The etiology of oxidative stress in insulin resistance

Samantha Hurrle, Walter H Hsu, Samantha Hurrle, Walter H Hsu

Abstract

Insulin resistance is a prevalent syndrome in developed as well as developing countries. It is the predisposing factor for type 2 diabetes mellitus, the most common end stage development of metabolic syndrome in the United States. Previously, studies investigating type 2 diabetes have focused on beta cell dysfunction in the pancreas and insulin resistance, and developing ways to correct these dysfunctions. However, in recent years, there has been a profound interest in the role that oxidative stress in the peripheral tissues plays to induce insulin resistance. The objective of this review is to focus on the mechanism of oxidative species generation and its direct correlation to insulin resistance, to discuss the role of obesity in the pathophysiology of this phenomenon, and to explore the potential of antioxidants as treatments for metabolic dysfunction.

Keywords: Adipokines; Antioxidants; Insulin resistance; Obesity; Oxidative stress; Type 2 diabetes.

Copyright © 2017 Chang Gung University. Published by Elsevier B.V. All rights reserved.

Figures

Fig. 1
Fig. 1
Insulin receptor signaling pathway including ROS influence. The normal pathway begins with insulin binding insulin tyrosine kinase receptor. The insulin receptor phosphorylates insulin receptor substrate-1 (IRS-1) which in turn phosphorylates PI3-kinase. PI3-kinase then phosphorylates PIP2 which then activates Akt , eventually leading to glucose transporter 4 (GLUT4) translocation to the plasma membrane of skeletal muscle cells and adipocytes, thus allowing the cell to absorb extracellular glucose, lowering interstitial glucose levels and thus plasma glucose concentration. Abbreviations used: PIP2 and PIP3: phosphatidylinositol species; Rac: Rac GTPase; ROS: Reactive oxygen species; JNK1: c-Jun N-terminal kinase 1; CK-2: Casein kinase 2; NF-kB: nuclear factor kB; IF-kB: Inhibitory factor kB; p38 MAPK: p38 mitogen activated protein kinase; Akt: protein kinase B.
Fig. 2
Fig. 2
Link between obesity and insulin resistance.
Fig. 3
Fig. 3
Radical stability in ascorbic acid.

