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Review
. 2012 Sep;17(5):348-56.
doi: 10.1007/s12199-012-0271-0. Epub 2012 Feb 24.

Preventive and improvement effects of exercise training and supplement intake in white adipose tissues on obesity and lifestyle-related diseases

Affiliations
Review

Preventive and improvement effects of exercise training and supplement intake in white adipose tissues on obesity and lifestyle-related diseases

Takuya Sakurai et al. Environ Health Prev Med. 2012 Sep.

Abstract

Recent increases in the number of obese individuals and individuals suffering from lifestyle-related diseases, such as type 2 diabetes, that accompany obesity have become a serious social problem. White adipose tissue (WAT) is more than a mere organ for storage of energy; it is also a highly active metabolic and endocrine organ that secretes physiologically active substances collectively known as adipokines, including tumor necrosis factor-α and adiponectin. Dysregulated expression of adipokines in WAT that is hypertrophied by obesity has been closely associated with the phenomenon of insulin resistance. Therefore, WAT is currently considered to be one of the tissues that promote lifestyle-related diseases. Reduction of excess WAT that results from obesity is seen as an important strategy in preventing and improving lifestyle-related diseases. This review shows that exercise training as well as intake of supplements, such as polyphenols, is one strategy for this, because this regimen can result in reduction of WAT mass, which affects the expression and secretory response of adipokines.

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Figures

Fig. 1
Fig. 1
Effects of exercise training on the adrenergic receptor-mediated, adipocyte lipolytic response. When β-adrenergic receptor (β-AR) binds to an agonist and associates with a stimulatory G protein (Gs), adenylate cyclase (AC) is activated by Gs α subunit (Gαs) and cyclic AMP (cAMP) is produced. cAMP stimulates cAMP-dependent kinase (PKA), and hormone-sensitive lipase (HSL) is phosphorylated and activated. The activated HSL hydrolyzes triglycerides (TG). On the contrary, TG degradation is suppressed by the inhibition of cAMP production by α2-AR through the inhibitory G protein α subunit (Gαi). Insulin inhibits the lipolytic response via downregulation of cAMP production by activated phosphodiesterase 3B. Exercise training (TR) increases the association efficiency of the β-AR and Gs, and leads to a reduction in the amount of Gi protein. As a result, sensitivity and reactivity to β-AR agonists increase. FFA free fatty acid, IRS insulin receptor substrate, PI3K phosphatidylinositol-3 kinase
Fig. 2
Fig. 2
Schematic model for a proposed mechanism of TR-induced reduction of adipocyte numbers in white adipose tissue. TR suppresses adipocyte differentiation of stromal-vascular fraction (SVF) cells containing adipose tissue-derived stem cells (ADSC) in white adipose tissue (WAT). Possible mechanisms for the TR-induced inhibition of adipogenesis may be enhanced expression of pre-adipocyte factor-1 (Pref-1), and decreased expression of peroxisome proliferator-activated receptor γ (PPARγ), through upregulation of the hypoxia-inducible factor-1α (HIF-1α) level in SVF cells. However, the ability of SVF cells containing ADSC to differentiate into vascular endothelial cells is retained after TR
Fig. 3
Fig. 3
Model of the development of chronic inflammation in WAT. Adipocytes begin to grow as a result of factors such as excess energy intake and lack of exercise, and MCP-1 is secreted from these enlarged cells. Macrophages infiltrate into WAT by the action of MCP-1, and as a result, increased expression of inflammatory adipokines [TNF-α, MCP-1, and interleukin-6 (IL-6)] and decreased expression of anti-inflammatory adipokines (adiponectin) occur in WAT
Fig. 4
Fig. 4
Schematic model for the antioxidative/anti-inflammatory effects of TR and polyphenol intake in WAT. TR and polyphenol intake are thought to provide decreased expression of inflammation-related adipokines through reduction of oxidative stress in WAT. Mn-SOD manganese-containing superoxide dismutase, NOX2 nicotinamide adenine dinucleotide phosphate oxidase 2

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