Aerobic Exercise, Gene Expression and Chronic Diseases

Author(s):  
J. Chen
2011 ◽  
Vol 43 (14) ◽  
pp. 895-902 ◽  
Author(s):  
Lindsey B. Gano ◽  
Anthony J. Donato ◽  
Gary L. Pierce ◽  
Hamza M. Pasha ◽  
Katherine A. Magerko ◽  
...  

We tested the hypothesis that peripheral blood mononuclear cells (PBMC) of older adults demonstrate a proinflammatory/-oxidative gene expression profile that can be improved by regular aerobic exercise. PBMC were isolated from young ( n = 25, 18–33 yr) and middle-aged/older ( n = 40, 50–76 yr) healthy adults. The older adults had greater mRNA expression (real-time RT-PCR) of the proinflammatory/-oxidant transcription factor nuclear factor-κB (1.58-fold, P < 0.05) and receptor for advanced glycation end products (1.12-fold, P < 0.05), the proinflammatory cytokines tumor necrosis factor-α (1.90-fold, P < 0.05) and monocyte chemoattractant protein-1 (1.47-fold, P < 0.05), and the oxidant-producing enzymes nicotinamide adenine dinucleotide phosphate-oxidase (0.91-fold, P < 0.05) and inducible nitric oxide synthase (2.60-fold, P < 0.05). In 11 subjects (58–70 yr), maximal oxygen consumption (+11%) and exercise time (+19%) were increased (both P < 0.001), and expression of the above proinflammatory/-oxidative genes was or tended to be decreased in PBMC after vs. before 2 mo of aerobic exercise (brisk walking ∼6 days/wk, 50 min/day, 70% of maximal heart rate). Expression of interleukin-6 was not different with age or exercise intervention. Age group- and exercise intervention-related differences in gene expression were independent of other factors. PBMC of healthy older adults demonstrate increased expression of several genes associated with inflammation and oxidative stress, which is largely ameliorated by habitual aerobic exercise. This proinflammatory/-oxidative gene signature may represent a therapeutic target for lifestyle and pharmacological prevention and treatment strategies.


2020 ◽  
pp. 1-14
Author(s):  
H.O. Ness ◽  
K. Ljones ◽  
M. Pinho ◽  
M.A. Høydal

Regular aerobic exercise training has a wide range of beneficial cardiac effects, but recent data also show that acute very strenuous aerobic exercise may impose a transient cardiac exhaustion. The aim of this study was to assess the response to acute high-intensity aerobic exercise on properties of mitochondrial respiration, cardiomyocyte contractile function, Ca2+ handling and transcriptional changes for key proteins facilitating Ca2+ handling and endoplasmic reticulum (ER) stress responses in type 2 diabetic mice. Diabetic mice were assigned to either sedentary control or an acute bout of exercise, consisting of a 10×4 minutes high-intensity interval treadmill run. Mitochondrial respiration, contractile and Ca2+ handling properties of cardiomyocytes were analysed 1 hour after completion of exercise. Gene expression levels of key Ca2+ handling and ER stress response proteins were measured in cardiac tissue samples harvested 1 hour and 24 hours after exercise. We found no significant changes in mitochondrial respiration, cardiomyocyte contractile function or Ca2+ handling 1 hour after the acute exercise. However, gene expression of Atp2a2, Slc8a1 and Ryr2, encoding proteins involved in cardiomyocyte Ca2+ handling, were all significantly upregulated 24 hours after the acute exercise bout. Acute exercise also altered gene expression of several key proteins in ER stress response and unfolded protein response, including Grp94, total Xbp1, Gadd34, and Atf6. The present results show that despite no significant alterations in functional properties of cardiomyocyte function, Ca2+ handling or mitochondrial respiration following one bout of high intensity aerobic exercise training, the expression of genes involved in Ca2+ handling and key components in ER stress and the unfolded protein response were changed. These transcriptional changes may constitute important steps in initiating adaptive remodelling to exercise training in type 2 diabetes.


