contribution to the training response of the epigenome as a mediator between genes and environment
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shared by Nathan Goodyear on 20 Dec 11
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Obesity - Effects of Lifestyle Changes to Reduce Risks of Diabetes and Associated Cardi... - 0 views
www.nature.com/...oby2009388a.html
obesity Type II Diabetes DM risks lifestyle effects cardiovascular exercise diet modification
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JAMA Network | JAMA: The Journal of the American Medical Association | Low-Fat Dietary ... - 0 views
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shared by Nathan Goodyear on 17 Nov 12
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Estradiol, Tamoxifen, and Flaxseed A... [J Clin Endocrinol Metab. 2012] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...22930784
diet estradiol flaxseed breast cancer Ca inflammation cytokines IL-1alpha IL-1Beta IL-1Ra
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Tamoxifen and more importantly, flaxseed increases endogenous IL-1Ra that is a known inhibitor of the pro-inflammatory cytokines IL-1alpha and IL-1beta. These pro-inflammatory cytokines are associated with breast cancer. Conclusion: diet modification can effect inflammatory cytokines associated with breast cancer. This should be explored as true preventative therapies for women. This study also found a positive association with estradiol and IL-1Beta in breast tissue and SC fat; inversely associated with IL-Ra in the breast.
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An integrative analysis reveals coordinated reprogramming of the epigenome and the tran... - 0 views
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Differential DNA methylation was predominantly observed in enhancers, gene bodies and intergenic regions and less in CpG islands or promoters
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highly consistent and associated modifications in methylation and expression, concordant with observed health-enhancing phenotypic adaptations, are induced by a physiological stimulus
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The health benefits following exercise training are elicited by gene expression changes in skeletal muscle, which are fundamental to the remodeling process
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there is increasing evidence that more short-term environmental factors can influence DNA methylation
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dietary factors have the potency to alter the degree of DNA methylation in different tissues, 9,10 including skeletal muscle
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In one study, a single bout of endurance-type exercise was shown to affect methylation at a few promoter CpG sites
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In the context of diabetes, exercise training has been shown to affect genome-wide methylation pattern in skeletal muscle,13 as well as in adipose tissue.
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the findings from this tightly controlled human study strongly suggest that the regulation and maintenance of exercise training adaptation is to a large degree associated to epigenetic changes, especially in regulatory enhancer regions
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Endurance training [after training (T2) vs. before training (T1)] induced significant (false discovery rate, FDR< 0.05) methylation changes at 4919 sites across the genome in the trained leg
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a complementary approach revealed that over 600 CpG sites correlated to the increase in citrate synthase activity, an objective measure of training response (Figure S4 and Dataset S14). This might imply that some of these sites could influence the degree of training response.
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As expected by a physiological environmental trigger on adult tissue, the observed effect size on DNA methylation was small in comparison to disease states such as cancer
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negative correlation was more prominent for probes in promoter/5′UTR/1st exon regions, while gene bodies had a stronger peak of positive correlation
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The significant changes in DNA methylation, that primarily occurred in enhancer regions, were to a large extent associated with relevant changes in gene expression
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The main findings of this study were that 3 months of endurance training in healthy human volunteers induced significant methylation changes at almost 5000 sites across the genome and significant differential expression of approximately 4000 genes
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DMPs that increased in methylation were mainly associated to structural remodeling of the muscle and glucose metabolism, while the DMPs with decreased methylation were associated to inflammatory/immunological processes and transcriptional regulation
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This suggests that the changes in methylation seen with training were not a random effect across the genome but rather a controlled process that likely contributes to skeletal muscle adaptation to endurance training
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Correlation of the changes in DNA methylation to the changes in gene expression showed that the majority of significant methylation/expression pairs were found in the groups representing either increases in expression with a concomitant decrease in methylation or vice versa
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The fraction of genes showing both significant decrease in methylation and upregulation was 7.5% of the DEGs or 2.3% of all genes detected in muscle tissue with at least one measured DNA methylation position. Correspondingly, 7.0% of the DEGs or 2.1% of all genes showed both significant increase in methylation and downregulation
