The prevalence of hypogonadism (often defined as serum testosterone < 300 ng dl−1 ) ranges from 6% [10] to as high as 38%
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shared by Nathan Goodyear on 14 Aug 14
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The role of testosterone in the m... [J Steroid Biochem Mol Biol. 2009] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...19444934
low T Testosterone low T low Testosterone lipids glucose diabetes metabolic syndrome SHBG metabolic syndrome IR insulin resistance
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Testosterone plays an important role in glucose and lipid metabolism. Thus, low Testosterone, will result in increased disruption in the homeostasis of glucose and lipids resulting in increased weight, insulin resistance, diabetes, metabolic syndrome... Low SHBG was also shown to be associated with MetS
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shared by Nathan Goodyear on 01 Dec 14
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Testosterone and benign prostatic hyperplasia Jarvis TR, Chughtai B, Kaplan SA, - Asian... - 0 views
www.ajandrology.com/preprintarticle.asp
Testosterone BPH low T low Testosterone prostate cancer men male hormone hormones
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The process of BPH, however, continues as men age and despite the fact their serum testosterone decreases
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Liu et al. [12] demonstrated that in a group of older males (mean age 59.8 years) that there was not a significant correlation of serum testosterone levels (total, free or bioavailable) with either prostate volume or International Prostate Symptom Score (IPSS)
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in eugonadal men, studies have demonstrated that the prostate can increase in volume by approximately 12%
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There seems to be little doubt that the treatment with testosterone of a young hypogonadal male leads to significant growth of the prostate
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Behre et al. [22] demonstrated increased prostate volume and prostate-specific antigen (PSA) levels in hypogonadal men
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Most studies, however, have shown no effect of exogenous androgens on PSA or prostate volume for older hypogonadal males
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They argue that the prostate is relatively insensitive to changes in androgen concentration at normal levels or in mild hypogonadism because the AR is saturated by androgens and therefore maximal androgen-AR binding is achieved. Conversely, the prostate is very sensitive to changes in androgen levels when testosterone is low
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visceral obesity (one of the most significant components of metabolic syndrome) is associated with prostate volume and influences prostate growth during TRT.
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This hypothesis of inflammation induced LUTS is also argued to be a mechanism for improvement of LUTS with PDE5I
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The concept, therefore, that treatment with TRT of hypogonadal males with metabolic syndrome might lead to improvement/stabilization of their LUTS, appears to be confirmed in recent work by Francomano et al.
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There was also an improvement in components of the patient's metabolic syndrome (such as BMI, waist circumference, hemoglobin A1c [HbA1c], insulin sensitivity, and lipid profile) as well as inflammatory markers and C-reactive protein.
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They concluded that TRT was safe in this group of men, and hypothesize that TRT mitigates the pro-inflammatory factors associated with metabolic syndrome.
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Nutrients | Free Full-Text | Vitamin C Status Correlates with Markers of Metabolic and ... - 0 views
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The CHALICE (Canterbury Health, Ageing and Lifecourse) study is a unique New Zealand study comprising a comprehensive database of determinants of health
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The CHALICE cohort of 404 individuals aged 50 years had an average vitamin C intake of ~110 mg/day, which should provide adequate plasma concentrations [14]. Despite this, a significant proportion of the participants had inadequate plasma vitamin C status
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plasma vitamin C was negatively associated with blood triglycerides, HbA1c and insulin, and positively associated with HDL levels.
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No correlation was found between plasma vitamin C and the two indicators of heart health; blood pressure and cardiovascular risk score.
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A high proportion (63%) of our participants had inadequate plasma vitamin C concentrations (i.e., <50 µmol/L)
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The association of low vitamin C with obesity in this study replicates results in the literature [35,40,41,42,43,44], and it is apparent that individuals with higher weight require higher intakes of vitamin C to reach adequate vitamin C status
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higher plasma vitamin C status is associated with lower circulating levels of blood triglycerides, insulin and HbA1c
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A role for vitamin C in the prevention or management of diabetes and/or metabolic syndrome has been suggested
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In this study, we also demonstrate lower levels of mild cognitive impairment in those with high vitamin C status
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The odds of mild cognitive impairment were twice as high for those below 23 μmol/L plasma vitamin C concentration.