2019 ◽  
Vol 508 (3) ◽  
pp. 871-876 ◽  
Author(s):  
Patrick G. Saracino ◽  
Michael L. Rossetti ◽  
Jennifer L. Steiner ◽  
Bradley S. Gordon

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Nabanita Kundu ◽  
Cleyton Domingues ◽  
Peter Kokkinos ◽  
Eric Nylen ◽  
Sabyasachi Sen

Approximately 422 million people have diabetes worldwide (2014) and it is predicted that diabetes will rise by nearly 54% by 2030. Aerobic exercise is known to show positive effect on health of diabetic and pre diabetic patients. The effect of exercise has been studied extensively using plasma biochemistry but cellular data is scares. Previously, we have shown endothelial progenitor cells (EPCs) can act as a strong cellular biomarker of endothelial function following aerobic exercise as an intervention. In this study, we are examining the effect of aerobic exercise on adipocyte derived MSCs to study stromal cell differentiation and as a cellular surrogate of fat metabolism. Methods: Overweight and obese subjects (n=5) were enrolled in a 12 week exercise intervention study. The biweekly exercise sessions were supervised by a trained exercise physiologist and consisted of a 1 hour sessions that included warm-up and cool-down and 30 min of combined aerobic and resistance training at an exercise intensity of 50-80% of heart rate reserve. Physical and biochemical parameters were tested pre and post exercise. Subcutaneous abdominal fat biopsies were obtained and fat derived stromal cells were cultured in vitro for 2-3 weeks. MSCs were analyzed for mRNA gene expression (qRT-PCR) and cellular oxygen consumption rate (OCR), pre and post 12 week exercise. Results: With exercise, A1C reduced significantly. An increase of METs was also noticed post exercise. Both basal and maximal respiration increased significantly post exercise when compared with commercially obtained MSCs. Simultaneously, mitochondrial genes COX4 and ATP5B (p= 0.01, 1.4 fold, 0.02, 1.5 fold respectively), Glucose transporter, GLUT1 (p=0.04, 1.8 fold), antioxidants GPX3 and CAT (p= 0.01, 3.2 fold and p=0.04, 1.5 fold respectively) upregulated whereas pro-inflammatory cyclo-oxygenase-2 (p=0.04, 2.5 fold) gene reduced significantly, post exercise. Regarding differentiation potential of multipotent MSCs, post exercise, we noted enhanced expression of bone markers such Alkaline Phosphatase (p= 0.03, 2.7 fold) BGLAP and RUNX2 (1.3 and 1.2 fold) and also for collagen marker COL2 (2.4 fold) expression. For adipogenic differentiation potential PPARG mRNA expression was reduced. Interestingly, serum value of osteocalcin increased significantly from 15.0 (5.5) to 16.3(6.1) ng/ml (9% increase, p=0.03) with 1% increase in bone alkaline phosphatase level, post exercise. Conclusion: We conclude that exercise augments cellular glucose transporters (GLUT1), anti-oxidants and reduce MSC inflammation and up-regulates mitochondrial function and gene expression profile of MSCs. Increased serum value of osteocalcin complement increased gene expression of bone formation markers indicating a cross talk between fat derived MSCs and bone formation, post exercise.


2019 ◽  
Vol 18 (1) ◽  
Author(s):  
K. González-Becerra ◽  
O. Ramos-Lopez ◽  
E. Barrón-Cabrera ◽  
J. I. Riezu-Boj ◽  
F. I. Milagro ◽  
...  

Abstract Background Chronic illnesses like obesity, type 2 diabetes (T2D) and cardiovascular diseases, are worldwide major causes of morbidity and mortality. These pathological conditions involve interactions between environmental, genetic, and epigenetic factors. Recent advances in nutriepigenomics are contributing to clarify the role of some nutritional factors, including dietary fatty acids in gene expression regulation. This systematic review assesses currently available information concerning the role of the different fatty acids on epigenetic mechanisms that affect the development of chronic diseases or induce protective effects on metabolic alterations. Methods A targeted search was conducted in the PubMed/Medline databases using the keywords “fatty acids and epigenetic”. The data were analyzed according to the PRISMA-P guidelines. Results Consumption fatty acids like n-3 PUFA: EPA and DHA, and MUFA: oleic and palmitoleic acid was associated with an improvement of metabolic alterations. On the other hand, fatty acids that have been associated with the presence or development of obesity, T2D, pro-inflammatory profile, atherosclerosis and IR were n-6 PUFA, saturated fatty acids (stearic and palmitic), and trans fatty acids (elaidic), have been also linked with epigenetic changes. Conclusions Fatty acids can regulate gene expression by modifying epigenetic mechanisms and consequently result in positive or negative impacts on metabolic outcomes.