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we show that DNA methylation changes are associated to gene expression changes in roughly 20% of unique genes that significantly changed with training
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Examples of structural genes include COL4A1, COL4A2 and LAMA4. These genes have also been identified as important for differences in responsiveness to endurance training
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Among the metabolic genes, MDH1 catalyzes the reversible oxidation of malate to oxaloacetate, utilizing the NAD/NADH cofactor system in the citric acid cycle and NDUFA8 plays an important role in transferring electrons from NADH to the respiratory chain
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In the present study, methylation predominantly changed in enhancer regions with enrichment for binding motifs for different transcription factors suggesting that enhancer methylation may be highly relevant also in exercise biology
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Of special interest in the biology of endurance training may be that MRFs, through binding to the PGC-1α core promoter, can regulate this well-studied co-factor for mitochondrial biogenesis
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That endurance training led to an increased methylation in enhancer regions containing motifs for the MRFs and MEFs is somewhat counterintuitive since it should lead to the repression of the action of the above discussed transcription factors
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this study demonstrates that the transcriptional alterations in skeletal muscle in response to a long-term endurance exercise intervention are coupled to DNA methylation changes
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We suggest that the training-induced coordinated epigenetic reprogramming mainly targets enhancer regions, thus contributing to differences in individual response to lifestyle interventions
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a physiological health-enhancing stimulus can induce highly consistent modifications in DNA methylation that are associated to gene expression changes concordant with observed phenotypic adaptations
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Exercise alters gene expression via methylation--the power of epigenetics. Interestingly, the majority of the methylation was outside the CPG island regions. This 3 month study found methylation of 5,000 sites across the genome resulting in altered expression of apps 4,000 genes. The altered muscle changes of the endurance training was linked to DNA methylation changes.
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shared by harshitatyagi on 24 Aug 22
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Can Keto Diet Lead You To Positive Pregnancy Results - 0 views
fortunetelleroracle.com/...itive-pregnancy-results-652446
Keto Diet Ketogenic Diet Low Carbohydrate Diet Keto Food Keto diet for weigh loss Pregnancy
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Distribution and Posttranslational Modification of Synaptic ERα in the Adult ... - 1 views
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shared by Nathan Goodyear on 08 Nov 16
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Lifestyle modification increases serum testosterone level and decrease central blood pr... - 0 views
www.ncbi.nlm.nih.gov/...25753766
low T low Testosterone Testosterone men male hormones hormones exercise obesity overweight obese
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shared by Nathan Goodyear on 11 Jun 12
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Alzheimer's disease--synergistic effects of ... [J Neural Transm. 1998] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...9720973
AD AGE advanced glycation end products Alzheimer's disease neurofibrillary tangles Beta-amyloid protein microglia brain neurology oxidative stress alzheimer
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AGEs are protein modifications that contribute to the formation of the histopathological and biochemical hallmarks of AD: amyloid plaques, neurofibrillary tangles and activated microglia
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shared by Nathan Goodyear on 13 Jun 12
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JAMA Network | JAMA: The Journal of the American Medical Association | Low-Fat Dietary ... - 0 views
jama.jamanetwork.com/article.aspx
low fat diet CVD CHD cardiovascular disease risk stroke MI heart attack health
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shared by Nathan Goodyear on 16 Sep 13
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Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslip... - 0 views
www.nutritionandmetabolism.com/...5
fructose metabolic syndrome metabolic syndrome insulin resistance obesity nutrition metabolism
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Of key importance is the ability of fructose to by-pass the main regulatory step of glycolysis, the conversion of glucose-6-phosphate to fructose 1,6-bisphosphate, controlled by phosphofructokinase
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Thus, while glucose metabolism is negatively regulated by phosphofructokinase, fructose can continuously enter the glycolytic pathway. Therefore, fructose can uncontrollably produce glucose, glycogen, lactate, and pyruvate, providing both the glycerol and acyl portions of acyl-glycerol molecules. These particular substrates, and the resultant excess energy flux due to unregulated fructose metabolism, will promote the over-production of TG (reviewed in [53]).
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Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
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reduction in circulating leptin both in the short and long-term as well as a 30% reduction in ghrelin (an orexigenic gastroenteric hormone) in the fructose group compared to the glucose group.