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animal models have shown that the brain is the last organ to be depleted of the vitamin during prolonged deficiency
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A recent animal study has shown that moderate vitamin C deficiency may play a role in accelerating amyloid plaque accumulation in Alzheimer’s disease
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New study: vitamin C levels correlate with cognitive and metabolic health. What is your vitamin C level? Despite the adequate levels of vitamin C intake, a large % of the individuals had inadequate vitamin C levels which points to a demand issue. Higher oxidative stress, chronic inflammation... would drive demand for vitamin C higher. Lower vitamin C levels were associated with more metabolic disease, ie. DM, and more cognitive decline.
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High-Dose Vitamin C for Cancer Therapy - PMC - 0 views
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diabetes [8], atherosclerosis [9], the common cold [10], cataracts [11], glaucoma [12], macular degeneration [13], stroke [14], heart disease [15], COVID-19 [16], and cancer.
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Iron is found in the human body in the form of haemoglobin in red blood cells and growing erythroid cells.
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iron is taken up by the majority of cells in the form of a transferrin (Tf)-Fe(III) complex that binds to the cell surface receptor transferrin receptor 1 (TfR1)
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the endosomal six transmembrane epithelial antigen of the prostate 3 (STEAP3) reduces Fe(III) (ferric ion) to Fe(II) (ferrous ion), which is subsequently transferred across the endosomal membrane by divalent metal transporter 1 (DMT1)
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DHA is quickly converted to Vit-C within the cell, by interacting with reduced glutathione (GSH) [45,46,47]. NADPH then recycles the oxidized glutathione (glutathione disulfide (GSSG)) and converts it back into GSH
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Fe(II) catalyzes the formation of OH• and OH− during the interaction between H2O2 and O2•− (Haber–Weiss reaction)
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Ascorbate can efficiently reduce free iron, thus recycling the cellular Fe(II)/Fe(III) to produce more OH• from H2O2 than can be generated during the Fenton reaction, which ultimately leads to lipid, protein, and DNA oxidation
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Asc•− and H2O2 were generated in vivo upon i.v Vit-C administration of around 0.5 g/kg of body weight and that the generation was Vit-C-dose reliant
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increase in the expression of various iron-intake pathways or the downregulation of iron exporter proteins and storage pathways
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Advanced breast tumor patients had substantially greater Fe(II) levels in their blood than the control groups without the disease
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Vit-C is supplied, it oxidizes to DHA, and then is readily transported by GLUT-1 in mutant cells of KRAS or BRAF competing with glucose [46]. DHA is quickly converted into ascorbate inside the cell by NADPH and GSH [46,107]. This decrease reduces the concentration of cytosolic antioxidants and raises the intracellular ROS amounts
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ROS activates poly (ADP-ribose) polymerase (PARP), which depletes NAD+ (a critical co-factor of GAPDH); thus, further reducing the GAPDH associated with a multifaceted metabolic rewiring
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high-dose Vit-C recruited metabolites and increased the enzymatic activity in the pentose phosphate pathway (PPP), blocked the tri-carboxylic acid (TCA) cycle, and increased oxygen uptake, disrupting the intracellular metabolic balance and resulting in irreversible cell death, due to an energy crisis
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Due to its great volatility at neutral pH [76], bolus therapy with mega-dose DHA has only transitory effects on tumor cells, both in vitro and in vivo.
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shared by Nathan Goodyear on 08 Oct 12
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Toll-like receptor signaling links dietary fatty acids to the metabolic syndrome - 0 views
www.ncbi.nlm.nih.gov/...PMC3099529
TLR toll-like receptors toll-like receptors fatty acids fat metabolic syndrome obesity overweight inflammation dietary
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the innate immune response is the first line of defense against invading pathogens, wherein highly conserved pathogen-associated molecular patterns (PAMPs) are recognized by cognate pattern recognition receptors (PRRs
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adipose tissue contains a substantial population of macrophages, and macrophage-driven adipose inflammation contributes significantly to the pathogenesis of obesity
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Collectively, activation of the innate immune system is strongly associated with ASCVD, insulin resistance, and obesity, and recent evidence suggests that much of this association can be traced to a unique family of PRRs known as TLRs
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TLRs are a family of type I transmembrane receptors, currently thought to comprise at least 13 members in mammals, that specifically recognize a variety of microbial PAMPs and trigger host cellular responses
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Free SFAs have indeed been demonstrated to elicit TLR4-dependent and TLR2-dependent responses in several cell types.
