1
|
Turrens JF: Mitochondrial formation of
reactive oxygen species. J Physiol. 552:335–344. 2003. View Article : Google Scholar : PubMed/NCBI
|
2
|
Tiganis T: Reactive oxygen species and
insulin resistance: The good, the bad and the ugly. Trends
Pharmacol Sci. 32:82–89. 2011. View Article : Google Scholar : PubMed/NCBI
|
3
|
Nishikawa T and Araki E: Impact of
mitochondrial ROS production in the pathogenesis of diabetes
mellitus and its complications. Antioxid Redox Signal. 9:343–353.
2007. View Article : Google Scholar : PubMed/NCBI
|
4
|
Newsholme P, Haber EP, Hirabara SM,
Rebelato EL, Procopio J, Morgan D, Oliveira-Emilio HC, Carpinelli
AR and Curi R: Diabetes associated cell stress and dysfunction:
Role of mitochondrial and non-mitochondrial ROS production and
activity. J Physiol. 583:9–24. 2007. View Article : Google Scholar : PubMed/NCBI
|
5
|
Riemer J, Bulleid N and Herrmann JM:
Disulfide formation in the ER and mitochondria: Two solutions to a
common process. Science. 324:1284–1287. 2009. View Article : Google Scholar : PubMed/NCBI
|
6
|
Panzhinskiy E, Ren J and Nair S: Protein
tyrosine phosphatase 1B and insulin resistance: role of endoplasmic
reticulum stress/reactive oxygen species/nuclear factor kappa B
axis. PLoS One. 8:e772282013. View Article : Google Scholar : PubMed/NCBI
|
7
|
Freedman RB, Hirst TR and Tuite MF:
Protein disulphide isomerase: Building bridges in protein folding.
Trends Biochem Sci. 19:331–336. 1994. View Article : Google Scholar : PubMed/NCBI
|
8
|
Figueira TR, Barros MH, Camargo AA,
Castilho RF, Ferreira JC, Kowaltowski AJ, Sluse FE, Souza-Pinto NC
and Vercesi AE: Mitochondria as a source of reactive oxygen and
nitrogen species: From molecular mechanisms to human health.
Antioxid Redox Sign. 18:2029–2074. 2013. View Article : Google Scholar
|
9
|
Bedard K and Krause KH: The NOX family of
ROS-generating NADPH oxidases: Physiology and pathophysiology.
Physiol Rev. 87:245–313. 2007. View Article : Google Scholar : PubMed/NCBI
|
10
|
Mukherjee SP, Lane RH and Lynn WS:
Endogenous hydrogen peroxide and peroxidative metabolism in
adipocytes in response to insulin and sulfhydryl reagents. Biochem
Pharmacol. 27:2589–2594. 1978. View Article : Google Scholar : PubMed/NCBI
|
11
|
May JM and de Haën C: Insulin-stimulated
intracellular hydrogen peroxide production in rat epididymal fat
cells. J Biol Chem. 254:2214–2220. 1979.PubMed/NCBI
|
12
|
Seo JH, Ahn Y, Lee SR, Yeo Yeol C and Hur
Chung K: The major target of the endogenously generated reactive
oxygen species in response to insulin stimulation is phosphatase
and tensin homolog and not phosphoinositide-3 kinase (PI-3 kinase)
in the PI-3 kinase/Akt pathway. Mol Biol Cell. 16:348–357. 2005.
View Article : Google Scholar : PubMed/NCBI
|
13
|
Gericke A, Munson M and Ross AH:
Regulation of the PTEN phosphatase. Gene. 374:1–9. 2006. View Article : Google Scholar : PubMed/NCBI
|
14
|
Ross AH and Gericke A: Phosphorylation
keeps PTEN phosphatase closed for business. Proc Natl Acad Sci USA.