References

    1. Centers for Disease Control and Prevention . HHS; 2014. National diabetes statistics report: estimates of diabetes and its burden in the United States.
    1. World Health Organization Media Centre . WHO Press; 2016. Global report on diabetes.
    1. Aguilar M., Bhuket T., Torres S., Liu B., Wong R. Prevalence of the metabolic syndrome in the United States, 2003–2012. JAMA. 2015;313:1973–1974.
    1. Sies H. The concept of oxidative stress after 30 years. In: Gelpi R., Boveris A., Poderoso J., editors. Advances in biochemistry in health and disease. Springer; New York: 2016. pp. 3–11.
    1. Schrieber M., Chandel N. ROS function in redox signaling and oxidative stress. Curr Biol. 2014;24:453–462.
    1. Brand M. Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling. Free Radic Biol Med. 2016;100:14–31.
    1. Gao C., Zhu C., Zhao Y., Chen X., Ji C., Zhang C. Mitochondrial dysfunction is induced by high levels of glucose and free fatty acids in 3T3-L1 adipocytes. Mol Cell Endocrinol. 2010;320:25–33.
    1. Marinho S., Real C., Cyrne L., Soares H., Antunes F. Hydrogen peroxide sensing, signaling and regulation of transcription factors. Redox Biol. 2014;2:535–562.
    1. Dikalov S. Cross talk between mitochondria and NADPH oxidases. Free Rad Biol Med. 2011;51:1289–1301.
    1. Hancer N., Qiu W., Cherella C., Li Y., Copps K., White M. Insulin and metabolic stress stimulate multisite serine/threonine phosphorylation of insulin receptor substrate 1 and inhibit tyrosine phosphorylation. J Biol Chem. 2014;29:12467–12484.
    1. Cooper G. 7th ed. Sinauer; Massachusetts: 2013. The cell: a molecular approach.
    1. Blanco C., McGill-Vargas L., Gastaldelli A., Seidner S., McCurnin D., Leland M. Peripheral insulin resistance and impaired insulin signaling contribute to abnormal glucose metabolism in preterm baboons. Endocrinology. 2015;156:813–823.
    1. Ma J., Nakagawa Y., Kojima I., Shibata H. Prolonged insulin stimulation down-regulates GLUT4 through oxidative stress-mediated retromer inhibition by a protein kinase CK2-dependent mechanism in 3T3-L1 adipocytes. J Biol Chem. 2013;298:133–142.
    1. Campa C., Ciraolo E., Ghigo A., Germena G., Hirsch E. Crossroads of PI3K and rac pathways. Small GTPases. 2015;6:71–80.
    1. Henriksen E., Diamond-Stanic M., Marchionne E. Oxidative stress and the etiology of insulin resistance and type 2 diabetes. Free Radic Biol Med. 2011;51:993–999.
    1. Tsai H., Wang W., Lin C., Pai P., Lai T., Tsai C. NADPH oxidase-derived superoxide anion-induced apoptosis is mediated via the JNK dependent activation of NF-kB in cardiomyocytes exposed to high glucose. J Cell Physiol. 2012;227:1347–1357.
    1. Al-Lahham R., Deford J., Papaconstantinou J. Mitochondrial-generated ROS down regulates insulin signaling via activation of p38 MAPK stress response pathway. Mol Cell Endocrinol. 2015;419:1–11.
    1. Boucher J., Kleinridders A., Kahn C. Insulin receptor signalling in normal and insulin resistant states. Cold Spring Harb Perspect Biol. 2014;6:1–23.
    1. Jheng H., Tsai P., Guo S., Kuo L., Chang C., Su I. Mitochondrial fission contributes to mitochondrial dysfunction and insulin resistance in skeletal muscle. Mol Cell Biol. 2012;32:309–319.
    1. Paio M., Kang K., Lee I., Kim H., Kim S., Choi J. Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis. Toxicol Lett. 2011;201:92–100.
    1. Matsuda M., Shimomura I. Increased oxidative stress in obesity: implications for metabolic syndrome, diabetes, hypertension, dyslipidemia, atherosclerosis, and cancer. Obes Res Clin Pract. 2013;7:330–341.
    1. Cohen D., LeRoith D. Obesity, type 2 diabetes, and cancer: the insulin and IGF connection. Endocr Relat Cancer. 2012;19:F27–F45.
    1. Gaggini M., Morelli M., Buzzigoli E., DeFronzo R., Bugianesi E., Gastaldelli A. Non-alcoholic fatty liver disease (NAFLD) and its connection with insulin resistance, dyslipidemia, atherosclerosis and coronary heart disease. Nutrients. 2013;5:1544–1560.
    1. Esser N., Legrand-Poels S., Piette J., Scheen A., Paquot N. Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes. Diabetes Res Clin Pract. 2014;105:141–150.
    1. Boden G. Obesity, insulin resistance, and free fatty acids. Curr Opin Endocrinol Diabetes Obes. 2011;18:139–143.
    1. Heinonen S., Muniandy M., Buzkova J., Mardinoglu A., Rodriguez A., Fruhbeck G. Mitochondria-related transcriptional signature is downregulated in adipocytes in obesity: a study of young healthy MZ twins. Diabetologia. 2017;60:169–181.
    1. Salzano S., Checconi P., Hanschmann E., Lillig C., Bowler L., Chan P. Linkage of inflammation and oxidative stress via release of glutathionylated peroxiredoxin-2, which acts as a danger signal. Proc Natl Acad Sci U S A. 2014;111:12157–12162.
    1. Lee M., Wu Y., Fried S. Adipose tissue heterogeneity: implications of depot differences in adipose tissue for obesity complications. Mol Asp Med. 2013;34:1–11.
    1. Franceschi C., Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. J Gerontol. 2014;69:4–9.