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Endogenous SFAs released from adipocytes activate cocultured macrophages via TLR4 [18], indicating the potential for cellular crosstalk in adipose tissue. Collectively, there is a growing body of evidence that SFAs promote, whereas long chain PUFA antagonize, TLR4-dependent and TLR2-dependent signaling in multiple cell models
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In an elegant study, Shi et al. [16] demonstrated that SFAs activate TLR4-dependent signaling in both macrophages and adipocytes, and mice lacking TLR4 are protected against insulin resistance driven by intravenous lipid infusion
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In addition to effects in macrophages and adipocytes, SFAs can activate TLR4 in the hypothalamus, which triggers a central inflammatory response that results in resistance to anorexigenic signals
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This finding strongly supports the work of Hwang and coworkers [19–22] demonstrating that ω-3 PUFAs can effectively counteract SFA-induced TLR4 activation in cultured macrophages and dendritic cells.
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Sex Hormone-Binding Globulin and Insulin-Like Growth Factor-Binding Protein-1 as Indica... - 0 views
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Inflammation as a Link between Obesity and Metabolic Syndrome - 0 views
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the role of the gut microbiota in energy metabolism and metabolic disease - 0 views
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Gender differences in serum high-molecular-weight adiponectin levels in metabolic syndrome - 0 views
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Differences in the Apparent Metabolic Clearance Rate of Testosterone in Young and Older... - 0 views
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shared by Nathan Goodyear on 08 May 13
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Testosterone: a metabolic hormone in health and disease - 0 views
joe.endocrinology-journals.org/...R25.full
male hormone hormones testosterone hypogonadal-obesity-adipocytokine hypothesis
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E2 and the inflammatory adipocytokines tumour necrosis factor α (TNFα) and interleukin 6 (IL6) inhibit hypothalamic production of GNRH and subsequent release of LH and FSH from the pituitary
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Leptin, an adipose-derived hormone with a well-known role in regulation of body weight and food intake, also induces LH release under normal conditions via stimulation of hypothalamic GNRH neurons
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In human obesity, whereby adipocytes are producing elevated amounts of leptin, the hypothalamic–pituitary axis becomes leptin resistant
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there is evidence from animal studies that leptin resistance, inflammation and oestrogens inhibit neuronal release of kisspeptin
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Beyond hypothalamic action, leptin also directly inhibits the stimulatory action of gonadotrophins on the Leydig cells of the testis to decrease testosterone production; therefore, elevated leptin levels in obesity may further diminish androgen status
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increasing insulin resistance assessed by glucose tolerence test and hypoglycemic clamp was shown to be associated with a decrease in Leydig cell testosterone secretion in men
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ADT for the treatment of prostatic carcinoma in some large epidemiological studies has been shown to be associated with an increased risk of developing MetS and T2DM
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Non-diabetic men undergoing androgen ablation show increased occurrence of new-onset diabetes and demonstrate elevated insulin levels and worsening glycaemic control
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Prostate cancer patients with pre-existing T2DM show a further deterioration of insulin resistance and worsening of diabetic control following ADT
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The response to testosterone replacement of insulin sensitivity is in part dependent on the androgen receptor (AR)
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Low levels of testosterone have been associated with an atherogenic lipoprotein profile, characterised by high LDL and triglyceride levels
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a positive correlation between serum testosterone and HDL has been reported in both healthy and diabetic men
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GLUT4 and IRS1 were up-regulated in cultured adipocytes and skeletal muscle cells following testosterone treatment at low dose and short-time incubations
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orchidectomy of male Wistar rats and associated testosterone deficiency induced increased absorption of glucose from the intestine
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(Kelley & Mandarino 2000). Frederiksen et al. (2012a) recently demonstrated that testosterone may influence components of metabolic flexibility as 6 months of transdermal testosterone treatment in aging men with low–normal bioavailable testosterone levels increased lipid oxidation and decreased glucose oxidation during the fasting state.
