Lipid-induced β-cell dysfunction and oxidative stress

被引:2
作者
Oprescu, Andrei I.
Giacca, Adria
机构
[1] Univ Toronto, Inst Med Sci, Toronto, ON M4X 1K9, Canada
[2] Univ Toronto, Dept Physiol, Toronto, ON M4X 1K9, Canada
来源
FUTURE LIPIDOLOGY | 2007年 / 2卷 / 04期
关键词
beta-cells; islets; lipotoxicity; type; 2; diabetes;
D O I
10.2217/17460875.2.4.455
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Type 2 diabetes is characterized by both insulin resistance and defective insulin secretion. Obesity is the major predisposing factor for Type 2 diabetes and is associated with excessive release of fatty acids from the expanded adipose tissue, leading to elevated plasma free fatty acid, known to induce insulin resistance and decrease p-cell function and mass. The purpose of this review is to discuss the mechanisms of the effect of prolonged fat exposure on pancreatic p-cells, known as lipotoxicity, with particular regard to p-cell function. The role of oxidative stress is emphasized, as it was shown by recent studies to play a significant role in the development of lipotoxicity and Type 2 diabetes.
引用
收藏
页码:455 / 463
页数:9
相关论文
共 99 条
[91]   Inhibition of interleukin-1β-induced COX-2 and EP3 gene expression by sodium salicylate enhances pancreatic islet β-cell function [J].
Tran, POT ;
Gleason, CE ;
Robertson, RP .
DIABETES, 2002, 51 (06) :1772-1778
[92]   Lipotoxicity of β-cells in obesity and in other causes of fatty acid spillover [J].
Unger, RH ;
Zhou, YT .
DIABETES, 2001, 50 :S118-S121
[93]   Gene and protein kinase expression profiling of reactive oxygen species-associated lipotoxicity in the pancreatic β-cell line MIN6 [J].
Wang, XL ;
Li, H ;
De Leo, D ;
Guo, WB ;
Koshkin, V ;
Fantus, IG ;
Giacca, A ;
Chan, CB ;
Der, S ;
Wheeler, MB .
DIABETES, 2004, 53 (01) :129-140
[94]   MECHANISMS OF THE STIMULATION OF INSULIN RELEASE BY SATURATED FATTY-ACIDS - A STUDY OF PALMITATE EFFECTS IN MOUSE BETA-CELLS [J].
WARNOTTE, C ;
GILON, P ;
NENQUIN, M ;
HENQUIN, JC .
DIABETES, 1994, 43 (05) :703-711
[95]   Fatty acid and phorbol ester-mediated interference of mitogenic signaling via novel protein kinase C isoforms in pancreatic β-cells (INS-1) [J].
Wrede, CE ;
Dickson, LM ;
Lingohr, MK ;
Briaud, I ;
Rhodes, CJ .
JOURNAL OF MOLECULAR ENDOCRINOLOGY, 2003, 30 (03) :271-286
[96]   Insulin receptor signaling in the β-cell influences insulin gene expression and insulin content -: Evidence for autocrine β-cell regulation [J].
Xu, GG ;
Rothenberg, PL .
DIABETES, 1998, 47 (08) :1243-1252
[97]   LONG-TERM EXPOSURE OF RAT PANCREATIC-ISLETS TO FATTY-ACIDS INHIBITS GLUCOSE-INDUCED INSULIN-SECRETION AND BIOSYNTHESIS THROUGH A GLUCOSE FATTY-ACID CYCLE [J].
ZHOU, YP ;
GRILL, VE .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (02) :870-876
[98]   LONG-TERM EXPOSURE TO FATTY-ACIDS AND KETONES INHIBITS B-CELL FUNCTIONS IN HUMAN PANCREATIC-ISLETS OF LANGERHANS [J].
ZHOU, YP ;
GRILL, V .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1995, 80 (05) :1584-1590
[99]   A fatty acid-induced decrease in pyruvate dehydrogenase activity is an important determinant of beta-cell dysfunction in the obese diabetic db/db mouse [J].
Zhou, YP ;
Berggren, PO ;
Grill, V .
DIABETES, 1996, 45 (05) :580-586