Weight gain has been associated with a higher gut permeability
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Chylomicron formation and glucagon-like peptide 1 receptor are involved in activation o... - 0 views
www.jnutbio.com/...abstract
chylomicron inflammation atherosclerosis CAD arteriosclerosis plaque vascular disease
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Fructose consumption: potential mechanisms for its effects t... : Current Opinion in Li... - 0 views
journals.lww.com/...tial_mechanisms_for_its.5.aspx
fructose insulin resistance lipids triglycerides fat adipose tissue adipose
shared by Nathan Goodyear on 27 Aug 14
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Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk - 0 views
jme.endocrinology-journals.org/...R51.full
metabolic endotoxemia obesity insulin resistance cardiovascular disease LPS inflammation
shared by Nathan Goodyear on 04 Aug 14
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The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal components through pattern-recognition receptors
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TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
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The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6, which are also elevated in obese and insulin-resistant patients
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Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
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LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
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In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
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In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
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the gut microbiota has been recently proposed to be an environmental factor involved in the control of body weight and energy homeostasis by modulating plasma LPS levels
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dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a bacterially related factor might be responsible for high-fat diet-induced obesity.
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This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
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n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
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it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
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this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
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these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
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This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can beneficially affect the host's weight and adiposity.
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endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
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in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
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LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
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Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
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The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
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All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
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LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
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When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed, with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions such as obesity and metabolic syndrome
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It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
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On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
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high-fat diet mice presented with ME, which positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and F4/80 (a specific marker of mature macrophages) mRNAs
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prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
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Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative stress, and macrophage infiltration markers
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This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
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high-fat feeding is associated with adipose tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
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markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
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As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.
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Curcumin inhibits hepatic protein-tyrosine phosphatase 1B and prevents hypertriglycerid... - 0 views
www.ncbi.nlm.nih.gov/...20222050
curcumin polyphenols leptin obesity leptin resistance insulin insulin resistance fructose diet
shared by Nathan Goodyear on 05 Jun 16
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Hormonal Modulation in Aging Patients with Erectile Dysfunction and Metabolic Syndrome - 0 views
www.ncbi.nlm.nih.gov/...PMC3888699
low T Testosterone hypogonadism MetS metabolic syndrome men male hormone hormones
shared by Nathan Goodyear on 05 Feb 14
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Hypogonadism and MetS are strongly associated [12, 13, 16], having even been demonstrated that with the increasing number of MetS parameters there is a proportional raise in the incidence of hypogonadism
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the presence of MetS did not prove to be a significant determinant of hypogonadism, as it did not lead to a decline in T levels, in MetS patients with already established hypogonadism, the increasing number of MetS features was associated with further decline in T
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In the setting of MetS, hypertriglyceridemia and increased WC have been reported as the most important determinants of hypogonadism
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recent literature consistently associates obesity not only with higher risk of hypogonadism [4, 6, 27] but also with lower T levels
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Visceral adiposity has been particularly related with reduction of T and SHBG levels (independent of other metabolic disorders)
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WC was one of the MetS parameters with the greatest influence in T levels decrease, presenting itself as a strong risk factor for hypogonadism development
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MetS-related T decline was not accompanied by an increase in pituitary LH levels, suggesting impairment in gonadotropin secretion
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The molecules behind this smoothing compensatory effect of GnRH/LH are still unknown, but estrogens and insulin, as well as leptin, TNF-α, and other adipokines, were proposed candidates
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fat stores undertake an increase aromatization of androgens, therefore raising estrogen levels [9, 15], which in turn decrease LH secretion
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our data contradicts the concept that estradiol exerts a negative feedback on hypothalamic GnRH secretion
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taking into account that high estradiol levels have already been described as the only abnormality in a subset of patients with ED, the hypothesis that the later might not only be caused by androgen deficiency is becoming increasingly evident
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it has been reported that the chronic exposure to phosphodiesterase type 5 inhibitors (PDE5i), widely used for the treatment of ED, may influence serum estradiol levels
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thyroid disorders (specially hyperthyroidism) have been related to ED and hypogonadism, and so must be considered in a sexual-dysfunction setting
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It is clear from the current literature that collecting a more thorough hormonal panel might be a wise approach to further uncover hormonal relations
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We concluded that in ED patients with hypogonadism and MetS, the attenuated response of HPG axis (normal or low LH levels) might not always be due to an underlying adiposity-dependent estrogen-raising effect.
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our findings indicate that ED, aging, and estradiol might have a stronger connection than what is currently described in the literature.
