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Edgar Anderson

Losing Weight Through Professional Help - 1 views

It is not easy being an obese because you always become the subject of ridicule. It is for this reason that I really exerted enough efforts going to the gym in order to lose weight. Yet, I did not ...

started by Edgar Anderson on 25 Sep 12 no follow-up yet
Nathan Goodyear

Dynamic Regulation of Estrogen Receptor-β Expression by DNA Methylation Durin... - 0 views

ajp.amjpathol.org/...fulltext

prostate cancer ER beta ER-beta methylation male men hormone hormones

shared by Nathan Goodyear on 21 Jan 14 - No Cached
  • Nathan Goodyear on 21 Jan 14
     
    Methylation of the ER beta gene promoter region decreases ER beta expression and this has been associated with carcinogenesis of the prostate.
Nathan Goodyear

Sex steroids and cardiovascular disease Yeap BB - Asian J Androl - 0 views

www.ajandrology.com/article.asp

cardiovascular disease CVD sex estradiol carotid intima-media thickness hormones hormone men Testosterone estrogen

shared by Nathan Goodyear on 15 Jan 14 - No Cached
  • Levels of SHBG are higher in older men, therefore levels of free T decline more steeply than total T as men's age increases.
  • calculations based on mass action equations may not reflect precisely free T measured using a reference method
  • free T declines more steeply with age than total T in both cross-sectional [35] and longitudinal studies, [36] as does free E2 in comparison to total E2
  • ...22 more annotations...
  • T may slow development of or progression of atherosclerosis by modulating effects on insulin resistance, inflammation, endothelial function, preclinical atherosclerosis or the vasculature.
  • these cross-sectional and longitudinal studies support a relationship between low circulating T with CIMT and higher E2 with its progression
  • lower levels of T are biomarkers for aortic vascular disease
  • circulating free T was negatively associated with the presence of AAA
  • luteinizing hormone (LH) was positively associated.
  • low levels of total or bioavailable T were associated with aortic atherosclerosis manifested as calcified deposits detected by radiography
  • Men with total or free T in the lowest quartile had increased adjusted ORs for PAD defined as ABI <0.90, as did men with free E2 in the highest quartile of values
  • The apparent association of SHBG with intermittent claudication reflects the correlation of total T with SHBG, while the contribution of E2 to risk of PAD remains unclear
  • men with total T in the lowest quartile of values (<11.7 nmol l−1 ) experienced an increased incidence of stroke or transient ischemic attack
  • lower total T with increased incidence of CVD events
  • cohort studies in mostly older men have supported the association of lower androgen levels with higher mortality
  • lower total or free T levels were associated with mortality in older men, but with discordant results for cause-specific mortality and for associations of E2
  • several large studies identifying lower endogenous levels of total or free T as independent predictors of all-cause or CVD-related deaths in middle-aged and older men
  • T exhibits anti-inflammatory effects, enhances flow-mediated brachial artery reactivity, and reduces arterial stiffness
  • Short-term T therapy had a beneficial effect on exercise-induced myocardial ischemia in middle-aged men with coronary artery disease or chronic stable angina, [95],[96],[97] and reduced angina frequency in older men with diabetes and coronary artery disease
  • T therapy resulted in an increase in treadmill test duration and time to ST segment depression
  • there are interventional studies supporting a protective effect of exogenous T against myocardial ischemia in men with coronary artery disease
  • employ conservative doses
    • Nathan Goodyear
      Nathan Goodyear on 16 Jan 14
       
      This dosing is 100 fold higher then peak production of a  young man at 20-22.
  • Observational studies indicate that lower levels of endogenous T in older men are associated with the presence of carotid atherosclerosis, aortic and peripheral vascular disease, and incidence of CVD events and mortality
  • Interventional studies have shown beneficial effects of exogenous T on vascular function and on exercise-induced myocardial ischemia in men with coronary artery disease
    • Nathan Goodyear
      Nathan Goodyear on 16 Jan 14
       
      the therapies employed in these studies were massively overdosed.
  • Nathan Goodyear on 15 Jan 14
     
    Nice review of all the sex hormones and their relationship to CVD in men.  
Nathan Goodyear

