Disruption of circadian rhythms accelerates development of diabetes through pancreatic beta-cell loss and dysfunction.
Disruption of circadian rhythms accelerates development of diabetes through pancreatic beta-cell loss and dysfunction.
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DOI：
10.1177/0748730411416341
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发表时间：
2011-10
影响因子：
3.5
通讯作者：
Matveyenko AV
中科院分区：
文献类型：
--
作者：
Gale JE;Cox HI;Qian J;Block GD;Colwell CS;Matveyenko AV
Type 2 diabetes mellitus (T2DM) is complex metabolic disease that arises as a consequence of interactions between genetic predisposition and environmental triggers. One recently described environmental trigger associated with development of T2DM is disturbance of circadian rhythms due to shift work, sleep loss, or nocturnal lifestyle. However, the underlying mechanisms behind this association are largely unknown. To address this, the authors examined the metabolic and physiological consequences of experimentally controlled circadian rhythm disruption in wild-type (WT) Sprague Dawley and diabetes-prone human islet amyloid polypeptide transgenic (HIP) rats: a validated model of T2DM. WT and HIP rats at 3 months of age were exposed to 10 weeks of either a normal light regimen (LD: 12:12-h light/dark) or experimental disruption in the light-dark cycle produced by either (1) 6-h advance of the light cycle every 3 days or (2) constant light protocol. Subsequently, blood glucose control, beta-cell function, beta-cell mass, turnover, and insulin sensitivity were examined. In WT rats, 10 weeks of experimental disruption of circadian rhythms failed to significantly alter fasting blood glucose levels, glucose-stimulated insulin secretion, beta-cell mass/turnover, or insulin sensitivity. In contrast, experimental disruption of circadian rhythms in diabetes-prone HIP rats led to accelerated development of diabetes. The mechanism subserving early-onset diabetes was due to accelerated loss of beta-cell function and loss of beta-cell mass attributed to increases in beta-cell apoptosis. Disruption of circadian rhythms may increase the risk of T2DM by accelerating the loss of beta-cell function and mass characteristic in T2DM.
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影响因子：
7.7
作者：
Huang, Chang-jiang;Lin, Chia-yu;Butler, Peter C.
通讯作者：
Butler, Peter C.
昼夜节律的代谢和能量学的融合。
DOI：
10.1126/science.1195027
发表时间：
2010-12-03
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Bass J;Takahashi JS
通讯作者：
Takahashi JS
影响因子：
30.8
作者：
Prokopenko I;Langenberg C;Florez JC;Saxena R;Soranzo N;Thorleifsson G;Loos RJ;Manning AK;Jackson AU;Aulchenko Y;Potter SC;Erdos MR;Sanna S;Hottenga JJ;Wheeler E;Kaakinen M;Lyssenko V;Chen WM;Ahmadi K;Beckmann JS;Bergman RN;Bochud M;Bonnycastle LL;Buchanan TA;Cao A;Cervino A;Coin L;Collins FS;Crisponi L;de Geus EJ;Dehghan A;Deloukas P;Doney AS;Elliott P;Freimer N;Gateva V;Herder C;Hofman A;Hughes TE;Hunt S;Illig T;Inouye M;Isomaa B;Johnson T;Kong A;Krestyaninova M;Kuusisto J;Laakso M;Lim N;Lindblad U;Lindgren CM;McCann OT;Mohlke KL;Morris AD;Naitza S;Orrù M;Palmer CN;Pouta A;Randall J;Rathmann W;Saramies J;Scheet P;Scott LJ;Scuteri A;Sharp S;Sijbrands E;Smit JH;Song K;Steinthorsdottir V;Stringham HM;Tuomi T;Tuomilehto J;Uitterlinden AG;Voight BF;Waterworth D;Wichmann HE;Willemsen G;Witteman JC;Yuan X;Zhao JH;Zeggini E;Schlessinger D;Sandhu M;Boomsma DI;Uda M;Spector TD;Penninx BW;Altshuler D;Vollenweider P;Jarvelin MR;Lakatta E;Waeber G;Fox CS;Peltonen L;Groop LC;Mooser V;Cupples LA;Thorsteinsdottir U;Boehnke M;Barroso I;Van Duijn C;Dupuis J;Watanabe RM;Stefansson K;McCarthy MI;Wareham NJ;Meigs JB;Abecasis GR
通讯作者：
Abecasis GR
影响因子：
7.7
作者：
Matveyenko, Aleksey V.;Butler, Peter C.
通讯作者：
Butler, Peter C.
影响因子：
2.2
作者：
DIAZ, B;BLAZQUEZ, E
通讯作者：
BLAZQUEZ, E