Obesity and models of obesity induced by ingestion of HF-diet in rodents are associated with chronically elevated circulating levels of LPS
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shared by Nathan Goodyear on 16 Aug 14
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The effect of a low-fat, plant-based lifestyle intervention (CHIP) on serum HDL levels ... - 0 views
www.ncbi.nlm.nih.gov/...PMC3849684
diet nutrition metabolic syndrome metabolism plant-based low fat diet low-fat HDL
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Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet - NEJM - 0 views
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shared by Nathan Goodyear on 15 Feb 17
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Effect of low-fat diet on female sex hormone levels. - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...3480374
nutrition diet low fat diet hormones female hormones estrogen Testosterone
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shared by Nathan Goodyear on 04 Oct 17
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Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in ... - 0 views
www.ncbi.nlm.nih.gov/...PMC4523075
LPS lipopolysaccharides leptin CCK cholecystokinin metabolism weight appetite diet nutrition inflammation
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chronic low-dose administration of LPS induces leptin-resistance in vagal afferent neurons and abolition of CCK-induced inhibition of food intake
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HF fat feeding has been shown to enhance gastrointestinal permeability promoting the translocation of LPS to the circulation
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LPS leads to an increase in SOCS3 expression [20]. SOCS3 is a negative regulator of leptin signaling
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the data provides a mechanism linking changes in gut microbiota induced by ingestion of HF diets to dysregulation of food intake and body weight
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Chronic low-dose LPS treatment induced TLR4 activation and MyD88 signaling in vagal afferent neurons, associated with increased SOCS3 expression and reduced leptin-signaling, characterized by the absence of leptin-induced pSTAT3.
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SOCS3 is an important mechanism by which leptin resistance develops in vagal afferent neurons and coincides with the onset of hyperphagia
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We demonstrate that this chronic low dose LPS is sufficient to induce leptin–resistance in vagal afferent neurons, reduced sensitivity to the satiating effects of CCK, and loss of vagal afferent plasticity
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it suggests that the increase in food intake and body weight we observed at week 6 in the LPS treated rats may be caused by LPS-induced leptin resistance.
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shared by Nathan Goodyear on 01 Jun 17
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Long-Term Immunomodulatory Effects of a Mediterranean Diet in Adults at High ... - 0 views
jn.nutrition.org/...1684.short
mediterranean mediterranean diet heart health heart nutrition cardiovascular disease inflammation hsCRP CRP TNF-alpha
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shared by Nathan Goodyear on 18 Jan 12
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Targeting gut microbiota in obesity: effects of prebiotics and probiotics : Article : N... - 0 views
www.nature.com/...nrendo.2011.126.html
LPS lipopolysaccharides gut microbiota dysbiosis inflammation obesity metabolic endotoxemia health probiotics
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Associations between circulating LPS level, consumption of a high-fat diet and the presence of obesity and type 2 diabetes mellitus have been confirmed in humans
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associations have been proposed between high-fat diet, metabolic endotoxemia and levels of inflammatory markers (TLRs and SOCS3) in mononuclear cells
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metabolic endotoxemia is associated with systemic and adipose tissue inflammation in pregnant women with obesity
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A growing amount of evidence indicates that changes in the integrity of the intestinal barrier occur both in the proximal and the distal part of the gut, which can contribute to the entrance of LPS into the systemic circulation
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The low-grade systemic inflammation that characterizes the obese phenotype is controlled by peptides that are produced in the gut. These peptides are influenced by the presence or absence of the gut microbiota
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these findings suggest that the gut microbiota modulates the biological systems that regulate the availability of nutrients, energy storage, fat mass development and inflammation in the host, which are all components of the obese phenotype
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good look of how the the gut health, or lack there of, can influence energy homeostasis and contribute to obesity. This article points to the presence of LPS playing a role in metabolic endotoxemia. It does discuss the importance of the microbiota and their possible role in the low-grade systemic inflammation condition that is obesity.
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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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Testosterone and glucose metabolism in men: current concepts and controversies - 0 views
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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
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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
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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
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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
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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
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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
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This is supported by observational studies showing that weight gain and development of diabetes accelerate the age-related decline in testosterone
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The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
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Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
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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
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This suggests that weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
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There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
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successful weight loss combined with optimisation of glycaemic control may be sufficient to normalise circulating testosterone levels in the majority of such men
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weight loss, optimisation of diabetic control and assiduous care of comorbidities should remain the first-line approach.
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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
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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).
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Effects of testosterone therapy on body composition were metabolically favourable with modest decreases in fat mass and increases in lean body mass
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This suggests that testosterone has limited effects on glucose metabolism in relatively healthy men with only mildly reduced testosterone.
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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.
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the evidence from controlled studies show that testosterone therapy consistently reduces fat mass and increases lean body mass, but inconsistently decreases insulin resistance.
