中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2006年
40期
172-175
,共4页
肥胖症%糖尿病%抵抗素%瘦素%肿瘤坏死因子α%脂联素%白细胞介素6
肥胖癥%糖尿病%牴抗素%瘦素%腫瘤壞死因子α%脂聯素%白細胞介素6
비반증%당뇨병%저항소%수소%종류배사인자α%지련소%백세포개소6
背景:通过分析脂肪细胞因子对机体的能量代谢及脂肪积累的调节作用,探讨脂肪组织的负反馈机制在肥胖、2型糖尿病形成中的作用.资料来源:应用计算机检索美国国立医学图书馆PubMed数据库1962-01/2005-11有关脂肪细胞因子的负反馈作用,肥胖和2型糖尿病的文章,检索词为"adipocytokines,obesity,tumor necrosis factor-α,interleukin-6,leptin,adiponectin,resistin and PGAR",限定语言种类为英语.资料选择:选择原创性研究论文作为参考,同时限定论文的内容必须与机体的能量代谢及脂肪积累有关;去除重复性研究、综述和其他与机体的能量代谢及脂肪积累关系不大的资料.资料提炼:共收集相关文献158篇,排除重复性研究和与本文主题相关性较小的文献123篇,本文共纳入文献35篇.资料综合:最近的研究表明脂肪组织能够分泌脂肪细胞因子以调节自身的容量.当体脂增加,脂肪细胞因子的调节作用会抑制脂肪合成,增加脂肪分解.脂肪细胞因子主要是通过抵抗胰岛素作用和减少胰岛素分泌来抑制脂肪合成,使脂肪分解增加,游离脂肪酸水平升高,抑制了血糖的利用.结论:当肥胖达到一定程度,脂肪细胞因子的负反馈作用可能是导致2型糖尿病发生的原因之一.
揹景:通過分析脂肪細胞因子對機體的能量代謝及脂肪積纍的調節作用,探討脂肪組織的負反饋機製在肥胖、2型糖尿病形成中的作用.資料來源:應用計算機檢索美國國立醫學圖書館PubMed數據庫1962-01/2005-11有關脂肪細胞因子的負反饋作用,肥胖和2型糖尿病的文章,檢索詞為"adipocytokines,obesity,tumor necrosis factor-α,interleukin-6,leptin,adiponectin,resistin and PGAR",限定語言種類為英語.資料選擇:選擇原創性研究論文作為參攷,同時限定論文的內容必鬚與機體的能量代謝及脂肪積纍有關;去除重複性研究、綜述和其他與機體的能量代謝及脂肪積纍關繫不大的資料.資料提煉:共收集相關文獻158篇,排除重複性研究和與本文主題相關性較小的文獻123篇,本文共納入文獻35篇.資料綜閤:最近的研究錶明脂肪組織能夠分泌脂肪細胞因子以調節自身的容量.噹體脂增加,脂肪細胞因子的調節作用會抑製脂肪閤成,增加脂肪分解.脂肪細胞因子主要是通過牴抗胰島素作用和減少胰島素分泌來抑製脂肪閤成,使脂肪分解增加,遊離脂肪痠水平升高,抑製瞭血糖的利用.結論:噹肥胖達到一定程度,脂肪細胞因子的負反饋作用可能是導緻2型糖尿病髮生的原因之一.
배경:통과분석지방세포인자대궤체적능량대사급지방적루적조절작용,탐토지방조직적부반궤궤제재비반、2형당뇨병형성중적작용.자료래원:응용계산궤검색미국국립의학도서관PubMed수거고1962-01/2005-11유관지방세포인자적부반궤작용,비반화2형당뇨병적문장,검색사위"adipocytokines,obesity,tumor necrosis factor-α,interleukin-6,leptin,adiponectin,resistin and PGAR",한정어언충류위영어.자료선택:선택원창성연구논문작위삼고,동시한정논문적내용필수여궤체적능량대사급지방적루유관;거제중복성연구、종술화기타여궤체적능량대사급지방적루관계불대적자료.자료제련:공수집상관문헌158편,배제중복성연구화여본문주제상관성교소적문헌123편,본문공납입문헌35편.자료종합:최근적연구표명지방조직능구분비지방세포인자이조절자신적용량.당체지증가,지방세포인자적조절작용회억제지방합성,증가지방분해.지방세포인자주요시통과저항이도소작용화감소이도소분비래억제지방합성,사지방분해증가,유리지방산수평승고,억제료혈당적이용.결론:당비반체도일정정도,지방세포인자적부반궤작용가능시도치2형당뇨병발생적원인지일.
BACKGROUND: To explore the effect of negative feedback mechanism of adipose tissue in the pathogenesis of obesity and type 2 diabetes through analyzing the function of the adipocytokines in regulating energy metabolism and fat accumulation.DATA SOURCES: We searched in the PubMed database of National Library of Medicine in USA for the articles on negative feedback action of adipocytokine, obesity and type 2 diabetes published from Jan 1962 to Nov 2005, using the key words of "adipocytokines, obesity, tumor necrosis factor-α, interleukin-6, leptin, adiponectin, resistin and PGAR" and limited the language to English.STUDY SELECTION: The articles of original researches and associated with energy metabolism and fat accumulation were included. The articles of repetitive researches, reviews and little associated with energy metabolism and fat accumulation were excluded.DATA EXTRACTION: A total of 158 articles were collected, of which 35 were closely correlated with this paper, and the 123 excluded articles were all repetitive studies, reviews and little correlated with this paper.DATA SYNTHESIS: Researches show that the fat tissue is able to secrete adipocytokines to regulate the fat mass, While the mass of body fat increases, the adipocytokines will inhibit lipogenesis and promote lipolysis.Adipocytokines can either resist the action of insulin or suppress the secretion of insulin. Thus lead to lipogenesis inhibition, lipolysis increasing and suppressing the utilization of blood glucose.CONCLUSION: When man develops obesity going up to certain degree,the negative feedback action of adipocytokines may lead to insulin resistance and type 2 diabetes.