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Review
. 2015 Apr 15;6(3):456-80.
doi: 10.4239/wjd.v6.i3.456.

Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitus

Surapon Tangvarasittichai  1
Affiliations
Review

Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitus

Surapon Tangvarasittichai. World J Diabetes. .

Abstract

Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus (T2DM) and this appears to underlie the development of cardiovascular disease, T2DM and diabetic complications. Increased oxidative stress appears to be a deleterious factor leading to insulin resistance, dyslipidemia, β-cell dysfunction, impaired glucose tolerance and ultimately leading to T2DM. Chronic oxidative stress, hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant, have high oxidative energy requirements, decrease the gene expression of key β-cell genes and induce cell death. If β-cell functioning is impaired, it results in an under production of insulin, impairs glucose stimulated insulin secretion, fasting hyperglycemia and eventually the development of T2DM.

Keywords: Dyslipidemia; Insulin resistance; Oxidative stress; Type 2 diabetes mellitus.

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Figures

Figure 1
Figure 1
Summarized of obesity and metabolic syndrome elevate in oxidative stress. T2DM: Type 2 diabetes mellitus; MetS: Metabolic syndrome.
Math 1
Math 1
Math(A1).
Figure 2
Figure 2
Increased oxidative stress by xanthine oxidase. NADH: Nicotinamide adenine dinucleotide.
Figure 3
Figure 3
The chain reaction of lipid peroxidation.
Math 2
Math 2
Math(A1).
Figure 4
Figure 4
Summarized the increasing reactive oxygen species in obesity, metabolic syndrome and salt sensitive hypertension. FFA: Free fatty acid; MetS: Metabolic syndrome; HT: Hypertension; IGT: Impaired glucose tolerance.
Figure 5
Figure 5
Summarizes the reactive oxygen species associations with atherosclerosis and sources of reactive oxygen species production in type 2 diabetes. oxLDL: Oxidized low density lipoprotein; FFA: Free fatty acids; AGEs: Advanced glycation end-products; VSMC: Vascular smooth muscle cells; ROS: Reactive oxygen species.
Figure 6
Figure 6
Insulin resistancedevelopment and consequence of β-cell dysfunction. FFA: Free fatty acid.
Figure 7
Figure 7
Summarized the etiology of the type 2 diabetes mellitus pathogenesis. FFA: Free fatty acid; NF-κB: Nuclear factor-κB; TNF-α: Tumor necrosis factor α.
Figure 8
Figure 8
Connection between life style, oxidative stress, insulin resistance, inflammation and atherosclerosis. FFA: Free fatty acid; NO: Nitric oxide; MNC: Mononuclear cells; PMN: Polymorpho nuclear cells; CRP: C-reactive protein; MIF: Migration inhibitory factor.
See this image and copyright information in PMC

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