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Interestingly, testosterone therapy does not consistently improve glucose metabolism despite a reduction in fat mass and an increase in lean mass
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the majority of RCTs (recently reviewed in Ng Tang Fui et al. (2013a)) showed that testosterone therapy does not reduce visceral fat
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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
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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
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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.
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data have not shown evidence that testosterone causes prostate cancer, or that it makes subclinical prostate cancer grow
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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
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shared by Nathan Goodyear on 20 Apr 16
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Metabolic characteristics of keto-adapted ultra-endurance runners - Metabolism - Clinic... - 0 views
www.metabolismjournal.com/...abstract
endurance athletes endurance sports exercise carbohydrates ketogenic diet
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shared by Nathan Goodyear on 08 Sep 17
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A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice: Cell Metabolism - 0 views
www.cell.com/...S1550-4131(17)30490-4
epigenitics diet nutrition ketogenic diet low carbohydrate diet low carb diet brain longevity
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shared by Nathan Goodyear on 16 Nov 16
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Anticonvulsant Mechanisms of the Ketogenic Diet - Bough - 2007 - Epilepsia - Wiley Onli... - 0 views
onlinelibrary.wiley.com/...full
ketogenic ketogenic diet seizures nutrition diet glucose mitochondria insulin ROS oxidative stress
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The ketogenic diet (KD) is a high-fat, low-protein, low-carbohydrate diet that has been employed as a treatment for medically refractory epilepsy for 86 years
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almost any diet that produces ketonemia and/or diminished blood glucose levels can induce an anticonvulsant effect.
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JAMA Network | JAMA: The Journal of the American Medical Association | Association of D... - 0 views
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shared by Nathan Goodyear on 13 Jun 12
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JAMA Network | JAMA: The Journal of the American Medical Association | Low-Fat Dietary ... - 0 views
jama.jamanetwork.com/article.aspx
low fat diet CVD CHD cardiovascular disease risk stroke MI heart attack health
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Decrease of serum total and free testosterone during a low-fat high-fibre diet - 0 views
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shared by Nathan Goodyear on 07 Oct 13
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Dietary Macronutrient Content Alters Cortisol Metabolism Independently of Body Weight C... - 0 views
jcem.endojournals.org/...4480.long
cortisol 11-betaHSD1 low carb diet low carb carbohydrates metabolism macronutrients
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The Effect of a Vegetarian vs Conventional Hypocaloric Diabetic Diet on Thigh Adipose T... - 0 views
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shared by Nathan Goodyear on 27 Jan 15
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International Journal of Impotence Research - Obesity, low testosterone levels and erec... - 0 views
www.nature.com/...ijir200842a.html
low T low Testosterone men male hormone hormones ED erectile dysfunction Testosterone diabetes metabolic syndrome obesity
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Studies have shown that ED may be an early biomarker of general endothelial dysfunction, atherosclerosis and CVD
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testosterone treatment of hypogonadal young and older men improves sexual function, increases lean mass and decreases fat mass
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In men with low serum testosterone (for example, <8 or 230 nmol l−1) with obesity, metabolic syndrome and diabetes mellitus, treatment with testosterone is warranted
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In obese middle-aged men, testosterone treatment reduced visceral adipocity, insulin resistance, serum cholesterol and glucose levels
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testosterone replacement has a favorable impact on body mass, insulin secretion and sensitivity, lipid profile and blood pressure in hypogonadal men with the metabolic syndrome as well as type 2 diabetes mellitus
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Testosterone significantly inhibits lipoprotein lipase activity, which reduces triglycerides uptake into adipocytes in the abdominal adipose tissue
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testosterone treatment decreased endogenous inflammatory cytokines (tumor necrosis factor-α and IL-1β) and lipids (total cholesterol) and increased IL-10 in hypogonadal men
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Testosterone treatment reduced leptin and adiponectin levels in hypogonadal type 2 diabetic men after 3 months of testosterone replacement
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Obesity adversely affects endothelial function and lowers serum testosterone levels through the development of insulin resistance and metabolic syndrome
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Metabolic disturbances as well as production of cytokines and adipokines by inflamed fat cells may be causal factors in the development of ED
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The onset of ED and the associated risk of CVD may be delayed through lifestyle modifications that affect obesity, such as diet and exercise
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Very low testosterone levels contribute to the development of ED in obesity, metabolic syndrome and type 2 diabetes mellitus
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Obesity is associated with low total testosterone levels that can be explained at least partially by lower sex hormone-binding globulin (SHBG) in obese men
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epidemiological studies have shown a negative correlation between BMI and total testosterone and to a lesser extent with free and bioavailable (biologically active) testosterone levels
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shared by Nathan Goodyear on 05 Feb 14
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Obesity-induced hypogonadism in the male: Prem... [Endocrinology. 2014] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...24424048
kisspeptin high fat diet diet fat LH FSH Testosterone Low T male hormone hormones
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