In early PET literature focusing on analysis of solitary pulmonary nodules, some researchers defined malignancy based on a SUVmax threshold of greater than 2.5
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Endogenous fructose production and metabolism in the liver contributes to the developme... - 0 views
www.nature.com/...ncomms3434.html
metabolic syndrome MetS metabolism fructose glucose liver fatty polyol pathway
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Influence of alpha-lipoic acid on lipid ... [Diabetes Obes Metab. 2004] - PubMed - NCBI - 0 views
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Numerous deletorious effects are seen in high fructose diets: elevated Triglyceride production, fatty liver, insulin resistance, increased VLDL production and secretion, increased deposit of TG in muscle and increased muscle insulin resistance. Alpha lipoic Acid is shown to counter these effects in rat model.
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Gut microbiota and non-alcoholic fatty liver disease: new insights - Aron-Wisnewsky - 2... - 0 views
onlinelibrary.wiley.com/...full
NAFLD gut gut flora gut microbiome gut microbiota metabolism non-alcoholic fatty liver LPS
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Non-Alcoholic Fatty Liver Disease and Fructose: Bad for Us, Better for Mice - 0 views
www.ncbi.nlm.nih.gov/...PMC3117982
HCFS NAFLD high fructose corn syrup non-alcoholic fatty liver disease obesity overweight epidemic
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How We Read Oncologic FDG PET/CT | Cancer Imaging | Full Text - 0 views
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Far more important than the SUVmax is the pattern rather than intensity of metabolic abnormality and the correlative CT findings
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Descriptively, we define SUV < 5 as “low intensity”, 5–10 as “moderate”, 10–15 as “intense” and >15 as “very intense”
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Evolving literature suggests that intensity of uptake is an independent prognostic factor and in some tumour subtypes superior to histopathologic characterisation.
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Our practice of thresholding the grey and colour scale to liver as detailed above results in similar image intensity to a fixed upper SUV threshold of 8 to 10
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The advantage of using the liver as a reference tissue is also aided by this organ having rather low variability in metabolic activity
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When the liver is abnormal and cannot be used as a reference organ, we use the default SUV setting of an upper SUV threshold of 8
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One of the most challenging aspects of oncologic FDG PET/CT review, however, is to recognise all the patterns of metabolic activity that are not malignant and which consequently confound interpretation
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Future articles in the “How I Read” series will address the specific details of reading PET/CT in various cancers
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For example, discordant low-grade activity in an enlarged lymph node in the setting of intense uptake in the primary tumour suggests it is unlikely malignant and more likely inflammatory or reactive
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By CT criteria the enlarged node is ‘pathologic’ but the discordantly low metabolic signature further characterises this is as non-malignant since such a node is not subject to partial volume effects and therefore the intensity of uptake should be similar to the primary site
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The exception is when the lymph node is centrally necrotic as a small rim of viable tumour is subject to partial volume effects with expectant lower intensity of uptake; integrating the CT morphology is therefore critical to reaching an accurate interpretation
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Small nodes that are visualised on PET are conversely much more likely to be metastatic as such nodes are subject to partial volume effects.
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The combination of FDG and a more specific tracer, which visualises the well-differentiated disease can be very useful to characterise this phenomenon
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For the majority of malignant processes, the intensity of metabolic abnormality correlates with degree of aggressiveness or proliferative rate.
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a negative PET/CT study in a patient with biopsy proven malignancy would be considered false-negative
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There, however, are a significant minority of tumours that utilise substrates other glucose such as glutamine or fatty acids as a source of the carbon atoms required for growth and proliferation
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This includes a subset of diffuse gastric adenocarcinomas, signet cell colonic adenocarcinomas and some sarcomas, particularly liposarcoma
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There may be a role for other radiotracers such as fluorothymidine (FLT) or amino acid substrates in this setting.
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Some tumours harbour mutations that result in defective aerobic mitochondrial energy metabolism, effectively simulating the Warburg effect
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Uterine fibroids, hepatic adenomas, fibroadenomas of the breast and desmoid tumours are benign or relatively benign lesions that can have quite high FDG-avidity.
