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Nathan Goodyear

Is erectile dysfunction a low-grade systemic inflammatory condition? - 0 views

eurheartj.oxfordjournals.org/...642.full

inflammation erectile dysfunction ED men sexual

shared by Nathan Goodyear on 02 Sep 13 - No Cached
  • Nathan Goodyear on 02 Sep 13
     
    ED is the result of low-grade, chronic inflammation.
Nathan Goodyear

Gonadal status and outcome of bariatric surgery in obese men - Aarts - 2013 - Clinical ... - 0 views

onlinelibrary.wiley.com/...full

low T Testosterone overweight obese bariatric surgery men male hormone hormones free testosterone

shared by Nathan Goodyear on 04 Feb 14 - No Cached
  • Nathan Goodyear on 04 Feb 14
     
    Small study of 13 men found that weight loss following bariatric surgery resulted in improved HPA function in 10/13.  Three men had resistant HPA dysfunction.  Free Testosterone was followed.
Nathan Goodyear

Endocrine milieu and erectile dysfunction: is oestradiol-testosterone imbalance, a risk... - 0 views

www.ncbi.nlm.nih.gov/...PMC3739617

erectile dysfunction ED low T Testosterone T:E2 Estradiol men male hormone hormones

shared by Nathan Goodyear on 05 Feb 14 - No Cached
  • Nathan Goodyear on 05 Feb 14
     
    This article points to the impact of T:E2 on ED in men.  A declining T:E2 increases ED in older men.  
Nathan Goodyear

Hormonal Modulation in Aging Patients with Erectile Dysfunction and Metabolic Syndrome - 0 views

www.ncbi.nlm.nih.gov/...PMC3888699

low T Testosterone hypogonadism MetS metabolic syndrome men male hormone hormones

shared by Nathan Goodyear on 05 Feb 14 - No Cached
  • Hypogonadism and MetS are strongly associated [12, 13, 16], having even been demonstrated that with the increasing number of MetS parameters there is a proportional raise in the incidence of hypogonadism
  • increasing number of MetS components is inversely associated with T levels
  • the presence of MetS did not prove to be a significant determinant of hypogonadism, as it did not lead to a decline in T levels, in MetS patients with already established hypogonadism, the increasing number of MetS features was associated with further decline in T
  • ...15 more annotations...
  • In the setting of MetS, hypertriglyceridemia and increased WC have been reported as the most important determinants of hypogonadism
  • recent literature consistently associates obesity not only with higher risk of hypogonadism [4, 6, 27] but also with lower T levels
  • Visceral adiposity has been particularly related with reduction of T and SHBG levels (independent of other metabolic disorders)
  • WC was one of the MetS parameters with the greatest influence in T levels decrease, presenting itself as a strong risk factor for hypogonadism development
  • MetS-related T decline was not accompanied by an increase in pituitary LH levels, suggesting impairment in gonadotropin secretion
  • The molecules behind this smoothing compensatory effect of GnRH/LH are still unknown, but estrogens and insulin, as well as leptin, TNF-α, and other adipokines, were proposed candidates
  • fat stores undertake an increase aromatization of androgens, therefore raising estrogen levels [9, 15], which in turn decrease LH secretion
  • our data contradicts the concept that estradiol exerts a negative feedback on hypothalamic GnRH secretion
  • taking into account that high estradiol levels have already been described as the only abnormality in a subset of patients with ED, the hypothesis that the later might not only be caused by androgen deficiency is becoming increasingly evident
  • it has been reported that the chronic exposure to phosphodiesterase type 5 inhibitors (PDE5i), widely used for the treatment of ED, may influence serum estradiol levels
  • thyroid disorders (specially hyperthyroidism) have been related to ED and hypogonadism, and so must be considered in a sexual-dysfunction setting
  • It is clear from the current literature that collecting a more thorough hormonal panel might be a wise approach to further uncover hormonal relations
    • Nathan Goodyear
      Nathan Goodyear on 05 Feb 14
       
      outstanding point.  This hits to the point that Low T is the effect not the cause.
  • We concluded that in ED patients with hypogonadism and MetS, the attenuated response of HPG axis (normal or low LH levels) might not always be due to an underlying adiposity-dependent estrogen-raising effect.
  • our findings indicate that ED, aging, and estradiol might have a stronger connection than what is currently described in the literature.
  • this study underlines the importance of the collection of a full hormonal panel in ED men
  • Nathan Goodyear on 05 Feb 14
     