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Decreased lipid oxidation coupled with diet-induced chronic FA elevation is linked to increased accumulation of myocellular lipid, in particular diacylglycerol and/or ceramide in myocytes
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In the Chang human adult liver cell line, insulin receptor mRNA expression was significantly increased following exposure to testosterone
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Testosterone deprivation via castration of male rats led to decreased expression of Glut4 in liver tissue, as well as adipose and muscle
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oestrogen was found to increase the expression of insulin receptors in insulin-resistant HepG2 human liver cell line
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FFA decrease hepatic insulin binding and extraction, increase hepatic gluconeogenesis and increase hepatic insulin resistance.
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Only one, albeit large-scale, population-based cross-sectional study reports an association between low serum testosterone concentrations and hepatic steatosis in men (Völzke et al. 2010)
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This suggests that testosterone may confer some of its beneficial effects on hepatic lipid metabolism via conversion to E2 and subsequent activation of ERα.
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hypogonadal men exhibiting a reduced lean body mass and an increased fat mass, abdominal or central obesity
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there was no change in visceral fat mass in aged men with low testosterone levels following 6 months of transdermal TRT, yet subcutaneous fat mass was significantly reduced in both the thigh and the abdominal areas when analysed by MRI (Frederiksen et al. 2012b)
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ADT of prostate cancer patients increased both visceral and subcutaneous abdominal fat in a 12-month prospective observational study (Hamilton et al. 2011)
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Catecholamines are the major lipolysis regulating hormones in man and regulate adipocyte lipolysis through activation of adenylate cyclase to produce cAMP
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deficiency of androgen action decreases lipolysis and is primarily responsible for the induction of obesity (Yanase et al. 2008)
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may be some regional differences in the action of testosterone on subcutaneous and visceral adipose function
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proinflammatory adipocytokines IL1, IL6 and TNFα are increased in obesity with a downstream effect that stimulates liver production of CRP
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observational evidence suggests that IL1β, IL6, TNFα and CRP are inversely associated with serum testosterone levels in patients
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This suggests a role for AR in the metabolic actions of testosterone on fat accumulation and adipose tissue inflammatory response
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testosterone treatment may have beneficial effects on preventing the pathogenesis of obesity by inhibiting adipogenesis, decreasing triglyceride uptake and storage, increasing lipolysis, influencing lipoprotein content and function and may directly reduce fat mass and increase muscle mass
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Early interventional studies suggest that TRT in hypogonadal men with T2DM and/or MetS has beneficial effects on lipids, adiposity and parameters of insulin sensitivity and glucose control
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Evidence that whole-body insulin sensitivity is reduced in testosterone deficiency and increases with testosterone replacement supports a key role of this hormone in glucose and lipid metabolism
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Impaired insulin sensitivity in these three tissues is characterised by defects in insulin-stimulated glucose transport activity, in particular into skeletal muscle, impaired insulin-mediated inhibition of hepatic glucose production and stimulation of glycogen synthesis in liver, and a reduced ability of insulin to inhibit lipolysis in adipose tissue
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shared by Nathan Goodyear on 12 Feb 13
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SIRT3 Weighs Heavily in the Metabolic Balance: A New Role for SIRT3 in Metabolic Syndrome - 0 views
biomedgerontology.oxfordjournals.org/...105.full
SIRT3 metabolic syndrome mitochondria acetylation high fat diet diet
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shared by Nathan Goodyear on 19 Feb 13
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Oral estrogen antagonizes the metabolic actions of growth hormone in growth hormone-def... - 0 views
ajpendo.physiology.org/...E1191.long
oral estrogen oral estrogen HGH human growth hormone growth hormone IGF-1 hormone hormones therapy
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One really wonders if estrogen should ever be given orally at all. Though this study is small, this is consistent with other studies that show that estrogen therapy, particularly oral therapy interferes with growth hormone signaling and thus action. Oral estrogen decreases IGF-1, increases growth hormone binding protein, lowers metabolism and reduces protein metabolism as monitored by leucine turnover.