Low Sex Hormone-Binding Globulin, Total Testosterone, and Symptomatic Androgen Deficien... - 0 views

press.endocrine.org/...jc.2005-1326

low testosterone T metabolic syndrome SHBG MetS men male hormone hormones

shared by Nathan Goodyear on 04 Feb 14 - No Cached
  • Nathan Goodyear on 04 Feb 14
     
    Low Total Testosterone, low SHBG, and symptoms of low T are associated with an increase risk (relative) of Mets, especially in normal weight men.
Nathan Goodyear

Testosterone and glucose metabolism in men: current concepts and controversies - 0 views

joe.endocrinology-journals.org/...R37.full

shared by Nathan Goodyear on 04 Feb 14 - No Cached
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      80% of E2 production in men, that will cause low T in men, comes from SQ adiposity.  This leads to increase in visceral adiposity.
  • Only 5% of men with type 2 diabetes have elevated LH levels (Dhindsa et al. 2004, 2011). This is consistent with recent findings that the inhibition of the gonadal axis predominantly takes place in the hypothalamus, especially with more severe obesity
  • Metabolic factors, such as leptin, insulin (via deficiency or resistance) and ghrelin are believed to act at the ventromedial and arcuate nuclei of the hypothalamus to inhibit gonadotropin-releasing hormone (GNRH) secretion
  • ...32 more annotations...
  • kisspeptin has emerged as one of the most potent secretagogues of GNRH release
  • Consistent with the hypothesis that obesity-mediated inhibition of kisspeptin signalling contributes to the suppression of the HPT axis, infusion of a bioactive kisspeptin fragment has been recently shown to robustly increase LH pulsatility, LH levels and circulating testosterone in hypotestosteronaemic men with type 2 diabetes
  • Figure 4
  • Interestingly, a recent 16-week study of experimentally induced hypogonadism in healthy men with graded testosterone add-back either with or without concomitant aromatase inhibitor treatment has in fact suggested that low oestradiol (but not low testosterone) may be responsible for the hypogonadism-associated increase in total body and intra-abdominal fat mass
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      This does not fit with the research on receptors, specifically estrogen receptors.  These studies that the authors are referencing are looking at "circulating" levels, not tissue levels.
  • A smaller study with a similar experimental design found that acute testosterone withdrawal reduced insulin sensitivity independent of body weight, whereas oestradiol withdrawal had no effects
  • Obesity and dysglycaemia and associated comorbidities such as obstructive sleep apnoea (Hoyos et al. 2012b) are important contributors to the suppression of the HPT axis
  • This is supported by observational studies showing that weight gain and development of diabetes accelerate the age-related decline in testosterone
  • Weight loss can reactivate the hypothalamic–pituitary–testicular axis
  • The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
  • Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
  • Several observational and randomised studies reviewed in Grossmann (2011) have shown that weight loss, whether by diet or surgery, leads to substantial increases in testosterone, especially in morbidly obese men
  • This suggests that weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
  • There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
  • in those men in whom glycaemic control worsened, testosterone decreased
  • successful weight loss combined with optimisation of glycaemic control may be sufficient to normalise circulating testosterone levels in the majority of such men
  • weight loss, optimisation of diabetic control and assiduous care of comorbidities should remain the first-line approach.
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      This obviously goes against marketing-based medicine
  • In part, the discrepant results may be due to the fact men in the Vigen cohort (Vigen et al. 2013) had a higher burden of comorbidities. Given that one (Basaria et al. 2010), but not all (Srinivas-Shankar et al. 2010), RCTs in men with a similarly high burden of comorbidities reported an increase in cardiovascular events in men randomised to testosterone treatment (see section on Testosterone therapy: potential risks below) (Basaria et al. 2010), testosterone should be used with caution in frail men with multiple comorbidities
  • The retrospective, non-randomised and non-blinded design of these studies (Shores et al. 2012, Muraleedharan et al. 2013, Vigen et al. 2013) leaves open the possibility for residual confounding and multiple other sources of bias. These have been elegantly summarised by Wu (2012).
  • Effects of testosterone therapy on body composition were metabolically favourable with modest decreases in fat mass and increases in lean body mass
  • This suggests that testosterone has limited effects on glucose metabolism in relatively healthy men with only mildly reduced testosterone.
  • it is conceivable that testosterone treatment may have more significant effects on glucose metabolism in uncontrolled diabetes, akin to what has generally been shown for conventional anti-diabetic medications.
  • the evidence from controlled studies show that testosterone therapy consistently reduces fat mass and increases lean body mass, but inconsistently decreases insulin resistance.
  • Interestingly, testosterone therapy does not consistently improve glucose metabolism despite a reduction in fat mass and an increase in lean mass
  • the majority of RCTs (recently reviewed in Ng Tang Fui et al. (2013a)) showed that testosterone therapy does not reduce visceral fat
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      visceral and abdominal adiposity are biologically different and thus the risks associated with the two are different.
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      yet low T is associated with an increase in visceral adiposity--confusing!
  • testosterone therapy decreases SHBG
  • testosterone is inversely associated with total cholesterol, LDL cholesterol and triglyceride (Tg) levels, but positively associated with HDL cholesterol levels, even if adjusted for confounders
  • Although observational studies show a consistent association of low testosterone with adverse lipid profiles, whether testosterone therapy exerts beneficial effects on lipid profiles is less clear
  • Whereas testosterone-induced decreases in total cholesterol, LDL cholesterol and Lpa are expected to reduce cardiovascular risk, testosterone also decreases the levels of the cardio-protective HDL cholesterol. Therefore, the net effect of testosterone therapy on cardiovascular risk remains uncertain.
  • data have not shown evidence that testosterone causes prostate cancer, or that it makes subclinical prostate cancer grow
  • compared with otherwise healthy young men with organic androgen deficiency, there may be increased risks in older, obese men because of comorbidities and of decreased testosterone clearance
  • recent evidence that fat accumulation may be oestradiol-, rather than testosterone-dependent
Nathan Goodyear