    low T strongly associated with metabolic syndrome in men.
Nathan Goodyear

http://onlinelibrary.wiley.com/store/10.1002/hep.21080/asset/21080_ftp.pdf;jsessionid=C... - 0 views

onlinelibrary.wiley.com/...FD1E43279D6DC7447C7FC1A.f04t01

vitamin C IV vitamin C IV intravenous cirrhosis

shared by Nathan Goodyear on 10 Feb 14 - No Cached
  • Nathan Goodyear on 10 Feb 14
     
    small study looked at patients with liver cirrhosis.  The authors used a low dose of IV vitamin C (5 grams) and found that this improved endothelial dysfunction.  Patients with cirrhosis were found to be low in vitamin C.  The IV vitamin C was well tolerated, despite a low dose.
Nathan Goodyear

Total Testosterone Levels and the Effect of Sildenafil on Type 2 Diabetics with Erectil... - 0 views

www.ncbi.nlm.nih.gov/...PMC3910416

low T Testosterone Diabetes sildenafil erectile dysfunction ED

shared by Nathan Goodyear on 17 Feb 14 - No Cached
  • Nathan Goodyear on 17 Feb 14
     
    Interesting study. In this study group, 36% of type II diabetes with ED had low Testosterone.  This fits with the estimated 40% of those with Diabetes have low T. What is really interesting about this study is that the degree of improvement with ED by Sildenfafil was dependent on the Testosterone level in the low T group.  Meanining that Testosterone therapy in these men would probably be more of a therapy directed at the cause and not Sildenafil.  Of course, the Testosterone therapy would benefit glucose regulation as well documented in the literature.
Nathan Goodyear

Androgenicity and venous endothelial function in post-menopausal women. - Abstract - Eu... - 1 views

europepmc.org/...sionid=W8hntONhSCdvQbfTjdRp.10

free androgen index Testosterone women hormone hormones CVD CRP inflammation endothelial

shared by Nathan Goodyear on 25 Feb 14 - No Cached
  • Nathan Goodyear on 25 Feb 14
     
    Increasing free androgen index associated with increasing vascular endothelial inflammation and dysfunction.
Nathan Goodyear

Oxidative Stress, Testosterone, and Cognition among Caucasian and Mexican-American Men ... - 0 views

iospress.metapress.com/...t1717503235m8667

Testosterone alzheimer memory disease stress oxidative oxidative stress men male hormone hormones cognition

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • Nathan Goodyear on 03 Mar 14
     
    Interesting study. This study points out the differences between individuals and groups i.e. Mexian-Americans and Caucasians in this study.  Men with low oxidative stress, Testosterone was associated with no cognitive dysfunction.  In contrast, with high oxidative stress, Testosterone therapy was associated with cognitive impairment in caucasians only.
Nathan Goodyear

Nature Clinical Practice Endocrinology & Metabolism | Testosterone and ill-health in ag... - 0 views

www.nature.com/...ncpendmet1050.html

low T Testosterone health men male hormone hormones metabolic syndrome metabolic syndrome MetS insulin resistance diabetes aging

