The Effects of Exercise Training on Obesity-Induced Dysregulated Expression of Adipokines in White Adipose Tissue

Sakurai, Takeshi; Ogasawara, Jun; Kizaki, Takako; Sato, Shogo; Ishibashi, Yoshinaga; Takahashi, Motoko; Kobayashi, Osamu; Oh‐ishi, Shuji; Nagasawa, Jun’ichi; Takahashi, Kazuto; Ishida, Hideyuki; Izawa, Tetsuya; Ohno, Hideki

doi:10.1155/2013/801743

Cited by 65 publications

(57 citation statements)

References 118 publications

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“…The dose response to exercise was apparent with body fat adjustment, but we also observed a significant difference between unadjusted baseline and final levels in leptin for the high-dose exercise group. Our findings are in line with others that have investigated the effect of exercise and changes in body composition on leptin levels (32). Following 12-month aerobic exercise interventions, Abbenhardt and colleagues observed a 13% reduction in leptin levels with exercise and Frank and colleagues a 7% reduction (15,33).…”

Section: Discussionsupporting

confidence: 92%

Exercise-Induced Dose-Response Alterations in Adiponectin and Leptin Levels Are Dependent on Body Fat Changes in Women at Risk for Breast Cancer

Sturgeon

DiGiovanni

Good

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Dysregulation of adipokines, such as adiponectin and leptin, is associated with a variety of chronic diseases, including cancer. Physical activity protects against breast cancer and one of the mechanisms which may underlie this association is exercise-induced changes in adipokine levels. The WISER Sister Trial was a three-armed randomized controlled trial in premenopausal women (n ¼ 137) with an elevated risk for breast cancer.Methods: A 5-menstrual-cycle-long dosed aerobic exercise intervention compared low-dose exercise (150 min/wk; n ¼ 44) or high-dose exercise (300 min/wk; n ¼ 48) with a control group asked to maintain usual activity levels (n ¼ 45). Exercise intensity progressed to and was maintained at 70% to 80% of age predicted heart rate max. Body composition and adipokine levels were measured at baseline and follow-up.

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Section: Discussionsupporting

confidence: 92%

Exercise-Induced Dose-Response Alterations in Adiponectin and Leptin Levels Are Dependent on Body Fat Changes in Women at Risk for Breast Cancer

Sturgeon

DiGiovanni

Good

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…This therefore suggests that the biological mechanisms by which exercise training provides benefits on the cardiovascular system, may underlie the protective associations demonstrated in the current study. Physical activity exerts cardioprotective effects via (i) improvement in cardiovascular risk factors such as blood pressure, biomarkers of insulin resistance, lipid and glucose levels, natriuretic peptides, and cardiac troponin T; [30][31][32] (ii) its anti-inflammatory actions, by reduction in levels of inflammatory markers such as IL-18 and C-reactive protein; [33,34] (iii) regulation of white adipose tissue mass and adipokine expression; [35] (iv) improvement in endothelial function which ultimately slows the atherosclerotic cascade; [36,37] (v) vagal control of heart rate and regulation of cardiac autonomic function; [38] and (vi) increase in cardiac output, left ventricular function, oxygen utilization, and the formation of collateral vessels. [36,39] In a meta-analysis of 160 randomized controlled trials, Lin and colleagues demonstrated that exercise significantly improved CRF with beneficial modulation of several cardiometabolic markers.…”

Section: Potential Biological Mechanismsmentioning

confidence: 99%

Associations of cardiovascular and all-cause mortality events with oxygen uptake at ventilatory threshold

Kunutsor

Kurl

Khan

et al. 2017

International Journal of Cardiology

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General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms Abbreviations BMI = body mass index CHD = coronary heart disease CRF = cardiorespiratory fitness CVD = cardiovascular disease HDL-C = high-density lipoprotein cholesterol HR = hazard ratio IDI = integrated-discrimination-improvement KIHD = Kuopio Ischaemic Heart Disease NRI = net reclassification improvement SCD = sudden cardiac death SD = standard deviation SBP = systolic blood pressure VT = ventilatory threshold VO2 = oxygen uptake ABSTRACTBackground: Oxygen uptake (VO2) at ventilatory threshold (VT), is a cardiopulmonary exercise testing parameter which may be a proxy for peak VO2. We aimed to assess the associations of VO2 at VT with sudden cardiac death (SCD), fatal coronary heart disease (CHD) and cardiovascular disease (CVD), and all-cause mortality.Methods and Results: VO2 at VT was assessed during a submaximal exercise test using respiratory gas analyzers in the Kuopio Ischemic Heart Disease cohort of 1,639 middle-aged men. Hazard ratios (HRs) (95% CIs) were assessed. During a median follow-up of 25.6 years, 121 SCDs, 202 fatal CHDs, 312 fatal CVDs, and 703 all-cause mortality events occurred. VO2 at VT was correlated with peak VO2 (r = 0.90) and linearly associated with each outcome. Comparing extreme quartiles of VO2 at VT, the HRs (95% CIs) for SCD, fatal CHD, fatal CVD, and all-cause mortality on adjustment for established risk factors Conclusions: There are linear and inverse associations of VO2 at VT with fatal cardiovascular and allcause mortality events, which are dependent on peak VO2. Inclusion of VO2 at VT in the standard established risk factors panel significantly improves the prediction and classification of long-term CVD mortality risk.

