1. Kor /
  2. Eng

  1. Kor /
  2. Eng

Major AchievementsFollowings are the major outstanding achievements of the SAIHST faculties

[엄성희 교수] Journal of Clinical Investigation. 2015 Jul 1;125(7):2736-47.
No -1
Date 2016/02/15

 

 

  
 

엄성희 교수

(의과대학 분자세포생물학교실, SAIHST겸직)

 

 Impact Factor ('13) = 13.765      BRIC한빛사 논문

 

 

2015 Jul 1;125(7):2736-47. doi: 10.1172/JCI77030. Epub 2015 Jun 15.
 

S6K1 controls pancreatic β cell size independently of intrauterine growth restriction.

 

Abstract

Type 2 diabetes mellitus (T2DM) is a worldwide heath problem that is characterized by insulin resistance and the eventual loss of β 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 β 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 β 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 β cell size or insulin levels in S6K1-/- embryos, suggesting that loss of S6K1 leads to an intrinsic β cell lesion. Consistent with this hypothesis, reexpression of S6K1 in β cells of S6K1-/- mice restored embryonic β cell size, insulin levels, glucose tolerance, and RPS6 phosphorylation, without rescuing IUGR. Together, these data suggest that a nutrient-mediated reduction in intrinsic β cell S6K1 signaling, rather than IUGR, during fetal development may underlie reduced β cell growth and eventual development of T2DM later in life.

 

PMID:26075820 [PubMed - indexed for MEDLINE]

PMCID: PMC4563673

 

(출처_PubMed)

 

 

엄성희 교수 연구소개     [프로필 보기]

 

비만과 당뇨병 등 대사성 질환들에서 나타나는 공통된 특징은 영양분과 에너지 항상성의 부조절임. 영양분과 에너지 항상성을 조절하는 신호전달체계에 대한 연구는 대사성 질환에 대한 병리 생리학적 이해를 증진시킬 수 있음. 본 연구실은 세포가 성장인자와 영양분으로부터 오는 신호를 어떻게 감지하고 연합시켜 여러 대사 작용을 매개하는 지와, 대사질환 같은 병리적 상태에서 이들 신호전달기전의 부조절이 어떻게 일어나는지에 관심을 가지고 연구해오고 있음. 이를 위해 생화학, 분자생물학적 실험과 동물모델, 환자 샘플을 이용하여 영양분과 에너지 항상성의 부조화를 일으키는 신호전달체계의 부조절에 관한 기작을 밝히려고 함.  이 연구는 대사성 질환 치료를 위한 전략을 개발하고 분자적 표적을 규명하는데 응용될 수 있을 것으로 사료됨. 
본 연구실은 한국연구재단, 보건산업진흥원, 삼성생명과학연구소, 포스코 청암 재단으로부터 연구지원을 받고 있음. 
2010년 제2기 포스코 청암재단 생명과학 분야 신진교수부문, 청암과학펠로쉽 (TJ Park Science Fellowship)을 수상하였고, 2015년 삼성미래기술육성재단의 삼성미래기술육성사업 (기초 과학)에 선정되어 연구를 진행하고 있음.  

 

 

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