JISSN | Full text | International Society of Sports Nutrition position stand: creatine ... - 0 views

www.jissn.com/6

creatine sports nutrition exercise

shared by Nathan Goodyear on 27 Jan 14 - No Cached
  • the energy supplied to rephosphorylate adenosine diphosphate (ADP) to adenosine triphosphate (ATP) during and following intense exercise is largely dependent on the amount of phosphocreatine (PCr) stored in the muscle
  • Creatine is chemically known as a non-protein nitrogen
  • It is synthesized in the liver and pancreas from the amino acids arginine, glycine, and methionine
  • ...26 more annotations...
  • Approximately 95% of the body's creatine is stored in skeletal muscle
  • About two thirds of the creatine found in skeletal muscle is stored as phosphocreatine (PCr) while the remaining amount of creatine is stored as free creatine
  • The body breaks down about 1 – 2% of the creatine pool per day (about 1–2 grams/day) into creatinine in the skeletal muscle
  • The magnitude of the increase in skeletal muscle creatine content is important because studies have reported performance changes to be correlated to this increase
  • "loading" protocol. This protocol is characterized by ingesting approximately 0.3 grams/kg/day of CM for 5 – 7 days (e.g., ≃5 grams taken four times per day) and 3–5 grams/day thereafter [18,22]. Research has shown a 10–40% increase in muscle creatine and PCr stores using this protocol
  • Additional research has reported that the loading protocol may only need to be 2–3 days in length to be beneficial, particularly if the ingestion coincides with protein and/or carbohydrate
  • A few studies have reported protocols with no loading period to be sufficient for increasing muscle creatine (3 g/d for 28 days)
  • Cycling protocols involve the consumption of "loading" doses for 3–5 days every 3 to 4 weeks
  • Most of these forms of creatine have been reported to be no better than traditional CM in terms of increasing strength or performance
  • Recent studies do suggest, however, that adding β-alanine to CM may produce greater effects than CM alone
  • These investigations indicate that the combination may have greater effects on strength, lean mass, and body fat percentage; in addition to delaying neuromuscular fatigue
  • creatine phosphate has been reported to be as effective as CM at improving LBM and strength
  • Green et al. [24] reported that adding 93 g of carbohydrate to 5 g of CM increased total muscle creatine by 60%
  • Steenge et al. [23] reported that adding 47 g of carbohydrate and 50 g of protein to CM was as effective at promoting muscle retention of creatine as adding 96 g of carbohydrate.
  • It appears that combining CM with carbohydrate or carbohydrate and protein produces optimal results
  • Studies suggest that increasing skeletal muscle creatine uptake may enhance the benefits of training
  • Nearly 70% of these studies have reported a significant improvement in exercise capacity,
  • Long-term CM supplementation appears to enhance the overall quality of training, leading to 5 to 15% greater gains in strength and performance
  • Nearly all studies indicate that "proper" CM supplementation increases body mass by about 1 to 2 kg in the first week of loading
  • short-term adaptations reported from CM supplementation include increased cycling power, total work performed on the bench press and jump squat, as well as improved sport performance in sprinting, swimming, and soccer
  • Long-term adaptations when combining CM supplementation with training include increased muscle creatine and PCr content, lean body mass, strength, sprint performance, power, rate of force development, and muscle diameter
  • subjects taking CM typically gain about twice as much body mass and/or fat free mass (i.e., an extra 2 to 4 pounds of muscle mass during 4 to 12 weeks of training) than subjects taking a placebo
  • The gains in muscle mass appear to be a result of an improved ability to perform high-intensity exercise via increased PCr availability and enhanced ATP synthesis, thereby enabling an athlete to train harder
  • there is no evidence to support the notion that normal creatine intakes (< 25 g/d) in healthy adults cause renal dysfunction
  • no long-term side effects have been observed in athletes (up to 5 years),
  • One cohort of patients taking 1.5 – 3 grams/day of CM has been monitored since 1981 with no significant side effects
  • Nathan Goodyear on 27 Jan 14
     
