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RISS 인기검색어
- 검색키워드
- 저자 : Vintersten, Kristina (검색결과 1 건)
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S6K1 controls pancreatic 관 cell size independently of intrauterine growth restriction.
Um, Sung Hee,Sticker-Jantscheff, Melanie,Chau, Gia Cac,Vintersten, Kristina,Mueller, Matthias,Gangloff, Yann-Gael,Adams, Ralf H,Spetz, Jean-Francois,Elghazi, Lynda,Pfluger, Paul T,Pende, Mario,Bernal- American Society for Clinical Investigation 2015 The Journal of clinical investigation Vol.125 No.7
<P>Type 2 diabetes mellitus (T2DM) is a worldwide heath problem that is characterized by insulin resistance and the eventual loss of 관 cell function. As recent studies have shown that loss of ribosomal protein (RP) S6 kinase 1 (S6K1) increases systemic insulin sensitivity, S6K1 inhibitors are being pursued as potential agents for improving insulin resistance. Here we found that S6K1 deficiency in mice also leads to decreased 관 cell growth, intrauterine growth restriction (IUGR), and impaired placental development. IUGR is a common complication of human pregnancy that limits the supply of oxygen and nutrients to the developing fetus, leading to diminished embryonic 관 cell growth and the onset of T2DM later in life. However, restoration of placental development and the rescue of IUGR by tetraploid embryo complementation did not restore 관 cell size or insulin levels in S6K1-/- embryos, suggesting that loss of S6K1 leads to an intrinsic 관 cell lesion. Consistent with this hypothesis, reexpression of S6K1 in 관 cells of S6K1-/- mice restored embryonic 관 cell size, insulin levels, glucose tolerance, and RPS6 phosphorylation, without rescuing IUGR. Together, these data suggest that a nutrient-mediated reduction in intrinsic 관 cell S6K1 signaling, rather than IUGR, during fetal development may underlie reduced 관 cell growth and eventual development of T2DM later in life.</P>
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