Novel aspects on signal-transduction in the pancreatic β-cell

被引:17
作者
Berggren, PO [1 ]
Leibiger, IB [1 ]
机构
[1] Karolinska Univ Hosp Solna L3, Rolf Luft Res Ctr Diabet & Endocrinol, Karolinska Inst, SE-17176 Stockholm, Sweden
关键词
signal-transduction; insulin release; inositol phosphates; Ca2+ channel; apolipoprotein CIII; apoptosis; insulin receptor; islet of Langerhans;
D O I
10.1016/j.numecd.2005.11.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The glucose-stimulus/insulin-secretion-coupling by the pancreatic beta-cell, which guarantees the maintenance of glucose homeostasis in man, is regulated by a sophisticated interplay between glucose and a plethora of additional factors. Besides other nutrients, incretins, nerval innervation, systemic growth factors as well as autocrine and paracrine regulatory loops within the islet of Langerhans modulate the function of the insulin-producing beta-cell. Although the modulatory rote of these factors is well appreciated, the underlying molecular mechanisms involved remain poorly understood. However, in most cases beta-cell membrane receptors coupled primarily to either G-proteins or tyrosine kinases, which subsequently activate respective second messenger cascades, are involved. In the present mini-review we will discuss the role of signaling through some of these receptor-operated effector systems in the light of pancreatic beta-cell, signal-transduction. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:S7 / S10
页数:4
相关论文
共 19 条
[1]   ATP-SENSITIVE K+ CHANNELS - A LINK BETWEEN B-CELL METABOLISM AND INSULIN-SECRETION [J].
ASHCROFT, FM ;
RORSMAN, P .
BIOCHEMICAL SOCIETY TRANSACTIONS, 1990, 18 (01) :109-111
[2]   Phosphorylated inositol compounds in β-cell stimulus-response coupling [J].
Barker, CJ ;
Leibiger, IB ;
Leibiger, B ;
Berggren, PO .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2002, 283 (06) :E1113-E1122
[3]   CA2+ AND PANCREATIC B-CELL FUNCTION [J].
BERGGREN, PO ;
LARSSON, O .
BIOCHEMICAL SOCIETY TRANSACTIONS, 1994, 22 (01) :12-18
[4]   Removal of Ca2+ channel β3 Subunit enhances Ca2+ oscillation frequency and insulin exocytosis [J].
Berggren, PO ;
Yang, SN ;
Murakami, M ;
Efanov, AM ;
Uhles, S ;
Köhler, M ;
Moede, T ;
Fernström, A ;
Appelskog, LB ;
Aspinwall, CA ;
Zaitsev, SV ;
Larsson, O ;
de Vargas, LM ;
Fecher-Trost, C ;
Weissgerber, P ;
Ludwig, A ;
Leibiger, B ;
Juntti-Berggren, L ;
Barker, CJ ;
Gromada, J ;
Freichel, M ;
Leibiger, IB ;
Flockerzi, V .
CELL, 2004, 119 (02) :273-284
[5]   Inositol hexakisphosphate stimulates non-Ca2+-mediated and primes Ca2+-mediated exocytosis of insulin by activation of protein kinase C [J].
Efanov, AM ;
Zaitsev, SV ;
Berggren, PO .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (09) :4435-4439
[6]   Involvement of protein kinase C-ε in inositol hexakisphosphate-induced exocytosis in mouse pancreatic β-cells [J].
Hoy, M ;
Berggren, PO ;
Gromada, J .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (37) :35168-35171
[7]   Inositol hexakisphosphate promotes dynamin mediated endocytosis [J].
Hoy, M ;
Efanov, AM ;
Bertorello, AM ;
Zaitsev, SV ;
Olsen, HL ;
Bokvist, K ;
Leibiger, B ;
Leibiger, IB ;
Zwiller, J ;
Berggren, PO ;
Gromada, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (10) :6773-6777
[8]   Apolipoprotein CIII promotes Ca2+-dependent β cell death in type 1 diabetes [J].
Juntti-Berggren, L ;
Refai, E ;
Appelskog, I ;
Andersson, M ;
Imreh, G ;
Dekki, N ;
Uhles, S ;
Yu, L ;
Griffiths, WJ ;
Zaitsev, S ;
Leibiger, I ;
Yang, SN ;
Olivecrona, G ;
Jörnvall, H ;
Berggren, PO .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (27) :10090-10094
[9]   INCREASED ACTIVITY OF L-TYPE CA2+ CHANNELS EXPOSED TO SERUM FROM PATIENTS WITH TYPE-I DIABETES [J].
JUNTTIBERGGREN, L ;
LARSSON, O ;
RORSMAN, P ;
AMMALA, C ;
BOKVIST, K ;
WAHLANDER, K ;
NICOTERA, P ;
DYPBUKT, J ;
ORRENIUS, S ;
HALLBERG, A ;
BERGGREN, PO .
SCIENCE, 1993, 261 (5117) :86-90
[10]   Receptors for insulin and insulin-like growth factor-1 and insulin receptor substrate-1 mediate pathways that regulate islet function [J].
Kulkarni, RN .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2002, 30 :317-322