    Nice review of the data, up to the publication date, on creatine.
Nathan Goodyear

The Androgen Derivative 5α-Androstane-3β,17β-Diol Inhibits Prostate Cancer Ce... - 0 views

cancerres.aacrjournals.org/...5445.full

prostate cancer 3-beta androstanediol DHT metabolite E-cadherin ER beta ER-beta male hormone hormones men

shared by Nathan Goodyear on 27 Jan 14 - No Cached
  • In the early stages, prostate cancer growth is dependent on circulating androgens
    • Nathan Goodyear
      Nathan Goodyear on 27 Jan 14
       
      This is in contrast to studies that show poor prognosis with Lower T at time of diagnosis of prostate cancer
  • 5α-reductase not only provides a potent amplification of the androgenic signal ( 4– 6), but it also prevents estrogen formation by subtracting testosterone from the action of aromatase ( 7, 8), thus blocking activation of the estrogen receptor subtypes (ERα and ERβ; refs. 9, 10)
  • ERβ is the prevailing subtype ( 11), and a growing body of evidence points to the protective role of this receptor in prostate cancer
  • ...3 more annotations...
  • It has been shown that the transformation of the dihydrotestosterone to 5α-androstane-3α,17β-diol (3α-diol) and 5α-androstane-3β,17β-diol (3β-Adiol), generates two metabolites unable to bind the androgen receptor, but possessing a very high affinity for the estrogen receptors
  • the effects of testosterone may result from the balance between the androgenic and the estrogenic molecules originating from its catabolism.
  • Recent data have been published postulating a direct estrogenic role of the 3β-hydroxylated derivatives of dihydrotestosterone in the prostate development and homeostasis
  • Nathan Goodyear on 27 Jan 14
     
    Here is the full article.
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

Lower-But-Normal Serum TSH level Is Associated With the Development or Progression of C... - 0 views

press.endocrine.org/...jc.2013-3385

TSH cognition dementia elderly aging brain hormone hormones functional hypothyroidism

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • Nathan Goodyear on 03 Mar 14
     
    This study points to an association between a low-normal TSH and cognitive decline in the elderly.  An association is not causative, but functional hypothyroidism does result in cognitive impairment, so the association would logically fit.  The results of this study do as well.
Nathan Goodyear