106:1297–1298. 2009. View Article : Google Scholar : PubMed/NCBI
|
15
|
Taniguchi CM, Emanuelli B and Kahn CR:
Critical nodes in signalling pathways: Insights into insulin
action. Nat Rev Mol Cell Biol. 7:85–96. 2006. View Article : Google Scholar : PubMed/NCBI
|
16
|
Cantley LC: The phosphoinositide 3-kinase
pathway. Science. 296:1655–1657. 2002. View Article : Google Scholar : PubMed/NCBI
|
17
|
Cheng CK, Fan QW and Weiss WA: PI3K
signaling in glioma-animal models and therapeutic challenges. Brain
pathol. 19:112–120. 2009. View Article : Google Scholar : PubMed/NCBI
|
18
|
Loh K, Deng H, Fukushima A, Cai X, Boivin
B, Galic S, Bruce C, Shields BJ, Skiba B, Ooms LM, et al: Reactive
oxygen species enhance insulin sensitivity. Cell Metab. 10:260–272.
2009. View Article : Google Scholar : PubMed/NCBI
|
19
|
Whelan SA, Dias WB, Thiruneelakantapillai
L, Lane MD and Hart GW: Regulation of insulin receptor substrate 1
(IRS-1)/AKT kinase-mediated insulin signaling by O-Linked
beta-N-acetylglucosamine in 3T3-L1 adipocytes. J Biol Chem.
285:5204–5211. 2010. View Article : Google Scholar : PubMed/NCBI
|
20
|
Cong LN, Chen H, Li Y, Zhou L, McGibbon
MA, Taylor SI and Quon MJ: Physiological role of Akt in
insulin-stimulated translocation of GLUT4 in transfected rat
adipose cells. Mol Endocrinol. 11:1881–1890. 1997. View Article : Google Scholar : PubMed/NCBI
|
21
|
Favaretto F, Milan G, Collin GB, Marshall
JD, Stasi F, Maffei P, Vettor R and Naggert JK: GLUT4 defects in
adipose tissue are early signs of metabolic alterations in
Alms1GT/GT, a mouse model for obesity and insulin resistance. PLoS
One. 9:e1095402014. View Article : Google Scholar : PubMed/NCBI
|
22
|
Chen YH, Heneidi S, Lee JM, Layman LC,
Stepp DW, Gamboa GM, Chen BS, Chazenbalk G and Azziz R: miRNA-93
inhibits GLUT4 and is overexpressed in adipose tissue of polycystic
ovary syndrome patients and women with insulin resistance.
Diabetes. 62:2278–2286. 2013. View Article : Google Scholar : PubMed/NCBI
|
23
|
Nakashima N, Sharma PM, Imamura T,
Bookstein R and Olefsky JM: The tumor suppressor PTEN negatively
regulates insulin signaling in 3T3-L1 adipocytes. J Biol Chem.
275:12889–12895. 2000. View Article : Google Scholar : PubMed/NCBI
|
24
|
Mehlem A, Hagberg CE, Muhl L, Eriksson U
and Falkevall A: Imaging of neutral lipids by oil red O for
analyzing the metabolic status in health and disease. Nat Protoc.
8:1149–1154. 2013. View Article : Google Scholar : PubMed/NCBI
|
25
|
Potashnik R, Bloch-Damti A, Bashan N and
Rudich A: IRS1 degradation and increased serine phosphorylation
cannot predict the degree of metabolic insulin resistance induced
by oxidative stress. Diabetologia. 46:639–648. 2003. View Article : Google Scholar : PubMed/NCBI
|
26
|
Yang P, Zhao Y, Zhao L, Yuan J, Chen Y,
Varghese Z, Moorhead JF, Chen Y and Ruan XZ: Paradoxical effect of
rapamycin on inflammatory stress-induced insulin resistance in
vitro and in vivo. Sci Rep. 5:149592015. View Article : Google Scholar : PubMed/NCBI
|
27
|
Lee SR, Yang KS, Kwon J, Lee C, Jeong W
and Rhee SG: Reversible inactivation of the tumor suppressor PTEN
by H2O2. J Biol Chem. 277:20336–20342. 2002.
View Article : Google Scholar : PubMed/NCBI
|
28
|
Jiang X, Huang L and Xing D:
Photoactivation of Dok1/ERK/PPARγ signaling axis inhibits excessive
lipolysis in insulin-resistant adipocytes. Cell Signal.
27:1265–1275. 2015. View Article : Google Scholar : PubMed/NCBI
|
29
|
Bernlohr DA, Bolanowski MA, Kelly TJ Jr
and Lane MD: Evidence for an increase in transcription of specific
mRNAs during differentiation of 3T3-L1 preadipocytes. J Biol Chem.