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • Levels of total and bioavailable testosterone and SHBG were reported to be inversely correlated with the prevalence of the metabolic syndrome in men aged 40–80 years
  • as were total testosterone and SHBG in men aged 65–96 years
  • and in a cross-sectional analysis of a large cohort of non-diabetic men aged 70–89 years
  • ...18 more annotations...
  • In longitudinal studies, decreased levels of total testosterone and SHBG predicted an increased incidence of metabolic syndrome in nonobese men
  • Free testosterone level is not associated with the prevalence of metabolic syndrome in middle-aged and older men
  • Levels of free, bioavailable and total testosterone are lower in men with T2DM than in age-matched controls,34, 35 and decreased total testosterone level predicts incident T2DM in middle-aged men.
  • men with T2DM commonly have low total or free testosterone levels
  • Total, bioavailable and free testosterone levels are inversely correlated with fasting insulin level and insulin resistance in middle-aged men without T2DM
  • total testosterone is positively correlated with insulin sensitivity in men with normal or impaired glucose tolerance or T2DM
  • low SHBG level is more strongly associated with metabolic syndrome than low total testosterone in aging men
  • the recognized association between low SHBG level and insulin resistance
  • Low levels of SHBG are also associated with smaller, denser LDL-cholesterol molecules in nondiabetic men,58 and were found to predict increased cardiovascular disease mortality in one study of older men
  • Low levels of SHBG might reflect obesity, insulin resistance and overall poor health
  • Compared with those who have normal testosterone levels, men aged 40 years or more with total testosterone levels <9.8 nmol/l or elevated LH level have greater CIMT
  • In men aged 73–94 years, total testosterone was inversely correlated with CIMT
  • a prospective analysis of men aged 73–91 years, progression of CIMT was not related to total testosterone level, but it was inversely related to free testosterone level
  • A study of men aged 55 years or more found that those with total and bioavailable testosterone levels in the highest tertile had a lower risk of severe aortic atherosclerosis (detected by radiography as abdominal aortic calcification) than those with the lowest testosterone levels.
  • a large study of men aged 69–80 years, those with total or free testosterone in the lowest quartile had increased odds of lower-extremity peripheral arterial disease
  • the possibility of reverse causation has to be considered, as systemic illness can result in decreased testosterone levels
  • previous case–control studies and longitudinal studies have failed to identify low testosterone levels as strong predictors of clinically significant coronary disease
  • Reviews of trials on testosterone therapy in men with either low or low-to-normal testosterone levels have not shown consistent beneficial effects either on lipid profiles or on actual cardiovascular events.24, 54, 55 These trials, however, have not been designed or powered to detect treatment-related differences in cardiovascular outcome
  • Nathan Goodyear on 03 Mar 14
     
    Declining Testosterone or low Testosterone is clearly associated with poor health in men.   Very nice review of the association between low Testosterone and metabolic dysfunction.  Low T is associated with increased metabolic syndrome, Diabetes, weight gain, insulin resistance...
Nathan Goodyear

Androgen Deprivation Therapy, Insulin Resistance, and Cardiovascular Mortality: An Inco... - 0 views

onlinelibrary.wiley.com/...full

androgen deprivation therapy androgen male men hormone hormones deprivation therapy prostate cancer cardiovascular disease insulin resistance diabetes metabolic syndrome mortality CVD

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • Nathan Goodyear on 03 Mar 14
     
    Androgen deprivation therapy is associated with increased diabetes, metabolic syndrome, insulin resistance, and cardiovascular mortality.  The longer the duration of therapy, the more the progression of metabolic dysfunction.  This process seems similar to chemotherapy i.e. secondary cancer due to chemotherapy.  The treatment of one disease, prostate cancer in this case, leads to an increase in the risk of the #1 killer in men--logic seems severely flawed there.
Nathan Goodyear

Acute and short term chronic testost... [J Clin Endocrinol Metab. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24606070

Testosterone hypogonadism adipnectin men male hormone hormones

shared by Nathan Goodyear on 17 Mar 14 - No Cached
  • Nathan Goodyear on 17 Mar 14
     
    Study finds that Testosterone regulates glucose metabolism, in part, through adiponectin production.  Early state of low T will slow the use of fats as a source of fuel and this results in an increased energy balance and results in the increased adiponectin production to increase metabolism.  Testosterone and adiponectin exist in an inverse relationship. This study does not mimic normal physiology.  Men with low T are unhealthy with significant metabolic dysfunction.  These young, "healthy" men were induced to a low T state--that is not a clear picture as the physiology of a "young healthy" man is quite different than that of one with low T.   Testosterone conversion to DHT increases GLUT4 and thus glucose uptake--another mechanism of Testosterone's effect on glucose metabolism.
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
  • ...56 more annotations...
  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Loss of mitochondrial bioenergetic capacity underlies the glucose avidity of carcinomas - 0 views

cancerres.aacrjournals.org/...9013.full.pdf

Warburg Warburg effect mitochondria mitochondrial bioenergetic capacity glucose cancer

shared by Nathan Goodyear on 11 Jul 13 - No Cached
  • Nathan Goodyear on 11 Jul 13
     
    Is cancer merely a result of mitochondrial and glucose dysfunction? Is cancer really just a energy problem? Good review of the Warburg effect at the biochemistry level in cancer.
Nathan Goodyear