Testosterone deficiency syndrome and cardiovascular health: An assessment of beliefs, k... - 0 views

www.ncbi.nlm.nih.gov/...PMC3929476

low T Testosterone cardiovascular disease physicians men male hormone hormones

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • The vast majority (88%) did not screen cardiac patients for TDS.
  • Testosterone deficiency has a prevalence of 7% in the general population, rising to 20% in elderly males
  • Males with CAD have lower testosterone levels than those with normal coronary angiograms of the same age,5 suggesting that the prevalence of testosterone deficiency is much higher in the CAD population
  • ...14 more annotations...
  • Men with hypertension, another established risk factor for CAD, have lower testosterone compared to normotensive men
  • Recent meta-analyses showed that testosterone levels are generally lower among patients with metabolic syndrome, regardless of the various definitions of metabolic syndrome that are used
  • Testosterone (total and bioavailable) and sex-hormone binding globulin (SHBG) are inversely associated with the prevalence of metabolic syndrome in men between the ages of 40 and 80, and this association persists across racial and ethnic backgrounds
  • ower levels of testosterone and SHBG predict a higher incidence of metabolic syndrome.
  • Low testosterone levels have been related to increased insulin resistance and cardiovascular mortality,12 even in the absence of overt type 2 diabetes mellitus.
  • testosterone levels (total and bioavailable) in middle-aged men are inversely correlated with insulin resistance
  • The Massachusetts Male Aging Study (MMAS) demonstrated that low levels of testosterone and SHBG are independent risk factors for the development of type 2 diabetes,
  • Andropausal men (age 58 ± 7 years) have a higher maximal carotid artery intima-media thickness
  • There is an inverse linear correlation between body mass index (BMI) and wait-to-hip ratio with testosterone and insulin-like growth factor-1 levels.
  • Testosterone supplementation for 1 year in hypogonadal men has been shown to cause a significant improvement in body weight, BMI, waist size, lipid profile, and C-reactive protein levels
  • TRT for 3 months in hypogonadal men with type 2 diabetes significantly improved fasting insulin sensitivity, fasting blood glucose and glycated hemoglobin.
  • Testosterone replacement can improve angina symptoms and delay the onset of cardiac ischemia, likely through a coronary vasodilator mechanism
  • ADT is associated with an increased risk of cardiovascular events, including myocardial infarction and cardiovascular mortality.
  • ADT significantly increases fat mass, decreases lean body mass,29,30 increases fasting plasma insulin and decreases insulin sensitivity31 and increases serum cholesterol and triglyceride levels
  • Nathan Goodyear on 03 Mar 14
     
    Startling study on the knowledge of Testosterone and cardiovascular disease in general practitioners and cardiologists in Canada.  Eight-eight percent did not screen patients with cardiovascular disease for low Testosterone.  A whopping 67% of physicians did not know that low T was a risk factor for cardiovascular disease, yet 62% believed Testosterone would increase exercise tolerance. The lack of knowledge displayed by physicians today is staggering and is an indictment of the governing bodies.  This was a survey conducted in Canada so there are obvious limitations to the strength/conclusion of this study.
Nathan Goodyear

Membrane Estrogen Receptors Stimulate Intracellular Calcium Release and Progesterone Sy... - 0 views

www.jneurosci.org/...12950.full

estradiol estrogen progesterone hypothalamus receptors ER ER-alpha ER alpha hormones CNS astrocytes brain calcium channels

shared by Nathan Goodyear on 10 Mar 14 - No Cached
  • Nathan Goodyear on 10 Mar 14
     
    Estradiol stimulates hypothalamic progesterone synthesis in astrocytes in rat model.  This occurs through activation of calcium channels and influx of calcium.  ER alpha appears to be the prominent ER involved.
Teresa conrad

Common Breast Cancer Treatments - 1 views

www.placidway.com/...Breast-Cancer-Treatment-Abroad

cancer

shared by Teresa conrad on 11 Mar 14 - No Cached
Teresa conrad liked it
  • Teresa conrad on 11 Mar 14
     
    A diagnosis of breast cancer can be a devastating bit of news to anyone. However, recent developments in treatments and medical advances that combat breast cancer offer today's women more choices, less discomfort and improved prognosis.
Nathan Goodyear

