanism contributing to the lack of fat accumulation involves not a loss, but an apparent inability of the adipose tissue to renew itself.
dcterms:title
The role of LMNA in adipose: a novel mouse model of lipodystrophy based on the Dunnigan-type familial partial lipodystrophy mutation The role of LMNA in adipose: a novel mouse model of lipodystrophy based on the Dunnigan-type familial partial lipodystrophy mutation
skos:prefLabel
The role of LMNA in adipose: a novel mouse model of lipodystrophy based on the Dunnigan-type familial partial lipodystrophy mutation The role of LMNA in adipose: a novel mouse model of lipodystrophy based on the Dunnigan-type familial partial lipodystrophy mutation
skos:notation
RIV/00064165:_____/09:4717!RIV10-MZ0-00064165
n3:aktivita
n15:N
n3:aktivity
N
n3:cisloPeriodika
6
n3:dodaniDat
n12:2010
n3:domaciTvurceVysledku
n9:6061982
n3:druhVysledku
n13:J
n3:duvernostUdaju
n11:S
n3:entitaPredkladatele
n14:predkladatel
n3:idSjednocenehoVysledku
339731
n3:idVysledku
RIV/00064165:_____/09:4717
n3:jazykVysledku
n16:eng
n3:klicovaSlova
Lipodystrophy; adipose tissue; metabolic syndrome
n3:klicoveSlovo
n10:metabolic%20syndrome n10:adipose%20tissue n10:Lipodystrophy
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[9B506A82471C]
n3:nazevZdroje
Journal of Lipid Research
n3:obor
n6:FB
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
8
n3:rokUplatneniVysledku
n12:2009
n3:svazekPeriodika
50
n3:tvurceVysledku
Edgemon, Keith Wojtanik, Kari M. Viswanadha, Srikant Poy, George Haluzík, Martin Reitman, Marc Londos, Constantine Lindsey, Brigette
n3:wos
000266114500005
s:issn
0022-2275
s:numberOfPages
12