Skip to main content

Home/ Seasons Wellness/ Group items tagged resistance syndrome

Rss Feed Group items tagged

Nathan Goodyear

[Plasma testosterone, obesity, metabolic syndrome and diabetes]. - Abstract - Europe Pu... - 0 views

  •  
    Androgen deprivation therapy leads to insulin resistance, metabolic syndrome, and type II diabetes in men. Testosterone therapy in men with IR, obesity, metabolic syndrome, and type II Diabetes will result in improved cardiovascular risk.  
Nathan Goodyear

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

  • 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
  •  
    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

  •  
    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

Higher Serum Testosterone Concentration in Older Women is Associated with Insulin Resis... - 0 views

  •  
    This study found that increasing Testosterone, as determined by serum, is associated with increased CVD, insulin resistance, and metabolic syndrome in postmenopausal women.  I believe that this massive Testosterone doping campaign that we are seeing in men and women is following the same patter seen with premarin and provera. 
Nathan Goodyear

Diagnosis and treatment of late-onset hypogonadism: Systematic review and meta-analysis... - 0 views

  •  
    Testosterone therapy is complex in hypogonadism.  Much of the marketing-based medicine of Low T today is in fact doping.  Increasing weight is clearly associated with a declining T level in men.  Testosterone therapy should be approach individually and therapies that use the one size fits all approach never work.  This is the case whether the use of synthetics or natural hormones are employed.  Testosterone has been shown to improve dysglycemia, MetS, reduce fat and increase muscle mass.  
Nathan Goodyear

The Dark Side of Testosterone Deficiency: II. Type 2 Diabetes and Insulin Resistance - ... - 0 views

  •  
    low Testosterone linked to insulin resistance, type II Diabetes, and increased  metabolic syndrome.  Low T is linked to increased visceral fat in this study.  
Nathan Goodyear

Toll-like Receptor Status in Obesity and Metabolic Syndrome: A Translational Perspectiv... - 0 views

  •  
    Only the abstract is available publicly.   Toll-like receptors, particularly TLR-4 has been shown to be associated with insulin resistance.  These TLRs have specific pathogen recognition sites.  TLRs are stimulated by fatty acids (FA) and endotoxemia from bacteria.  Thus, dietary intake of high trans fats, inflammation originating from the gut can be the source of insulin receptor dysfunction through TLRs.
Nathan Goodyear

PLOS ONE: Prediabetes Is Associated with an Increased Risk of Testosterone Deficiency, ... - 0 views

  •  
    This study found that low T was clearly associated with "pre diabetes" independent of weight and MetS.  All men that are overweight, obese, with metabolic syndrome, "pre diabetic" need evaluation of hormones, not just Testosterone.
Nathan Goodyear

Access : Testosterone and insulin resistance in the metabolic syndrome and T2DM in men ... - 0 views

  •  
    Testosterone plays role in insulin resistance, metabolic syndrome, and type II diabetes in men.
Nathan Goodyear

Statin Therapy Worsens Insulin Sensi... [J Clin Endocrinol Metab. 2013] - PubMed - NCBI - 0 views

  •  
    Statin therapy worsens insulin resistance in women with PCOS
Nathan Goodyear

Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslip... - 0 views

  • 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
  •  
    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

Endogenous Sex Hormones and Glucose Tolerance Status in Postmenopausal Women - 0 views

  •  
    Increase in free Testosterone, DHEA, and Estradiol in postmenopause women associated with increase in insulin resistance.
Nathan Goodyear

Glucose and insulin components of the metabol... [Am J Epidemiol. 2004] - PubMed - NCBI - 0 views

  •  
    Correlation between increasing male hormones (androgens) and poor glucose control and metabolic syndrome in post menopause women.
Nathan Goodyear

Association of Endogenous Sex Hormones and Insulin Resistance among Postmenopausal Wome... - 0 views

  •  
    In women, the postmenopause state is associated with a decrease in SHBG, and increase in free Testosterone and Estradiol.  No increase in Total Testosterone was found in this study.  This was associated with increased insulin resistance and MetS.
Nathan Goodyear

Association between hyperinsulinemia and endogeno... [Metabolism. 2002] - PubMed - NCBI - 0 views

  •  
    Increasing androgen levels associated with perimenopause/menopause transition.  This is associated with increasing insulin resistance.
Nathan Goodyear

JCI - Thyroid hormone resistance syndrome. Inhibition of normal receptor function by mu... - 0 views

  •  
    Thyroid hormone resistance is not a new term.  This study goes back to 1991.
Nathan Goodyear

Diabetology & Metabolic Syndrome | Full text | Visceral adiposity, insulin resistance a... - 0 views

  •  
    adipose tissue and it's biological activity contribution to cancer risk.  Good review of our current understanding on how adipose tissue increases the favorably of cancer.
Nathan Goodyear

'Metabolic syndrome' in the brain: deficiency in omega-3 fatty acid exacerbates dysfunc... - 0 views

  • n-3 deficient diet and fructose interventions disrupted insulin receptor signalling in hippocampus as evidenced by a decrease in phosphorylation of the insulin receptor and its downstream effector Akt
  •  
    rats fed high fructose diet and omega-3 diet found to have memory decline.  The purpose of this study was to look at the effects of Metabolic syndrome on the brain.
Nathan Goodyear

Insulin resistance and endothelial function are improved after folate and vitamin B12 t... - 0 views

  •  
    Vitamin B12 and Folic acid improves insulin resistance, endothelial dysfunction, and reduces homocysteine levels by 28% in those with metabolic syndrome.
Nathan Goodyear

Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity - 0 views

  • acute GC secretion during stress mobilizes peripheral amino acids from muscle as well as fatty acids and glycerol from peripheral fat stores to provide substrates for glucose synthesis by the liver
  • chronically elevated GC levels alter body fat distribution and increase visceral adiposity as well as metabolic abnormalities in a fashion reminiscent of metabolic syndrome
  • This local production may play an important role in the onset of obesity and insulin resistance.
  • ...9 more annotations...
  • In adipocytes, cortisol inhibits lipid mobilization in the presence of insulin, thus leading to triglyceride accumulation and retention.
  • Since the density of GC receptors is higher in intra-abdominal (visceral) fat than in other fat depots, the activity of cortisol leading to accumulation of fat is accentuated in visceral adipose tissue (24, 158), providing a mechanism by which excessive endogenous or exogenous GC lead to abdominal obesity and IR
  • obese patients generally have normal or subnormal plasma cortisol concentrations
  • This may be explained by an increased intratissular/cellular concentration of cortisol in adipose tissues
  • Intracellular GC may be produced from recycling of GC metabolites such as cortisone in adipose tissues
  • Local GC recycling metabolism is mediated by 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD1 and 11β-HSD2
  • Cortisol also increases 11β-HSD1 expression in human adipocytes
  • In humans, elevated 11β-HSD1 expression in visceral adipose tissue is also associated with obesity
  • even if obese patients generally have normal or subnormal plasma cortisol concentrations (131, 158), triglyceride accumulation in visceral adipose tissue may be due, at least in part, to the local production of GC in insulin- and GC-responsive organs such as adipose tissue, liver, and skeletal muscle
  •  
    another nice article on the dysregulation of cortisol and its role in insulin resistance, metabolic syndrome, and obesity.
1 - 20 of 30 Next ›
Showing 20 items per page