The Evolving Role of Oestrogens and Their Receptors in the Development and Progression ... - 0 views

www.europeanurology.com/...S0302-2838(08)01301-8

Estrogen Estradiol aromatase aromatase activity prostate cancer prostate cancer ER ER alpha

shared by Nathan Goodyear on 21 Aug 13 - No Cached
  • Nathan Goodyear on 21 Aug 13
     
    This study points out, that it is not the androgens, but the high aromatase activity and resultant Estradiol production that promotes prostate disease.  Take this together with high ER alpha dominance and one has a recipe for disease.
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

Fructose: A Key Factor in the Development of Metabolic Syndrome and Hypertension - 0 views

www.hindawi.com/...682673

fructose obesity metabolic syndrome

shared by Nathan Goodyear on 17 Sep 13 - No Cached
  • Nathan Goodyear on 17 Sep 13
     
    nice article how fructose contributes to fat accumulation.
Nathan Goodyear

Uric Acid Stimulates Fructokinase and Accelerates Fructose Metabolism in the Developmen... - 0 views

www.ncbi.nlm.nih.gov/...PMC3480441

non-alcoholic fatty liver fatty liver fructose uric acid

shared by Nathan Goodyear on 01 Oct 13 - No Cached
  • Nathan Goodyear on 01 Oct 13
     
    Vicious cycle.  High fructose intake increases uric acid production.  Hyperuricemia then leads to further Fructose metabolism.  This study finds that hyperuricemia upregulates the fructokinase enzyme that is the first step in fructose metabolism.  This upregulation will increase fructose metabolism and increase fat accumulation in the liver.
Nathan Goodyear

Fructose: A Key Factor in the Development of Metabolic Syndrome and Hypertension - 0 views

www.ncbi.nlm.nih.gov/...PMC3677638

fructose phosphofructokinase MetS metabolic syndrome metabolic syndrome insulin resistance ATP mitochondria uric acid

shared by Nathan Goodyear on 01 Oct 13 - No Cached
  • Nathan Goodyear on 01 Oct 13
     
    Fructose intake increases MetS and hypertension.  The high fructose intake upregulates phosphofructokinase which increases triglyceride production, bypassing central regulation.  This results in ATP depletion with reduced capacity to recover.  Thus attempts by the cells to increase ATP through AMP deaminase results in uric acid production.
Nathan Goodyear

Role of Pancreatic Cancer-derived Exosomes in Salivary Biomarker Development - 0 views

www.jbc.org/26888

saliva testing salivary pancreatic cancer

shared by Nathan Goodyear on 16 Oct 13 - No Cached
  • Nathan Goodyear on 16 Oct 13
     
    Saliva is proving to be an exciting medium for functional testing.  Recently, studies have found saliva as a great medium to evaluate for cancer biomarkers.  This study find pancreatic cancer biomarkers in saliva.
Nathan Goodyear

Hypoxia-inducible Factor 1 Activation by Aerobic Glycolysis Implicates the Warburg Effe... - 0 views

www.jbc.org/...23111.long

HIF-1alpha cancer Hypoxia-inducible Factor 1

shared by Nathan Goodyear on 17 Oct 13 - No Cached
  • HIF-1 activation is highly associated with cancer cell growth and survival, tumor development, tumor angiogenesis, and poor clinical prognosis
  • The adaptation of cancer cells to hypoxia is mediated via hypoxia-inducible Factor 1 (HIF-1),1 a key transcription factor that up-regulates a series of genes involved in glycolytic energy metabolism, angiogenesis, cell survival, and erythropoiesis. Included among these genes are vascular endothelial growth factor (VEGF), erythropoietin (EPO), glucose transporters (GLUT), and several glycolytic enzymes (12, 13).
  • Nathan Goodyear on 17 Oct 13
     
    good discussion of HIF-1alpha and cancer
Nathan Goodyear

Recent developments in mushrooms as anti-cancer therapeutics: a review - 0 views

www.ncbi.nlm.nih.gov/...PMC3339609

cancer mushrooms

shared by Nathan Goodyear on 28 Apr 14 - No Cached
  • Nathan Goodyear on 28 Apr 14
     
    mushrooms and cancer
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