Five branched chain and aromatic amino acids (isoleucine, leucine, valine, tyrosine, and phenylalanine) showed significant associations with future diabetes
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Nutritional Modulation of Insulin Resistance - 0 views
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macronutrient macronutrients nutrition insulin resistance glucose protein carbohydrates metabolism fats
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there is increasing evidence that longer term high-protein intake may have detrimental effects on insulin resistance [68, 117–123], diabetes risk [69], and the risk of developing cardiovascular disease
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significant and clinically relevant worsening of insulin sensitivity with an isoenergetic plant-based high-protein diet
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longer term high-protein intake has been shown to result in whole-body insulin resistance [68, 118], associated with upregulation of factors involved in the mammalian target of rapamycin (mTOR)/S6K1 signalling pathway [68], increased stimulation of glucagon and insulin within the endocrine pancreas, high glycogen turnover [118] and stimulation of gluconeogenesis [68, 118].
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it was recently shown in a large prospective cohort with 10 years followup that consuming 5% of energy from both animal and total protein at the expense of carbohydrates or fat increases diabetes risk by as much as 30% [69]. This reinforces the theory that high-protein diets can have adverse effects on glucose metabolism.
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Another recent study showed that low-carbohydrate high-protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are also associated with increased risk of cardiovascular disease [70], thereby indicating a potential link between high-protein Western diets, T2DM, and cardiovascular risk.
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Low-Fat High-Fiber Diet Decreased Serum and Urine Androgens in Men: The Journal of Clin... - 0 views
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diet nutrition Testosterone androgens men hormones male hormones
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The Ketogenic Diet and Sport: A Possible Marriage? : Exercise and Sport Sciences Reviews - 0 views
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nutrition diet ketogenic ketogenic diet sports athletes exercise sports medicine
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It is important to note that, although the blood level of glucose drops, it still remains at a physiological level (23), which is maintained through gluconeogenesis involving glucogenic amino acids and also glycerol released from triglycerides
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“physiological ketosis” where KB levels may rise to 7 to 8 mmol L-1 (but without any pH change). In “pathological diabetic ketoacidosis,” on the other hand, ketonemia can exceed 20 mmol L-1 and also cause lowering of blood pH
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in the initial phase of KD, about 16% of glucose comes from glycerol (released from triglyceride hydrolysis) and the bulk (60–65 g) from proteins via gluconeogenesis (proteins may be of either dietary or endogenous origin
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The importance of glycerol as a glucose source increases progressively during ketosis; in fact, glycerol passes from supplying 16% of total glucose to an average of 60% after many days (>7 d) of complete fasting (from 38% in lean individual to 79% in the obese).
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The possible reasons for the effectiveness of KD for weight loss may be listed as follows, in order of evidence, strongest first: Figure 3Image Tools 1. Appetite reduction: protein satiety, effects on appetite-related hormones such as ghrelin, and possibly a sort of direct appetite-blocking effect of KB 2. Reduced lipogenesis and increased fat oxidation 3. A reduction in respiratory quotient may indicate a greater metabolic efficiency in fat oxidation 4. A thermic effect of proteins and increased energy usage by gluconeogenesis
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all data regarding biochemical and molecular mechanisms suggest that it is very difficult to increase muscle mass during a KD; use of which really should be limited to the few days immediately before competition in bodybuilding.
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a long-term KD can interfere with some muscle hypertrophy mechanisms and this could be counterproductive if the aim of the athlete is to gain muscle mass
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Estrogen Mediates Metabolic Syndrome-Induced Erect... [J Sex Med. 2014] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...25243860
ED erectile dysfunction metabolic syndrome Estradiol E2 Testosterone male men hormones HFD high fat diet indued obesity
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animal model finds that high fat diet induces ED more through increased Estradiol production than low Testosterone. Of course the authors focused on the drugs to block E2 once produced, rather then reducing the T to E2 aromatase activity. This metabolic syndrome model implies that increased aromatase activity will be present.