Testosterone for the aging male; current evidence and recommended practice - 0 views

www.ncbi.nlm.nih.gov/...PMC2544367

low T low Testosterone testosterone low male

shared by Nathan Goodyear on 12 Jul 13 - No Cached
  • Nathan Goodyear on 12 Jul 13
     
    review of central and peripheral contribution to low T and metabolic dysfunction.
Nathan Goodyear

Focal brain inflammation and autism - 0 views

www.jneuroinflammation.com/...1742-2094-10-46.pdf

autism ASD autism spectrum disorder inflammation inflammatory cytokines

shared by Nathan Goodyear on 13 Aug 13 - No Cached
  • Nathan Goodyear on 13 Aug 13
     
    Inflammatory cytokines are increased in autism. Dysfunctional immune system is in part responsible for autism.
Nathan Goodyear

Molecular Autism | Full text | Non-synonymous single-nucleotide variations of the human... - 0 views

www.molecularautism.com/...22

autism ASD autism spectrum disorder oxytocin SNPs receptors

shared by Nathan Goodyear on 14 Aug 13 - No Cached
  • Nathan Goodyear on 14 Aug 13
     
    Oxytocin receptor SNPs may contribute to some of the biochemical dysfunction found in autism.
Nathan Goodyear

Oxytocin and autistic disorder: alterations in peptide forms - 0 views

www.sciencedirect.com/...S0006322301011398

autism ASD oxytocin autism spectrum disorder

shared by Nathan Goodyear on 14 Aug 13 - No Cached
  • Nathan Goodyear on 14 Aug 13
     
    Again, a small study, but oxytocin signaling disruption is clearly a part of the biochemical dysfunction found in autism.
Nathan Goodyear

Metabolic Effects of Fructose and the Worldwide Increase in Obesity - 0 views

physrev.physiology.org/...23.full

fructose obesity

shared by Nathan Goodyear on 19 Sep 13 - No Cached
  • Nathan Goodyear on 19 Sep 13
     
    Great review of fructose and it's role in increasing metabolic dysfunction and resultant obesity.
Nathan Goodyear

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

shared by Nathan Goodyear on 16 Sep 13 - Cached
  • For thousands of years humans consumed fructose amounting to 16–20 grams per day
  • daily consumptions amounting to 85–100 grams of fructose per day
  • 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
  • ...29 more annotations...
  • 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]).
  • Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
  • 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.
  • A prolonged elevation of TG was also seen in the high fructose subjects
  • 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
  • Chronic fructose consumption reduces adiponectin responses, contributing to insulin resistance
  • A definite relationship has also been found between metabolic syndrome and hyperhomocysteinemia
  • 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
  • Fructose stimulates TG production, but impairs removal, creating the known dyslipidemic profile
  • the effects of fructose in promoting TG synthesis are independent of insulinemia
  • 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
  • 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
  • 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
  • Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
  • fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
  • Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
  • 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
  • High fructose diets can have a hypertriglyceridemic and pro-oxidant effect
  • Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
  • Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
  • LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
  • Fructose has also been implicated in reducing PPARα levels
  • PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
  • decreased PPARα expression can result in reduced oxidation, leading to cellular lipid accumulation
  • fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
  • LDL particle size has been found to be inversely related to TG concentration
  • 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
  • High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
  • 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
  • Nathan Goodyear on 16 Sep 13
     
    Fructose and metabolic syndrome.  Good discussion of the impact of high fructose intake and metabolic dysfunction.  This study also does a great job of highlighting the historical change of fructose intake.
Nathan Goodyear

The Epidemiology of Uric Acid and Fructose - 0 views

www.ncbi.nlm.nih.gov/...PMC3197219

uric acid fructose metabolic syndrome inflammation vitamin C IV vitamin C

shared by Nathan Goodyear on 17 Sep 13 - No Cached
  • Previous studies have found that high doses of vitamin C supplementation lower serum uric acid via a uricosuric effect
  • fructose consumption coincided with the increasing trend of serum uric acid
  • Fructose is known to induce uric acid production by increasing ATP degradation to AMP, a uric acid precursor (85, 93, 94) and thus, within minutes after fructose infusion, serum uric acid levels rise
  • Nathan Goodyear on 17 Sep 13
     
    fructose intake, metabolic dysfunction, and elevated uric acid.
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