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“…Tang [19] found that high dose NPY inhibits the proliferation of 3T3-L1 cells and promotes adipocyte differentiation. Zhang et al [20] showed that NPY promotes adipogenesis in chickens by increasing production of new preadipocytes, lipid synthesis, and lipid storage.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y promotes adipogenic differentiation in primary cultured human adipose-derived stem cells

Liu

Fang

et al. 2018

Endocr J

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Abstract. Neuropeptide Y (NPY) is an important neurotransmitter in the control of energy metabolism. Several studies have shown that obesity is associated with increased levels of NPY in the hypothalamus. We hypothesized that the release of NPY has coordinated and integrated effects on energy metabolism in different tissues, such as adipocyte tissue, resulting in increased energy storage and decreased energy expenditure. Whether NPY has role in the molecular mechanism of human adipocyte tissue remains unclear. We established the model of human adipose derived stem cells (hADSCs) from human adipose tissue and differentiated it into adipocytes in the presence of NPY at different concentrations (10 -15 -10 -6 mmol/L). We then assessed hADSCs proliferation and differentiation by quantifying lipid accumulation and examining the expression levels of related adipocyte markers after differentiation. Furthermore, the specific markers of white adipocyte tissue (WAT) in hADSCs were also analyzed. The results showed that low doses of NPY stimulated hADSCs proliferation (p < 0.05), while high doses of NPY inhibited hADSCs proliferation (p < 0.05). NPY significantly promoted lipid accumulation and increased the size of lipid droplets during human adipogenic differentiation; the levels of adipocyte markers PPAR-γ and C/EBPα were also increased. At the same time, NPY also increased the levels of WAT markers Cidec and RIP140 after adipocyte differentiation. The results suggested high dose NPY inhibits the proliferation of hADSCs while promotes adipocyte differentiation and increases the expression of WAT markers. This may be the reason why increased levels of NPY can lead to a rise in body weight.Key words: Neuropeptide Y, Human adipose-derived stem cells, Adipocyte differentiation, White adipose tissue NEUROPEPTIDE Y (NPY) is a 36-amino acid neuropeptide, which is widely expressed in the central and peripheral nervous system. In the brain, NPY is found in many brain areas [1], including the hypothalamus, dentate gyrus, lateral thalamus and striatum, with the highest concentrations in the arcuate nucleus of the hypothalamus (Arc). NPY is implicated in the regulation of many physiological processes, including food intake and body energy balance. NPY also regulates cardiovascular, gastrointestinal, reproductive, endocrine and behavioural function [2][3][4]. Recently, studies have revealed that administration of NPY has profound metabolic effects throughout the body. One characteristic of obesity is the This overproduction of fat is associated with increased lipogenesis in different organs, such as liver and white adipose tissue (WAT). Several studies found that obesity is associated with elevated levels of NPY in the hypothalamus [5][6][7][8][9]. Adipose tissue is important for regulation of energy metabolism. A disturbance of metabolic processes, such as thermogenesis, lipogenesis and fatty acid oxidation, may contribute to the pathology of obesity. In order to increase our understanding of how NPY could be involved in the adipoc...

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The Effects of Exercise Training on Obesity-Induced Dysregulated Expression of Adipokines in White Adipose Tissue

Cited by 65 publications

References 118 publications

Exercise-Induced Dose-Response Alterations in Adiponectin and Leptin Levels Are Dependent on Body Fat Changes in Women at Risk for Breast Cancer

Exercise-Induced Dose-Response Alterations in Adiponectin and Leptin Levels Are Dependent on Body Fat Changes in Women at Risk for Breast Cancer

Associations of cardiovascular and all-cause mortality events with oxygen uptake at ventilatory threshold

Neuropeptide Y promotes adipogenic differentiation in primary cultured human adipose-derived stem cells

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