2013 ◽  
Vol 45 (14) ◽  
pp. 565-576 ◽  
Author(s):  
Pao-Yang Chen ◽  
Amit Ganguly ◽  
Liudmilla Rubbi ◽  
Luz D. Orozco ◽  
Marco Morselli ◽  
...  

Maternal nutrient restriction causes the development of adult onset chronic diseases in the intrauterine growth restricted (IUGR) fetus. Investigations in mice have shown that either protein or calorie restriction during pregnancy leads to glucose intolerance, increased fat mass, and hypercholesterolemia in adult male offspring. Some of these phenotypes are shown to persist in successive generations. The molecular mechanisms underlying IUGR remain unclear. The placenta is a critical organ for mediating changes in the environment and the development of embryos. To shed light on molecular mechanisms that might affect placental responses to differing environments we examined placentas from mice that had been exposed to different diets. We measured gene expression and whole genome DNA methylation in both male and female placentas of mice exposed to either caloric restriction or ad libitum diets. We observed several differentially expressed pathways associated with IUGR phenotypes and, most importantly, a significant decrease in the overall methylation between these groups as well as sex-specific effects that are more pronounced in males. In addition, a set of significantly differentially methylated genes that are enriched for known imprinted genes were identified, suggesting that imprinted loci may be particularly susceptible to diet effects. Lastly, we identified several differentially methylated microRNAs that target genes associated with immunological, metabolic, gastrointestinal, cardiovascular, and neurological chronic diseases, as well as genes responsible for transplacental nutrient transfer and fetal development.


2010 ◽  
Vol 109 (6) ◽  
pp. 1904-1912 ◽  
Author(s):  
Joseph M. Company ◽  
Frank W. Booth ◽  
M. Harold Laughlin ◽  
Arturo A. Arce-Esquivel ◽  
Harold S. Sacks ◽  
...  

Epicardial adipose tissue (EAT) is contiguous with coronary arteries and myocardium and potentially may play a role in coronary atherosclerosis (CAD). Exercise is known to improve cardiovascular disease risk factors. The purpose of this study was to investigate the effect of aerobic exercise training on the expression of 18 genes, measured by RT-PCR and selected for their role in chronic inflammation, oxidative stress, and adipocyte metabolism, in peri-coronary epicardial (cEAT), peri-myocardial epicardial (mEAT), visceral abdominal (VAT), and subcutaneous (SAT) adipose tissues from a castrate male pig model of familial hypercholesterolemia with CAD. We tested the hypothesis that aerobic exercise training for 16 wk would reduce the inflammatory profile of mRNAs in both components of EAT and VAT but would have little effect on SAT. Exercise increased mEAT and total heart weights. EAT and heart weights were directly correlated. Compared with sedentary pigs matched for body weight to exercised animals, aerobic exercise training reduced the inflammatory response in mEAT but not cEAT, had no effect on inflammatory genes but preferentially decreased expression of adiponectin and other adipocyte-specific genes in VAT, and had no effect in SAT except that IL-6 mRNA went down and VEGFa mRNA went up. We conclude that 1) EAT is not homogeneous in its inflammatory response to aerobic exercise training, 2) cEAT around CAD remains proinflammatory after chronic exercise, 3) cEAT and VAT share similar inflammatory expression profiles but different metabolic mRNA responses to exercise, and 4) gene expression in SAT cannot be extrapolated to VAT and heart adipose tissues in exercise intervention studies.


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