260:5563–5567. 1985.PubMed/NCBI
|
30
|
Turpin SM, Nicholls HT, Willmes DM,
Mourier A, Brodesser S, Wunderlich CM, Mauer J, Xu E, Hammerschmidt
P, Brönneke HS, et al: Obesity-induced CerS6-dependent C16:0
ceramide production promotes weight gain and glucose intolerance.
Cell Metab. 20:678–686. 2014. View Article : Google Scholar : PubMed/NCBI
|
31
|
Quan YY, Qin GQ, Huang H, Liu YH, Wang XP
and Chen TS: Dominant roles of Fenton reaction in sodium
nitroprusside-induced chondrocyte apoptosis. Free Radic Biol Med.
94:135–144. 2016. View Article : Google Scholar : PubMed/NCBI
|
32
|
Whiteman EL, Cho H and Birnbaum MJ: Role
of Akt/protein kinase B in metabolism. Trends Endocrinol Metab.
13:444–451. 2002. View Article : Google Scholar : PubMed/NCBI
|
33
|
Gonzalez E, Flier E, Molle D, Accili D and
McGraw TE: Hyperinsulinemia leads to uncoupled insulin regulation
of the GLUT4 glucose transporter and the FoxO1 transcription
factor. Proc Natl Acad Sci USA. 108:10162–10167. 2011. View Article : Google Scholar : PubMed/NCBI
|
34
|
Koseoglu S, Lu Z, Kumar C, Kirschmeier P
and Zou J: AKT1, AKT2 and AKT3-dependent cell survival is cell
line-specific and knockdown of all three isoforms selectively
induces apoptosis in 20 human tumor cell lines. Cancer Biol Ther.
6:755–762. 2007. View Article : Google Scholar : PubMed/NCBI
|
35
|
Bryant NJ, Govers R and James DE:
Regulated transport of the glucose transporter GLUT4. Nat Rev Mol
Cell Biol. 3:267–277. 2002. View
Article : Google Scholar : PubMed/NCBI
|
36
|
Goldstein BJ, Mahadev K, Wu X, Zhu L and
Motoshima H: Role of insulin-induced reactive oxygen species in the
insulin signaling pathway. Antioxid Redox Signal. 7:1021–1031.
2005. View Article : Google Scholar : PubMed/NCBI
|
37
|
Tonks NK: Protein tyrosine phosphatases:
From genes, to function, to disease. Nat Rev Mol Cell Biol.
7:833–846. 2006. View Article : Google Scholar : PubMed/NCBI
|
38
|
Bloch-Damti A and Bashan N: Proposed
mechanisms for the induction of insulin resistance by oxidative
stress. Antioxid Redox Signal. 7:1553–1567. 2005. View Article : Google Scholar : PubMed/NCBI
|
39
|
Ding H, Heng B, He W, Shi L, Lai C, Xiao
L, Ren H, Mo S and Su Z: Chronic reactive oxygen species exposure
inhibits glucose uptake and causes insulin resistance in C2C12
myotubes. Biochem Biophys Res Commun. 478:798–803. 2016. View Article : Google Scholar : PubMed/NCBI
|
40
|
Matsukawa J, Matsuzawa A, Takeda K and
Ichijo H: The ASK1-MAP kinase cascades in mammalian stress
response. J Biochem. 136:261–265. 2004. View Article : Google Scholar : PubMed/NCBI
|
41
|
Tobiume K, Matsuzawa A, Takahashi T,
Nishitoh H, Morita K, Takeda K, Minowa O, Miyazono K, Noda T and
Ichijo H: ASK1 is required for sustained activations of JNK/p38 MAP
kinases and apoptosis. EMBO Rep. 2:222–228. 2001. View Article : Google Scholar : PubMed/NCBI
|
42
|
Storz P and Toker A: Protein kinase D
mediates a stress-induced NF-kappaB activation and survival
pathway. EMBO J. 22:109–120. 2003. View Article : Google Scholar : PubMed/NCBI
|
43
|
Gual P, Le Marchand-Brustel Y and Tanti
JF: Positive and negative regulation of insulin signaling through
IRS-1 phosphorylation. Biochimie. 87:99–109. 2005. View Article : Google Scholar : PubMed/NCBI
|