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A plant-based diet for type 2 diabetes... [Diabetes Educ. 2010 Jan-Feb] - PubMed - NCBI - 0 views
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Ketogenic diets slow melanoma growth in vivo regardless of tumor genetics and metabolic... - 0 views
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melanoma malignant melanoma NRAS BRAF ketogenic diet
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Dietary composition in the treatment of polycystic ovary syndrome: a systematic review ... - 0 views
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Influence of high-carbohydrate mixed meals with different glycemic indexes on substrate... - 0 views
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Serum sex steroids and steroidogenesis-relate... [Diabetes Metab. 2014] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...24792219
androgens Testosterone DHT DihydroTestosterone weight fat insulin SHBG diabetes men male hormone hormones low T
shared by Nathan Goodyear on 07 May 14
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Overeating, which is a classical American diet, was found to increase weight, fat mass and fasting insulin. In contrast, SHBG, Testosterone and DHT were decreased. Enzymes responsible for androgen production i.e.3-beta-hydroxysteroid dehydrogenase and 17-beta-hydroxysteroiddehydrogenase, were decreased in muscles of those in this study. These changes were more pronounced in those with a family h/o of diabetes.
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Ketone bodies as a therapeutic for Alzheim... [Neurotherapeutics. 2008] - PubMed - NCBI - 0 views
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ketone bodies ketosis Alzheimer's disease Alzheimer's neurodegenerative disease
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Low Cost Liposuction in Dubai astutely escalating | Dubai Cosmetic Surgery - 0 views
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Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslip... - 0 views
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fructose metabolic syndrome metabolic syndrome insulin resistance obesity nutrition metabolism
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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
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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]).
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Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
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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.
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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
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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
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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
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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
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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
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Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
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fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
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Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
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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
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Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
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Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
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LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
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PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
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fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
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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
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High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
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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
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Cellular and Molecular Basis of Deiodinase-Regulated Thyroid Hormone Signaling - 0 views
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Anything and everything one would want to know regarding thyroid hormone signaling. Doctors, especially endocrinologists, need to read this. T4 is not or is ever inside target cells. The enzymes, deiodinase types 1, 2, and 3, are what control the thyroid hormone at the cellular levels. Deiodinase-2 is what generates T3 in the cytosol of the cell. In contrast, deiodinase-3 is what generates rT3 which is inactive. High Fat diet increases deiodinase-3.
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Gut Endotoxin Leading to a Decline IN Gonadal function (GELDING) - a novel theory for t... - 0 views
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GELDING theory GELDING LPS gut gut health inflammation low T low Testosterone Testosterone hypogonadism obesity
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trans-mucosal passage of bacterial lipopolysaccharide (LPS) from the gut lumen into the circulation is a key inflammatory trigger underlying male hypogonadism
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Obesity and a high fat/high calorie diet are both reported to result in changes to gut bacteria and intestinal wall permeability, leading to the passage of bacterial endotoxin (lipopolysaccharide- LPS) from within the gut lumen into the circulation (metabolic endotoxaemia), where it initiates systemic inflammation.
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Endotoxin is known to reduce testosterone production by the testis, both by direct inhibition of Leydig cell steroidogenic pathways and indirectly by reducing pituitary LH drive, thereby also leading to a decline in sperm production.
Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fa... - 0 views
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diet dysbiosis low T diabetes hypogonadism gut bacteria metabolic endotoxemia obesity low testosterone gut microbiota gut flora gut microbiome
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PPARs, Obesity, and Inflammation - 0 views
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obesity inflammation PPARs perioxisome proliferator-activated receptor
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Many of the inflammatory markers found in plasma of obese individuals appear to originate from adipose tissue
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obesity is a state of chronic low-grade inflammation that is initiated by morphological changes in the adipose tissue.