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Secondary causes of hyperlipidemia. [Med Clin North Am. 1994] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...8283927
triglycerides hypertriglyceridemia aromatase activity estrogen glucocorticoids
shared by Nathan Goodyear on 23 Sep 13
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Fructose decreases physical activity and increases body fat without affecting hippocamp... - 0 views
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The average liver mass of mice in the fructose treatment group was 20% heavier than for mice in the glucose group
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The fat pads of mice consuming the fructose diet were 69% heavier than the fat pads of animals consuming the glucose diet
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there are many studies showing that consumption of fructose in comparison to other monosaccharides results in increased de novo lipogenesis, dyslipidemia, insulin resistance, BW6, 7 and, most recently, impaired cognitive function
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in the present study, the intake of fructose by mice was more similar to that of typical human consumption in comparison to previous studies
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studies in humans confirm that fructose, but not glucose (when provided as 25% of energy requirements), in the context of an energy-balanced diet increases de novo lipogenesis and visceral adiposity along with dyslipidemia, decreases insulin sensitivity10, 12 and decreases in fat oxidation
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significant reduction (~20%) in physical activity in the fructose-fed animals in comparison to glucose
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a recent study reported that ingestion of fructose (25% energy intake, 10 weeks) in human volunteers also resulted in reduced energy expenditure in relation to a diet with the same glucose dose
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There is certainly evidence to suggest that, for example, exercise is able to prevent dyslipidemia in healthy subjects fed a weight-maintenance high-fructose diet (30%)54, which strongly suggests a protective role of physical activity in metabolic regulation.
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the potential negative effects of fructose in brain and cognitive function have been investigated, with a series of studies showing cognitive deficits in spatial memory and learning in adolescent and adult animals following access to a high fructose diet
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access to both fructose and sucrose, but not glucose, results in a 40% reduction in hippocampal neurogenesis
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Collectively these studies seem to suggest that fructose consumption can have a considerable impact on hippocampal function and learning, which is in direct contrast with what we observed.
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the impact of fructose is apparent only in BW, liver mass and body fat, but not in cognitive measures or rates of neurogenesis
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Effects of d-chiro-inositol in lean women with the... [Endocr Pract. 2002 Nov-Dec] - Pu... - 0 views
www.ncbi.nlm.nih.gov/...15251831
D-chiro-inositol insulin resistance PCOS hyperandrogenism metabolic syndrome
shared by Nathan Goodyear on 11 May 11
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women with the polycystic ovary syndrome, D-chiro-inositol reduces circulating insulin, decreases serum androgens, and ameliorates some of the metabolic abnormalities (increased blood pressure and hypertriglyceridemia) of syndrome X.
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Triglycerides Induce Leptin Resistance at the Blood-Brain Barrier - 0 views
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Decreasing triglycerides may potentiate the anorectic effect of leptin by enhancing leptin transport across the BBB.
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hypertriglyceridemia could explain impaired transport of leptin across the BBB in both starvation and obesity
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(n-3) Fatty Acids: Clinical Trials in People with Type 2 Diabetes - 0 views
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Fructose: A Key Factor in the Development of Metabolic Syndrome and Hypertension - 0 views
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HFCS consists of fructose and glucose mixed in a variety of concentrations, but most commonly as 55% fructose and 45% glucose
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In the United States, HFCS and sucrose are the major sources of fructose in the diet, and HFCS is a major ingredient in soft drinks, pastries, desserts, and various processed foods
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fructose and glucose are metabolized in completely different ways and utilize different GLUT transporters
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In the liver, fructose bypasses the two highly regulated steps of glycolysis, catalyzed by glucokinase/hexokinase and phosphofructokinase both of which are inhibited by increasing concentrations of their byproducts. Instead, fructose enters the pathway at a level that is not regulated and is metabolized to fructose-1-phosphate primarily by fructokinase or ketohexokinase
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Fructokinase has no negative feedback system, and ATP is used for the phosphorylation process. As a result, continued fructose metabolism results in intracellular phosphate depletion, activation of AMP deaminase, and uric acid generation which is harmful at the cellular level
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Uric acid inhibits endothelial NO both in vivo and in vitro, [15] and directly induces adipocyte dysfunction
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Serum uric acid increases rapidly after ingestion of fructose, resulting in increases as high as 2 mg/dL within 1 hour
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Uncontrolled fructose metabolism leads to postprandial hypertriglyceridemia, which increases visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver
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Several reviews have concluded that intake of both fructose and HFCS by children and adults was associated with an increased risk of obesity and metabolic syndrome