    1. Barnes M., Carson M., Nair M. Non-traditional cytokines: how catecholamines and adipokines influence macrophages in immunity, metabolism and the central nervous system. Cytokine. 2015;72:210–219.
    1. Kizer J. A tangled threesome: adiponectin, insulin sensitivity, and adiposity. Diabetes. 2013;62:1007–1009.
    1. Shehzad A., Iqbal W., Shehzad O., Lee Y. Adiponectin: regulation of its production and its role in human disease. Hormones. 2012;1:8–20.
    1. Awazawa M., Ueki K., Inabe K., Yamauchi T., Kubota N., Kaneko K. Adiponectin enhances insulin sensitivity by increasing hepatic IRS-2 expression via a macrophage-derived IL-6-dependent pathway. Cell Metab. 2011;13:401–412.
    1. Adams A., Kharitonenkov A. FGF21 drives a shift in adipocytokine tone to restore metabolic health. Aging. 2013;15:386–387.
    1. Heredia F., Gomez-Martinez S., Marcos A. Obesity, inflammation, and the immune system. Proc Nutr Soc. 2012;71:332–338.
    1. Matsuzawa Y. The metabolic syndrome and adipocytokines. Expert Rev Clin Immunol. 2014;3:39–46.
    1. Shuster A., Patlas M., Pinthus J., Mourtzakis M. The clinical importance of visceral adiposity: a critical review for methods for visceral adipose tissue analysis. Br J Radiol. 2012;85:1–10.
    1. Reczek C., Chandel N. ROS-dependent signal transduction. Curr Opin Cell Biol. 2015;33:8–13.
    1. Halliwell B., Gutteridge J. 5th ed. Oxford; United Kingdom: 2015. Free radicals in biology and medicine.
    1. Reece J., Campbell N., Cain M., Urry L., Wasserman S., Minorsky P. 10th ed. Cummings/Pearson; Massachusetts: 2014. Campbell biology.
    1. Pratt C., Cornely K. 3rd ed. Wiley; New Jersey: 2014. Essential biochemistry.
    1. Sleiman D., Al-Badri M., Azar S. Effect of Mediterranean diet in diabetes control and cardiovascular risk modification: a systematic review. Front Public Health. 2015;3:69.
    1. Mason S., Della Gatta P., Snow R., Russell A., Wadley G. Ascorbic acid supplementation improves skeletal muscle oxidative stress and insulin sensitivity in people with diabetes: findings of a randomized controlled study. Free Radic Biol Med. 2016;93:227–238.
    1. Etsuo N. Role of vitamin E as a lipid-soluble peroxyl radical scavenger: in vitro and in vivo evidence. Free Radic Biol Med. 2014;66:3–12.
    1. Ramezani A., Djazayeri A., Koohdani F., Nematipour E., Javanbakht M., Keshavarz S. Omega-3 fatty acids/vitamin E behave synergistically on adiponectin receptor-1 and adiponectin receptor-2 gene expressions in peripheral blood mononuclear cell of coronary artery disease patients. Curr Top Nutraceutical Res. 2015;13:23–32.
    1. Li D., Zhang Y., Liu Y., Sun R., Xia M. Purified anthocyanin supplementation reduces dyslipidemia, enhances antioxidant capacity, and prevents insulin resistance in diabetic patients. J Nutr. 2015;145:742–748.
    1. Suliburska J., Bogdanski P., Szulinska M., Stepien M., Pupek-Musialik D., Jablecka A. Effects of green tea supplementation on elements, total antioxidants, lipids, and glucose values in the serum of obese patients. Biol Trace Elem Res. 2012;149:315–322.
    1. Ihm S., Jang S., Kim O., Chang K., Oak M., Lee J. Decaffeinated green tea extract improves hypertension and insulin resistance in a rat model of metabolic syndrome. Atherosclerosis. 2012;224:377–383.
    1. Mann J., Lonn E., Yi Q., Gerstein H., Hoogwerf B., Pogue J. Effects of vitamin E on cardiovascular outcomes in people with mild-to-moderate renal insufficiency: results of the HOPE study. Kidney Int. 2004;65:1375–1380.
    1. Lee D., Folsom A., Harnack L., Halliwell B., Jacobs D. Does supplemental vitamin C increase cardiovascular disease risk in women with diabetes? Am J Clin Nutr. 2004;80:1194–1200.
    1. Parrow N., Leshin J., Levine M. Parenteral ascorbate as a cancer therapeutic: a reassessment based on pharmacokinetics. Antioxid Redox Signal. 2013;19:2141–2156.
    1. Padayatty S., Sun H., Wang Y., Riordan H., Hewitt S., Katz A. Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Intern Med. 2004;140:533–537.
    1. Borel P., Desmarchelier C., Nowicki M., Bott R., Tourniaire F. Can genetic variability in α-tocopherol bioavailability explain the heterogenous response to a-tocopherol supplements? Antioxid Redox Signal. 2014;22:669–678.
    1. Deng C., Sun Z., Tong G., Yi W., Ma L., Zhao B. α-Lipoic acid reduces infarct size and preserves cardiac function in rat myocardial ischemia/reperfusion injury through activation of PI3K/Akt/Nrf2 pathway. PLoS One. 2013;8:e58371.
    1. Inman D., Lambert W., Calkins D., Horner P. α-Lipoic acid antioxidant treatment limits glaucoma retinal ganglion cell death and dysfunction. PLoS One. 2013;8:e65389.
    1. Liu R. Health promoting components of fruits and vegetables in the diet. Adv Nutr. 2013;14:3845–3925.
    1. Ismail H., Scapozza L., Ruegg U., Dorchies O. Diapocynin, a dimer of NADPH oxidase inhibitor apocynin, reduces ROS production and prevents force loss in eccentrically contracting dystrophic muscle. PLoS Med. 2014;9:1–8.

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