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secretion of MCP-1, resistin, and other proinflammatory cytokines is increased by obesity, the adipose secretion of the anti-inflammatory protein adiponectin is decreased
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the peroxisome proliferators- activated receptor (PPAR) family are involved in the regulation of inflammation and energy homestasis
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upregulation of COX-2 is seen in alcoholic steatohepatitis and nonalcoholic steatohepatitis and has been directly linked to the progression of steatosis to steatohepatitis, the inhibitory effect of PPARα on COX-2 may reduce steatohepatitis
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PPARα agonists have a clear anorexic effect resulting in decreased food intake, evidence is accumulating that PPARα may also directly influence adipose tissue function, including its inflammatory status.
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PPARα may govern adipose tissue inflammation in three different ways: (1) by decreasing adipocyte hypertrophy, which is known to be connected with a higher inflammatory status of the tissue [3, 11, 59], (2) by direct regulation of inflammatory gene expression via locally expressed PPARα, or (3) by systemic events likely originating from liver
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two different molecular mechanisms have been proposed by which anti-inflammatory actions of PPARγ are effectuated: (1) via interference with proinflammatory transcription factors including STAT, NF-κB, and AP-1
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and (2) by preventing removal of corepressor complexes from gene promoter regions resulting in suppression of inflammatory gene transcription
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diet-induced obesity is associated with increased inflammatory gene expression in adipose tissue via adipocyte hypertrophy and macrophage infiltration
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PPARγ is able to reverse macrophage infiltration, and subsequently reduces inflammatory gene expression
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Inflammatory adipokines mainly originate from macrophages which are part of the stromal vascular fraction of adipose tissue [18, 19], and accordingly, the downregulation of inflammatory adipokines in WAT by PPARγ probably occurs via effects on macrophages
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By interfering with NF-κB signaling pathways, PPARγ is known to decrease inflammation in activated macrophages
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PPARs may influence the inflammatory response either by direct transcriptional downregulation of proinflammatory genes
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JCI - Inflammatory links between obesity and metabolic disease - 0 views
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The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time
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Multiple inflammatory inputs contribute to metabolic dysfunction, including increases in circulating cytokines (10), decreases in protective factors (e.g., adiponectin; ref. 11), and communication between inflammatory and metabolic cells
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Physiologic enhancement of the M2 pathways (e.g., eosinophil recruitment in parasitic infection) also appears to be capable of reducing metainflammation and improving insulin sensitivity (27).
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increasing adiposity results in a shift in the inflammatory profile of ATMs as a whole from an M2 state to one in which classical M1 proinflammatory signals predominate (21–23).
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Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63–65).
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inflammation in pancreatic islets can reduce insulin secretion and trigger β cell apoptosis leading to decreased islet mass, critical events in the progression to diabetes (33, 34)
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Since an estimated excess of 20–30 million macrophages accumulate with each kilogram of excess fat in humans, one could argue that increased adipose tissue mass is de facto a state of increased inflammatory mass
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Upon stimulation by LPS and IFN-γ, macrophages assume a classical proinflammatory activation state (M1) that generates bactericidal or Th1 responses typically associated with obesity
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DIO, metabolites such as diacylglycerols and ceramides accumulate in the hypothalamus and induce leptin and insulin resistance in the CNS (58, 59)
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saturated FAs, which activate neuronal JNK and NF-κB signaling pathways with direct effects on leptin and insulin signaling (60)
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Lipid infusion and a high-fat diet (HFD) activate hypothalamic inflammatory signaling pathways, resulting in increased food intake and nutrient storage (57)
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Maternal obesity is associated with endotoxemia and ATM accumulation that may affect the developing fetus (73)
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a risk factor for obesity in offspring, and involves inflammatory macrophage infiltration that can alter the maternal-fetal circulation (74
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Of these PRRs, TLR4 has received the most attention, as this receptor can be activated by free FAs to generate proinflammatory signals and activate NF-κB
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The adipokine adiponectin has long been recognized to have positive benefits on multiple cell types to promote insulin sensitivity and deactivate proinflammatory pathways.
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adiponectin stimulates ceramidase activity and modulates the balance between ceramides and sphingosine-1-phosphate
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Inhibition of ceramide production blocks the ability of saturated FAs to induce insulin resistance (101)