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Inflammation, oxidative stress, and obesity.

Fernández-Sánchez A, Madrigal-Santillán E, Bautista M, Esquivel-Soto J, Morales-González A, Esquivel-Chirino C, Durante-Montiel I, Sánchez-Rivera G, Valadez-Vega C, Morales-González JA - Int J Mol Sci (2011)

Bottom Line: The first of these is the mitochondrial and peroxisomal oxidation of fatty acids, which can produce ROS in oxidation reactions, while another mechanism is over-consumption of oxygen, which generates free radicals in the mitochondrial respiratory chain that is found coupled with oxidative phosphorylation in mitochondria.Upon the increase of adipose tissue, the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was found to be significantly diminished.Finally, high ROS production and the decrease in antioxidant capacity leads to various abnormalities, among which we find endothelial dysfunction, which is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide (NO), and an increase in endothelium-derived contractile factors, favoring atherosclerotic disease.

View Article: PubMed Central - PubMed

Affiliation: Instituto de Ciencias de la Salud, Universidad Autónoma del Estado de Hidalgo, Ex-Hacienda de la Concepción, Tilcuautla, 42080 Pachuca de Soto, Hgo, Mexico; E-Mails: alba_mfs@hotmail.com (A.F.-S.); eomsmx@yahoo.com.mx (E.M.-S.); mirandeli@hotmail.com (M.B.); m.valadezvega@lycos.com (C.V.-V.).

ABSTRACT
Obesity is a chronic disease of multifactorial origin and can be defined as an increase in the accumulation of body fat. Adipose tissue is not only a triglyceride storage organ, but studies have shown the role of white adipose tissue as a producer of certain bioactive substances called adipokines. Among adipokines, we find some inflammatory functions, such as Interleukin-6 (IL-6); other adipokines entail the functions of regulating food intake, therefore exerting a direct effect on weight control. This is the case of leptin, which acts on the limbic system by stimulating dopamine uptake, creating a feeling of fullness. However, these adipokines induce the production of reactive oxygen species (ROS), generating a process known as oxidative stress (OS). Because adipose tissue is the organ that secretes adipokines and these in turn generate ROS, adipose tissue is considered an independent factor for the generation of systemic OS. There are several mechanisms by which obesity produces OS. The first of these is the mitochondrial and peroxisomal oxidation of fatty acids, which can produce ROS in oxidation reactions, while another mechanism is over-consumption of oxygen, which generates free radicals in the mitochondrial respiratory chain that is found coupled with oxidative phosphorylation in mitochondria. Lipid-rich diets are also capable of generating ROS because they can alter oxygen metabolism. Upon the increase of adipose tissue, the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was found to be significantly diminished. Finally, high ROS production and the decrease in antioxidant capacity leads to various abnormalities, among which we find endothelial dysfunction, which is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide (NO), and an increase in endothelium-derived contractile factors, favoring atherosclerotic disease.

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This figure depicts the major adipokines and their roles. Adipose tissue produces several adipokines that exert metabolic effects, both in central and in peripheral tissues. The production of these adipokines is regulated by insulin, cathecholamines, and adiposity. TNF-alpha: Tumor necrosis factor-alpha; IL-6: Interleukin. (Courtesy of Cristina Fernández-Mejía, Ph.D.).
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f1-ijms-12-03117: This figure depicts the major adipokines and their roles. Adipose tissue produces several adipokines that exert metabolic effects, both in central and in peripheral tissues. The production of these adipokines is regulated by insulin, cathecholamines, and adiposity. TNF-alpha: Tumor necrosis factor-alpha; IL-6: Interleukin. (Courtesy of Cristina Fernández-Mejía, Ph.D.).

Mentions: In animals with obesity, there is a huge increase in white fat deposits due to the hyperplasia and hypertrophy of their adipocytes [8]. Hypertrophic-hyperplastic adipocytes exhibit a lower density of insulin receptors and a higher beta-3 adrenergic receptor, which facilitates the diapedesis of monocytes to visceral adipose stroma, initiating a proinflammatory cycle between adipo- and monocytes [10]. Adipose tissue is not only a triglyceride (TG)-storage tissue; studies in recent years have shown the role of white adipose tissue as a producer of certain substances with endocrine, paracrine, and autocrine action [2]. These bioactive substances are denominated adipokines or adipocytokines, among which are found plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-alpha (TNF-α), resistin, leptin, and adiponectin [11]. These substances derive primarily from white adipose tissue and play a role in the homeostasis of various physiological processes (Figure 1).


Inflammation, oxidative stress, and obesity.

