Abstract：
:Earlier, we reported that S6K1(-/-) mice have reduced body fat mass, have elevated rates of lipolysis, have severely decreased adipocyte size, and are resistant to high fat diet (HFD)-induced obesity. Here we report that adipocytes of S6K1(-/-) mice on a HFD have the capacity to increase in size to a degree comparable to that of wild-type (WT) mice, but not in number, indicating an unexpected lesion in adipogenesis. Tracing this lesion revealed that S6K1 is dispensable for terminal adipocyte differentiation, but is involved in the commitment of embryonic stem cells to early adipocyte progenitors. We further show that absence of S6K1 attenuates the upregulation of transcription factors critical for commitment to adipogenesis. These results led to the conclusion that a lack of S6K1 impairs the generation of de novo adipocytes when mice are challenged with a HFD, consistent with a reduction in early adipocyte progenitors.
journal_name
Dev Celljournal_title
Developmental cellauthors
Carnevalli LS,Masuda K,Frigerio F,Le Bacquer O,Um SH,Gandin V,Topisirovic I,Sonenberg N,Thomas G,Kozma SCdoi
10.1016/j.devcel.2010.02.018subject
Has Abstractpub_date
2010-05-18 00:00:00pages
763-74issue
5eissn
1534-5807issn
1878-1551pii
S1534-5807(10)00164-4journal_volume
18pub_type
杂志文章abstract：:Tissues have a natural capacity to replace dying cells and to heal wounds. This ability resides in resident stem cells, which self-renew, preserve, and repair their tissue during homeostasis and following injury. The skin epidermis and its appendages are subjected to daily assaults from the external environment. A hig...
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