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Both fat and fructose consumption usually results in low leptin concentrations which, in turn, leads to overeating in populations consuming energy from these particular macronutrients
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the liver takes up dietary fructose rapidly where it can be converted to glycerol-3-phosphate. This substrate favours esterification of unbound FFA to form the TG
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Although fructose does not appear to acutely increase insulin levels, chronic exposure seems to indirectly cause hyperinsulinemia and obesity through other mechanisms. One proposed mechanism involves GLUT5
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If FFA are not removed from tissues, as occurs in fructose fed insulin resistant models, there is an increased energy and FFA flux that leads to the increased secretion of TG
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In these scenarios, where there is excess hepatic fatty acid uptake, synthesis and secretion, 'input' of fats in the liver exceed 'outputs', and hepatic steatosis occurs
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Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
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fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
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Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
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the metabolic effects of fructose occur through rapid utilization in the liver due to the bypassing of the regulatory phosphofructokinase step in glycolysis. This in turn causes activation of pyruvate dehydrogenase, and subsequent modifications favoring esterification of fatty acids, again leading to increased VLDL secretion
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Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
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Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
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LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
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PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
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fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
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therefore the higher TG results in a smaller, denser, more atherogenic LDL particle, which contributes to the morbidity of the metabolic disorders associated with insulin resistance
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High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
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A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs normal hepatic carbohydrate metabolism leading to two major consequences (Figure 2): perturbations in glucose metabolism and glucose uptake pathways, and a significantly enhanced rate of de novo lipogenesis and TG synthesis, driven by the high flux of glycerol and acyl portions of TG molecules coming from fructose catabolism
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Colonization-Induced Host-Gut Microbial Metabolic Interaction - 0 views
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he gut microbiota enhances the host’s metabolic capacity for processing nutrients and drugs and modulate the activities of multiple pathways in a variety of organ systems.
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Acquisition of the gut microbiota was associated with rapid increase in body weight (4%) over the first 5 days of colonization
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The colonization process stimulated glycogenesis in the liver prior to triggering increases in hepatic triglyceride synthesis
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Expression and activity of major drug-metabolizing enzymes (Cyp3a11 and Cyp2c29) were also significantly stimulated
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The gut microbiota (GM) exhibits a relatively low level of diversity compared to those of most soil ecosystems and in humans it is comprised of usually no more than nine phyla of microorganisms, of which only two are dominant: the Firmicutes and the Bacteroidetes
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colonization of a germfree gut was rapid and remarkably stable, establishing within only a week after first exposure
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a study conducted on germfree rats by Nicholls et al. showed that 3 weeks were necessary to obtain a stabilization and “normalization”
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the microbiota status affects the systemic metabolism of the host, modulating the metabolic fingerprint of topographically remote organs such as the liver and the kidney
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Gut colonization induces a rapid weight gain associated with stimulation of hepatic glycogenesis and triglyceride synthesis
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PLOS ONE: The Gut Microbiota and Developmental Programming of the Testis in Mice - 0 views
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The intra-testicular level of testosterone in GF mice was found to be significantly lower than in SPF and CBUT mice
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This study establishes a novel role for the commensal gut microbiota in the regulation of testicular development and function
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Absence of the normal microbiota influences the formation and the integrity of the BTB as well as the intra-testicular levels of testosterone and serum levels of LH and FSH.
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Nutritional, socioeconomic, lifestyle and environmental factors (among others) are involved in the regulation of normal spermatogenesis.
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he gut microbiota is one such potential source of environmental factors/products that has developed an intimate symbiotic relationship with host's physiology.
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Manipulation of the gut microbiotia through dietary modification, pre- and probiotics can therefore be beneficial for the host's reproductive health.
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In the current study, colonizing GF mice with CBUT resulted in an increased sperm production, suggesting that bacterial products, e.g. of fermentation, directly or indirectly, can affect the testis.
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A recent study demonstrated that dietary supplementation of the probiotics Lactobacillus reuteri increased and restored testosterone levels in aging mice
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This suggests that butyrate most likely regulates testosterone production at the testicular level by stimulation of gene expression in Leydig cells and with little or no effect at the pituitary- hypothalamic levels.