Fernández-Sánchez A, Madrigal-Santillán E, Bautista M, Esquivel-Soto J, Morales-González A, Esquivel-Chirino C, Durante-Montiel I, Sánchez-Rivera G, Valadez-Vega C, Morales-González JA - Int J Mol Sci (2011)

This figure depicts the major adipokines and their roles. Adipose tissue produces several adipokines that exert metabolic effects, both in central and in peripheral tissues. The production of these adipokines is regulated by insulin, cathecholamines, and adiposity. TNF-alpha: Tumor necrosis factor-alpha; IL-6: Interleukin. (Courtesy of Cristina Fernández-Mejía, Ph.D.).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3116179&req=5

f1-ijms-12-03117: This figure depicts the major adipokines and their roles. Adipose tissue produces several adipokines that exert metabolic effects, both in central and in peripheral tissues. The production of these adipokines is regulated by insulin, cathecholamines, and adiposity. TNF-alpha: Tumor necrosis factor-alpha; IL-6: Interleukin. (Courtesy of Cristina Fernández-Mejía, Ph.D.).
Mentions: In animals with obesity, there is a huge increase in white fat deposits due to the hyperplasia and hypertrophy of their adipocytes [8]. Hypertrophic-hyperplastic adipocytes exhibit a lower density of insulin receptors and a higher beta-3 adrenergic receptor, which facilitates the diapedesis of monocytes to visceral adipose stroma, initiating a proinflammatory cycle between adipo- and monocytes [10]. Adipose tissue is not only a triglyceride (TG)-storage tissue; studies in recent years have shown the role of white adipose tissue as a producer of certain substances with endocrine, paracrine, and autocrine action [2]. These bioactive substances are denominated adipokines or adipocytokines, among which are found plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-alpha (TNF-α), resistin, leptin, and adiponectin [11]. These substances derive primarily from white adipose tissue and play a role in the homeostasis of various physiological processes (Figure 1).

Bottom Line: The first of these is the mitochondrial and peroxisomal oxidation of fatty acids, which can produce ROS in oxidation reactions, while another mechanism is over-consumption of oxygen, which generates free radicals in the mitochondrial respiratory chain that is found coupled with oxidative phosphorylation in mitochondria.Upon the increase of adipose tissue, the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was found to be significantly diminished.Finally, high ROS production and the decrease in antioxidant capacity leads to various abnormalities, among which we find endothelial dysfunction, which is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide (NO), and an increase in endothelium-derived contractile factors, favoring atherosclerotic disease.

View Article: PubMed Central - PubMed

Affiliation: Instituto de Ciencias de la Salud, Universidad Autónoma del Estado de Hidalgo, Ex-Hacienda de la Concepción, Tilcuautla, 42080 Pachuca de Soto, Hgo, Mexico; E-Mails: alba_mfs@hotmail.com (A.F.-S.); eomsmx@yahoo.com.mx (E.M.-S.); mirandeli@hotmail.com (M.B.); m.valadezvega@lycos.com (C.V.-V.).

ABSTRACT
Obesity is a chronic disease of multifactorial origin and can be defined as an increase in the accumulation of body fat. Adipose tissue is not only a triglyceride storage organ, but studies have shown the role of white adipose tissue as a producer of certain bioactive substances called adipokines. Among adipokines, we find some inflammatory functions, such as Interleukin-6 (IL-6); other adipokines entail the functions of regulating food intake, therefore exerting a direct effect on weight control. This is the case of leptin, which acts on the limbic system by stimulating dopamine uptake, creating a feeling of fullness. However, these adipokines induce the production of reactive oxygen species (ROS), generating a process known as oxidative stress (OS). Because adipose tissue is the organ that secretes adipokines and these in turn generate ROS, adipose tissue is considered an independent factor for the generation of systemic OS. There are several mechanisms by which obesity produces OS. The first of these is the mitochondrial and peroxisomal oxidation of fatty acids, which can produce ROS in oxidation reactions, while another mechanism is over-consumption of oxygen, which generates free radicals in the mitochondrial respiratory chain that is found coupled with oxidative phosphorylation in mitochondria. Lipid-rich diets are also capable of generating ROS because they can alter oxygen metabolism. Upon the increase of adipose tissue, the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was found to be significantly diminished. Finally, high ROS production and the decrease in antioxidant capacity leads to various abnormalities, among which we find endothelial dysfunction, which is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide (NO), and an increase in endothelium-derived contractile factors, favoring atherosclerotic disease.

Show MeSH
Related in: MedlinePlus