Role of AMPK in pancreatic beta cell function

被引:84
作者
Fu, Accalia [1 ]
Eberhard, Chandra E. [1 ]
Screaton, Robert A. [1 ,2 ,3 ]
机构
[1] Childrens Hosp Eastern Ontario, Res Inst, Ottawa, ON K1H 8L1, Canada
[2] Univ Ottawa, Dept Pediat, Ottawa, ON K1N 6N5, Canada
[3] Univ Ottawa, Dept Cellular & Mol Med, Ottawa, ON K1N 6N5, Canada
关键词
AMPK; Beta cell; Glucose stimulated insulin secretion; Pancreas; Islet; Mitochondria; ACTIVATED PROTEIN-KINASE; STIMULATED INSULIN-SECRETION; GLUCOSE-HOMEOSTASIS; IN-VIVO; HEPATIC STEATOSIS; OVER-EXPRESSION; SKELETAL-MUSCLE; KEY REGULATOR; AICA-RIBOSIDE; LKB1;
D O I
10.1016/j.mce.2012.06.020
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Pharmacological activation of AMP activated kinase (AMPK) by metformin has proven to be a beneficial therapeutic approach for the treatment of type II diabetes. Despite improved glucose regulation achieved by administration of small molecule activators of AMPK, the potential negative impact of enhanced AMPK activity on insulin secretion by the pancreatic beta cell is an important consideration. In this review, we discuss our current understanding of the role of AMPK in central functions of the pancreatic beta cell, including glucose-stimulated insulin secretion (GSIS), proliferation, and survival. In addition we discuss the controversy surrounding the role of AMPK in insulin secretion, underscoring the merits and caveats of methods used to date. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:127 / 134
页数:8
相关论文
共 83 条
  • [1] Stimulation of AMP-activated protein kinase (AMPK) is associated with enhancement of Glut1-mediated glucose transport
    Abbud, W
    Habinowski, S
    Zhang, JZ
    Kendrew, J
    Elkairi, FS
    Kemp, BE
    Witters, LA
    Ismail-Beigi, F
    [J]. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2000, 380 (02) : 347 - 352
  • [2] Akkan A G, 1994, Diabetes Res, V25, P13
  • [3] Complete polarization of single intestinal epithelial cells upon activation of LKB1 by STRAD
    Baas, AF
    Kuipers, J
    van der Wel, NN
    Batlle, E
    Koerten, HK
    Peters, PJ
    Clevers, HC
    [J]. CELL, 2004, 116 (03) : 457 - 466
  • [4] LKB1 and SAD kinases define a pathway required for the polarization of cortical neurons
    Barnes, Anthony P.
    Lilley, Brendan N.
    Pan, Y. Albert
    Plummer, Lisa J.
    Powell, Ashton W.
    Raines, Alexander N.
    Sanes, Joshua R.
    Polleux, Franck
    [J]. CELL, 2007, 129 (03) : 549 - 563
  • [5] Barthel A, 2002, ENDOCRINOLOGY, V143, P3183, DOI 10.1210/endo.143.8.8792
  • [6] Loss of AMP-activated protein kinase α2 subunit in mouse β-cells impairs glucose-stimulated insulin secretion and inhibits their sensitivity to hypoglycaemia
    Beall, Craig
    Piipari, Kaisa
    Al-Qassab, Hind
    Smith, Mark A.
    Parker, Nadeene
    Carling, David
    Viollet, Benoit
    Withers, Dominic J.
    Ashford, Michael L. J.
    [J]. BIOCHEMICAL JOURNAL, 2010, 429 : 323 - 333
  • [7] Increased oxygen radical formation and mitochondrial dysfunction mediate beta cell apoptosis under conditions of AMP-activated protein kinase stimulation
    Cai, Ying
    Martens, Geert A.
    Hinke, Simon A.
    Heimberg, Harry
    Pipeleers, Daniel
    Van de Casteele, Mark
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 2007, 42 (01) : 64 - 78
  • [8] AMPK is essential for energy homeostasis regulation and glucose sensing by POMC and AgRP neurons
    Claret, Marc
    Smith, Mark A.
    Batterham, Rachel L.
    Selman, Colin
    Choudhury, Agharul I.
    Fryer, Lee G. D.
    Clements, Melanie
    Al-Qassab, Hind
    Heffron, Helen
    Xu, Allison W.
    Speakman, John R.
    Barsh, Gregory S.
    Viollet, Benoit
    Vaulont, Sophie
    Ashford, Michael L. J.
    Carling, David
    Withers, Dominic J.
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2007, 117 (08) : 2325 - 2336
  • [9] da Silva Xavier Gabriela, 2003, Biochem J, V371, P761, DOI 10.1042/BJ20021812
  • [10] Preservation of β-Cell Function: The Key to Diabetes Prevention
    DeFronzo, Ralph A.
    Abdul-Ghani, Muhammad A.
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2011, 96 (08) : 2354 - 2366