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shared by wheelchairindia9 on 19 Apr 15
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Golden Motor Electric Wheelchair - 0 views
www.wheelchairindia.com/...GM-LITE-POWER-WHEELCHAIR
Power Wheelchairs Controlled Wheelchair Users accessories and equipment Best Power Wheelchair reduces downward sliding motorized Standing Wheelchair Golden Motor Electric Wheelchair
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Powerchairs are generally four-wheeled or six-wheeled and non-folding, however some folding designs exist and other designs may have some ability to partially dismantle for transit. Four general styles of powerchair drive systems exist: front, centre or rear wheel drive and all-wheel drive. Powered wheels are typically somewhat larger than the trailing/castoring wheels, while castoring wheels are typically larger than the castors on a manual chair. Centre wheel drive powerchairs have castors at both front and rear for a six-wheel layout. Angel Wheelchair Electric standing wheelchair Standing up, driving function by power. Head and signal light (controlled by joystick). Adjustable headrest. Adjustable footplate. Detachable backrest Rigid steel framework W/liquid coating Flip-backward armrest Max speed: 9.15KM/H Front castor: 2.80/2.50-4 pneumatic castor (9") Rear wheels: 3.00-8 pneumatic tire (14") Available seat width: A (46 cm), D (42 cm) Max loading: A size: 135 kg Net weight w/o battery: 62.7 kg A powerchairs is a wheelchair that is propelled by means of an electric motor rather than manual power. Power wheelchairs are useful for those unable to propel a manual wheelchair or who may need to use a wheelchair for distances or over terrain which would be fatiguing in a manual wheelchair. They may also be used not just by people with 'traditional' mobility impairments, but also by people with cardiovascular and fatigue based condition. An powerwheelchair powers more than just chair. It gives the power to safely travel long distances on own. It empowers to navigate through home, backyard, school, workplace or local park. It gives power to do the things,want to do. It gives power. When accidents occur that leave permanent leg injuries, or as age sets in and joint pain becomes unbearable, the power chair acts as a gateway to continue living life to the fullest. The powerwheelchairs in our lineup are all battery powered, yet each device fills
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What dietary modification best improves insulin sensitivity and why? - Weickert - 2012 ... - 0 views
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cereal-fibre intake, under isoenergetic conditions, improves whole-body IR in both short-term and more prolonged studies
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Low-level lead exposure, metabolic syndrome, and h... [Environ Health Perspect. 2006] -... - 0 views
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The results suggest that elderly men with MetS were more susceptible to autonomic dysfunction in association with chronic lead exposure as measured in patella. The modification by MetS is consistent with a role for oxidative stress in lead toxicity on the cardiovascular system.
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shared by Nathan Goodyear on 27 Jan 15
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International Journal of Impotence Research - Obesity, low testosterone levels and erec... - 0 views
www.nature.com/...ijir200842a.html
low T low Testosterone men male hormone hormones ED erectile dysfunction Testosterone diabetes metabolic syndrome obesity
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Studies have shown that ED may be an early biomarker of general endothelial dysfunction, atherosclerosis and CVD
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testosterone treatment of hypogonadal young and older men improves sexual function, increases lean mass and decreases fat mass
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In men with low serum testosterone (for example, <8 or 230 nmol l−1) with obesity, metabolic syndrome and diabetes mellitus, treatment with testosterone is warranted
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In obese middle-aged men, testosterone treatment reduced visceral adipocity, insulin resistance, serum cholesterol and glucose levels
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testosterone replacement has a favorable impact on body mass, insulin secretion and sensitivity, lipid profile and blood pressure in hypogonadal men with the metabolic syndrome as well as type 2 diabetes mellitus
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Testosterone significantly inhibits lipoprotein lipase activity, which reduces triglycerides uptake into adipocytes in the abdominal adipose tissue
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testosterone treatment decreased endogenous inflammatory cytokines (tumor necrosis factor-α and IL-1β) and lipids (total cholesterol) and increased IL-10 in hypogonadal men
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Testosterone treatment reduced leptin and adiponectin levels in hypogonadal type 2 diabetic men after 3 months of testosterone replacement
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Obesity adversely affects endothelial function and lowers serum testosterone levels through the development of insulin resistance and metabolic syndrome
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Metabolic disturbances as well as production of cytokines and adipokines by inflamed fat cells may be causal factors in the development of ED
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The onset of ED and the associated risk of CVD may be delayed through lifestyle modifications that affect obesity, such as diet and exercise
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Very low testosterone levels contribute to the development of ED in obesity, metabolic syndrome and type 2 diabetes mellitus
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Obesity is associated with low total testosterone levels that can be explained at least partially by lower sex hormone-binding globulin (SHBG) in obese men
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epidemiological studies have shown a negative correlation between BMI and total testosterone and to a lesser extent with free and bioavailable (biologically active) testosterone levels
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shared by Nathan Goodyear on 04 Mar 15
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Testosterone and weight loss: the evidence - 0 views
www.ncbi.nlm.nih.gov/...PMC4154787
low T low Testosterone Testosterone men male hormone hormones obesity obese fat adipose tissue visceral fat muscle waist circumference BMI
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Nitrogen Excretion in Cancer Cachexia and Its Modification by a High Fat Diet in Mice - 0 views
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