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shared by Nathan Goodyear on 15 Jan 13
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Is the Gut Microbiota a New Factor Contributing to Obesity and Its Metabolic Disorders? - 0 views
www.hindawi.com/...879151
dysbiosis gut bacteria microbiota obesity inflammation metabolic syndrome metabolic endotoxemia
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shared by Nathan Goodyear on 11 Oct 12
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ScienceDirect.com - Cell Metabolism - Estrogen Receptors and the Metabolic Network - 0 views
www.sciencedirect.com/...S1550413111003123
ER-alpha ER-beta estrogen receptor receptors metabolic syndrome MetS hormone hormones
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The pro-opiomelanocortin (POMC) neurons have an anorexigenic action and, when activated, reduce food intake through the release of two peptides, α-melanocyte-stimulating hormone (α-MSH) and cocaine-and-amphetamine-regulated transcripts (CART). The neuropeptide Y (NPY) neurons, on the other hand, release NPY hormone and agouti gene-related protein (AgRP), which prevent the binding of α-MSH to MC3R and MC4R, increasing food intake
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The main hypothalamic areas involved in food intake and satiety are the arcuate nucleus (ARC), the lateral hypothalamus (LH), the paraventricular nucleus (PVN), the ventromedial hypothalamus (VMH), and the dorsomedial hypothalamus (DMH)
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Leptin is a potent anorexigenic and catabolic hormone secreted by adipose cells that reduces food intake and increases energy expenditure
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E2 not only modulates leptin receptor mRNA in the ARC and VMH, but also increases hypothalamic sensitivity to leptin, altering peripheral fat distribution
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ghrelin. It acts on growth hormone secretagogue receptors (GHSR1a) located in the ARC and is a potent stimulator of food intake
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It thus appears that of the two ERs, ERα plays a predominant role in the CNS regulation of lipid and carbohydrate homeostasis.
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Stimulation of MCH neurons increases food intake and fat accumulation while its inhibition leads to decreased food intake and reduced fat accumulation.
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The PVN is the region of the hypothalamus with the highest expression of ERβ and is reported to be weakly ERα positive
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GLUT4 is highly expressed in muscle and represents a rate-limiting step in the insulin-induced glucose uptake
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data suggest that in the physiological range, E2 is beneficial for insulin sensitivity, whereas hypo- or hyperestrogenism is related to insulin resistance
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In aging female rats, E2 treatment improves glucose homeostasis mainly through its ability to increase muscle GLUT4 content on the cell membrane
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It is evident that ERα and ERβ have distinct actions and that much more research is needed to clearly identify the function of each receptor in muscle.
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E2 prevents accumulation of visceral fat, increases central sensitivity to leptin, increases the expression of insulin receptors in adipocytes, and decreases the lipogenic activity of lipoprotein lipase in adipose tissue
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In rats, ovariectomy increases body weight, intra-abdominal fat, fasting glucose and insulin levels, and insulin resistance followed by decreased phosphorylation of AMPK and its substrate acetyl-CoA carboxylase in adipose tissue
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decreased adiponectin, PPARγ coactivator-1α (PGC-1α), and uncoupling protein 2 (UCP2) and increased resistin
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Men with aromatase deficiency have truncal obesity, elevated blood lipids, and severe insulin resistance
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Although not all studies are in agreement, polymorphisms of ERα in humans have been associated with risk factors for CVDs
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Human subcutaneous and visceral adipose tissues express both ERα and ERβ, whereas only ERα mRNA has been identified in brown adipose tissue
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very nice article that looks at the balance of ER-alpha/ER-beta and their role in metabolic syndrome. This article discusses the balance of these receptors are tissue dependent in their effect. I like their conclusion: "...but these mechanisms will never be completely understood if they are not considered in the context of a whole system.
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shared by Nathan Goodyear on 03 Jul 13
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British Journal of Cancer - Role of glucose and ketone bodies in the metabolic control ... - 0 views
www.nature.com/...6601269a.html
glucose ketones cancer ketogenic diet ketogenic diet nutrition brain
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Ketogenic Diet Prevents Alterations in Brain Metabolism in Young but not Adult Rats aft... - 0 views
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shared by Nathan Goodyear on 05 Jun 16
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Responses of Gut Microbiota and Glucose and Lipid Metabolism to Prebiotics in Genetic O... - 0 views
www.ncbi.nlm.nih.gov/...PMC3198091
prebiotics probiotic Bifidobacterium leptin resistance leptin glucose lipids inflammation LPS
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Obesity and Gender influence cortisol secretion and metabolism in man - 0 views
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This study reveals the degree of metabolism dysfunction in obesity. This study suggests that cortisol metabolism is increased in obesity, which results in increased HPA activity resulting in increased peripheral cortisol production. The question to be asked: is serum, salivary, and urinary cortisol results revealing the same function of cortisol. The answer is no.