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Review
. 2021 Feb 11;22(4):1786.
doi: 10.3390/ijms22041786.

Oxidative Stress, Plant Natural Antioxidants, and Obesity

Affiliations
Review

Oxidative Stress, Plant Natural Antioxidants, and Obesity

Israel Pérez-Torres et al. Int J Mol Sci. .

Abstract

Oxidative stress is important in the pathophysiology of obesity, altering regulatory factors of mitochondrial activity, modifying the concentration of inflammation mediators associated with a large number and size of adipocytes, promoting lipogenesis, stimulating differentiation of preadipocytes to mature adipocytes, and regulating the energy balance in hypothalamic neurons that control appetite. This review discusses the participation of oxidative stress in obesity and the important groups of compounds found in plants with antioxidant properties, which include (a) polyphenols such as phenolic acids, stilbenes, flavonoids (flavonols, flavanols, anthocyanins, flavanones, flavones, flavanonols, and isoflavones), and curcuminoids (b) carotenoids, (c) capsaicinoids and casinoids, (d) isothiocyanates, (e) catechins, and (f) vitamins. Examples are analyzed, such as resveratrol, quercetin, curcumin, ferulic acid, phloretin, green tea, Hibiscus Sabdariffa, and garlic. The antioxidant activities of these compounds depend on their activities as reactive oxygen species (ROS) scavengers and on their capacity to prevent the activation of NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells), and reduce the expression of target genes, including those participating in inflammation. We conclude that natural compounds have therapeutic potential for diseases mediated by oxidative stress, particularly obesity. Controlled and well-designed clinical trials are still necessary to better know the effects of these compounds.

Keywords: antioxidants; natural products; obesity; oxidative stress.

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Conflict of interest statement

We declare we do not have any conflict of interest.

Figures

Figure 1
Figure 1
Pathways generating reactive oxygen species (ROS) and their impact on obesity Abbreviations: AgRP = agouti-related protein, Ang II = Angiotensin II, eNOS = endothelial nitric oxide synthase, H2O2 = hydrogen peroxide, IκBα = nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, GLUT 4 = gucose transporter type 4, IGF-1 = insulin-like growth factor 1, IGF-1R = insulin-like growth factor 1 receptor, IL = Interleucine, IR = insulin receptor, IRS 1 = insulin receptor substrate 1, LR = Leptin receptor, NF-κB = nuclear factor κ-light-chain-enhancer of activated B cells, NOX = nicotinamide adenine dinucleotide phosphate oxidase, NPY = neuropeptide Y, O2− = superoxide anion, PI3k = phosphoinositide 3-kinase, PPP = pentose phosphate pathway, ROS = reactive oxygen species, SOD = superoxide dismutase, TNF-α = factor de necrosis tumoral alfa, UPR = unfolded protein response. Blue arrows indicate flow through the pathway; red arrows indicate increases or decreases.
Figure 2
Figure 2
Types of adipocytes, their distribution, and their functions.
Figure 3
Figure 3
Summary of the interaction of antioxidant groups found in natural plants and the different metabolic pathways to induce anti obesogenic effects. The numbers correspond to the natural product and the “**” correspond to the enzymes stimulated by Nrf2. Abbreviations: Ang II = Angiotensin II, eNOS = endothelial nitric oxide synthase, H2O2 = hydrogen peroxide, GLUT 4 = glucose transporter type 4, GR = glutathione reductase, GSH = glutathione, GSSG = oxidized glutathione, IGF-1 = insulin-like growth factor 1, IGF-1R = insulin-like growth factor 1 receptor, IL = Interleukin, IR = insulin receptor, IRS 1 = insulin receptor substrate 1, LR = Leptin receptor, NF-κB = nuclear factor κ-light-chain-enhancer of activated B cells, NOS = nitric oxide synthase, NOX = nicotinamide adenine dinucleotide phosphate oxidase, O2− = superoxide anion, PI3k = phosphoinositide 3-kinase, PPAR = peroxisome proliferator–activated receptor, PPP = pentose phosphate patway, ROS = reactive oxygen species, SOD = superoxide dismutase, TNF-α = factor de necrosis tumoral alfa.

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