Molecular Mechanisms of Insulin Resistance: An Update

被引:0
作者
Gutierrez-Rodelo, Citlaly [1 ]
Roura-Guiberna, Adriana [1 ]
Alberto Olivares-Reyes, Jesus [1 ]
机构
[1] Inst Politecn Nacl, Lab Transducc Senales, Dept Bioquim, Ctr Invest & Estudios Avanzados, Ave Inst Politecn Nacl 2508, Mexico City 07360, DF, Mexico
来源
GACETA MEDICA DE MEXICO | 2017年 / 153卷 / 02期
关键词
Insulin; Insulin resistance; Inflammation; Endoplasmic reticulum stress; Mitochondrial dysfunction; ENDOPLASMIC-RETICULUM STRESS; PROTEIN-TYROSINE-PHOSPHATASE; ADIPOSE-TISSUE INFLAMMATION; KAPPA-B ACTIVATION; NITRIC-OXIDE; ER STRESS; MITOCHONDRIAL DYSFUNCTION; GLUCOSE-HOMEOSTASIS; SIGNALING PATHWAYS; OBESITY;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The biological actions of insulin are initiated by activating its membrane receptor, which triggers multiple signaling pathways to mediate their biological actions. Due to the importance of metabolic regulation and promoting functions of cell growth and proliferation, insulin actions are highly regulated to promote proper metabolic functioning and energy balance. If these mechanisms are altered, this can lead to a condition known as insulin resistance, which is the consequence of a deficient insulin signaling caused by mutations or post-translational modifications of the receptor or effector molecules located downstream. Insulin resistance is one of the main characteristics of pathological manifestations associated with type 2 diabetes mellitus, one of the leading causes of death in Mexico and worldwide. In recent years, it has been found that conditions such as inflammation, endoplasmic reticulum stress, and mitochondrial dysfunction promote insulin resistance. The aim of this review is to elucidate the molecular aspects of insulin resistance and the mechanisms involved in regulating its effects, with particular emphasis on the role of inflammation, endoplasmic reticulum stress, and mitochondrial dysfunction.
引用
收藏
页码:214 / 228
页数:15
相关论文
共 116 条
[1]   Endoplasmic reticulum stress [J].
Banhegyi, Gabor ;
Baumeister, Peter ;
Benedetti, Angelo ;
Dong, Dezheng ;
Fu, Yong ;
Lee, Amy S. ;
Li, Jianze ;
Mao, Changhui ;
Margittai, Eva ;
Ni, Min ;
Paschen, Wulf ;
Piccirella, Simona ;
Senesi, Silvia ;
Sitia, Roberto ;
Wang, Miao ;
Yang, Wei .
STRESS RESPONSES IN BIOLOGY AND MEDICINE: STRESS OF LIFE IN MOLECULES, CELLS, ORGANISMS, AND PSYCHOSOCIAL COMMUNITIES, 2007, 1113 :58-71
[2]   Insulin signalling in the heart [J].
Bertrand, Luc ;
Horman, Sandrine ;
Beauloye, Christophe ;
Vanoverschelde, Jean-Louis .
CARDIOVASCULAR RESEARCH, 2008, 79 (02) :238-248
[3]   Insulin in the brain: its pathophysiological implications for states related with central insulin resistance, type 2 diabetes and alzheimer's disease [J].
Blazquez, Enrique ;
Velazquez, Esther ;
Hurtado-Carneiro, Veronica ;
Miguel Ruiz-Albusac, Juan .
FRONTIERS IN ENDOCRINOLOGY, 2014, 5
[4]   Infusion of Glucose and Lipids at Physiological Rates Causes Acute Endoplasmic Reticulum Stress in Rat Liver [J].
Boden, Guenther ;
Song, Weiwei ;
Duan, Xunbao ;
Cheung, Peter ;
Kresge, Karen ;
Barrero, Carlos ;
Merali, Salim .
OBESITY, 2011, 19 (07) :1366-1373
[5]   The extracellular signal-regulated kinase isoform ERK1 is specifically required for in vitro and in vivo adipogenesis [J].
Bost, F ;
Aouadi, M ;
Caron, L ;
Even, P ;
Belmonte, N ;
Prot, M ;
Dani, C ;
Hofman, P ;
Pagès, G ;
Pouysségur, J ;
Le Marchand-Brustel, Y ;
Binétruy, B .
DIABETES, 2005, 54 (02) :402-411
[6]   Insulin Receptor Signaling in Normal and Insulin-Resistant States [J].
Boucher, Jeremie ;
Kleinridders, Andre ;
Kahn, C. Ronald .
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY, 2014, 6 (01)
[7]   ERKS - A FAMILY OF PROTEIN-SERINE THREONINE KINASES THAT ARE ACTIVATED AND TYROSINE PHOSPHORYLATED IN RESPONSE TO INSULIN AND NGF [J].
BOULTON, TG ;
NYE, SH ;
ROBBINS, DJ ;
IP, NY ;
RADZIEJEWSKA, E ;
MORGENBESSER, SD ;
DEPINHO, RA ;
PANAYOTATOS, N ;
COBB, MH ;
YANCOPOULOS, GD .
CELL, 1991, 65 (04) :663-675
[8]   Phosphorylation of IRS proteins, insulin action, and insulin resistance [J].
Boura-Halfon, Sigalit ;
Zick, Yehiel .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2009, 296 (04) :E581-E591
[9]   Ceramide-induced inhibition of Akt is mediated through protein kinase Cζ -: Implications for growth arrest [J].
Bourbon, NA ;
Sandirasegarane, L ;
Kester, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (05) :3286-3292
[10]   Selective versus total insulin resistance: A pathogenic paradox [J].
Brown, Michael S. ;
Goldstein, Joseph L. .
CELL METABOLISM, 2008, 7 (02) :95-96