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Common examples where patients have commenced active therapy but the referrer is requesting “staging” includes hormonal therapy (eg. tamoxifen) in breast cancer, oral capecitabine in colorectal cancer or high dose steroids in Hodgkin’s lymphoma
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Without intravenous contrast, additional identification of typical oncologic complications such as pulmonary embolism or venous thrombosis cannot be identified
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If the study is performed as an “interim” restaging study after commencement of therapy but before completion, in order to reach a valid or clinically useful conclusion findings must be interpreted in the context of known changes that occur at a specific timing and type of therapy
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The most well studied use of interim PET is in Hodgkin’s lymphoma where repeat PET after two cycles of ABVD-chemotherapy provides powerful prognostic information and may improve outcomes by enabling early change of management
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Adipose Tissue Inflammation in Obesity and Metabolic Syndrome - - Satoshi Nishimura - D... - 0 views
www.discoverymedicine.com/...obesity-and-metabolic-syndrome
inflammation obesity metabolic syndrome fat adipose tissue innate immune system humoral
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Activation of inflammatory pathways in adipocytes impairs triglyceride storage and increases release of free fatty acids, an excess of which is known to induce insulin resistance in muscle and liver
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It has been postulated that a paracrine loop involving free fatty acids and inflammatory cytokines establishes a vicious cycle between adipocytes and macrophages that propagates the inflammation
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not only does interrupting the accumulation of macrophages within obese adipose tissue suppresses adipose inflammation in various animal models, it also ameliorates systemic insulin resistance and metabolic abnormalities, suggesting macrophages are key effector cells involved in adipose inflammation
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CD8+ T cells within obese adipose tissue induce activation and migration of monocytes/macrophages, and in cooperation with the adipose tissue, they also induce macrophage differentiation. At the same time, obese adipose tissue activates CD8+ T cells, creating a vicious cycle involving CD8+ T cells, macrophages, and obese adipose tissue that propagates local inflammation
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In obese adipose tissue there is a shift to dominance of CD8+ and TH1 T cells, which appears to propagate inflammation
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Plasma lipoproteins: composition, structure and biochemistry - 0 views
lipidlibrary.aocs.org/...index.htm
apolipoproteins cholesterol VLDL chylomicrons LDL HDL lipoproteins biochemistry
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The most abundant lipid constituents are triacylglycerols, free cholesterol, cholesterol esters and phospholipids (phosphatidylcholine and sphingomyelin especially ), though fat-soluble vitamins and anti-oxidants are also transported in this way
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the lipoprotein aggregates should be described in terms of the different protein components or apoproteins (or 'apolipoproteins'
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these classes can be further refined by improved separation procedures, and intermediate-density lipoproteins (IDL) and subdivisions of the HDL (e.g. HDL1, HDL2, HDL3 and so forth
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Density is determined largely by the relative concentrations of triacylglycerols and proteins and by the diameters of the broadly spherical particles
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Lipoproteins are spherical (VLDL, LDL, HDL) to discoidal (nascent HDL) in shape with a core of non-polar lipids, triacylglycerols and cholesterol esters, and a surface monolayer, ~20Å thick, consisting of apoproteins, phospholipids and non-esterified cholesterol, which serves to present a hydrophobic face to the aqueous phase
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the various lipid components should not be considered as absolute, as they are in a state of constant flux
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the main groups are classified as chylomicrons (CM), very-low-density lipoproteins (VLDL), low-density lipoproteins (LDL) and high-density lipoproteins (HDL), based on the relative densities of the aggregates on ultracentrifugation
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The lipoproteins can be categorised simplistically according to their two main metabolic functions. The principal role of the chylomicrons and VLDL is to transport triacylglycerols ‘forward’ as a source of fatty acids from the intestines or liver to the peripheral tissues. In contrast, the HDL remove excess cholesterol from peripheral tissues and deliver it to the liver for excretion in bile in the form of bile acids (‘reverse cholesterol transport’). While these functions are considered separately here for convenience, it should be recognised that the processes are highly complex and inter-related, and they involve transfer of apoproteins, enzymes and lipid constituents among the heterogeneous mix of all the lipoprotein fractions.
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Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity - 0 views
ajpendo.physiology.org/...E1465.long
cortisol insulin resistance metabolic syndrome obesity overweight
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acute GC secretion during stress mobilizes peripheral amino acids from muscle as well as fatty acids and glycerol from peripheral fat stores to provide substrates for glucose synthesis by the liver
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chronically elevated GC levels alter body fat distribution and increase visceral adiposity as well as metabolic abnormalities in a fashion reminiscent of metabolic syndrome
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In adipocytes, cortisol inhibits lipid mobilization in the presence of insulin, thus leading to triglyceride accumulation and retention.
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Since the density of GC receptors is higher in intra-abdominal (visceral) fat than in other fat depots, the activity of cortisol leading to accumulation of fat is accentuated in visceral adipose tissue (24, 158), providing a mechanism by which excessive endogenous or exogenous GC lead to abdominal obesity and IR
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This may be explained by an increased intratissular/cellular concentration of cortisol in adipose tissues
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Intracellular GC may be produced from recycling of GC metabolites such as cortisone in adipose tissues
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Local GC recycling metabolism is mediated by 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD1 and 11β-HSD2
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even if obese patients generally have normal or subnormal plasma cortisol concentrations (131, 158), triglyceride accumulation in visceral adipose tissue may be due, at least in part, to the local production of GC in insulin- and GC-responsive organs such as adipose tissue, liver, and skeletal muscle
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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
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Levels of serum testosterone predict prevalent but not incident non... - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...25708291
Testosterone NAFLD non-alcoholic fatty liver liver disease men male hormone hormones
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A vicious circle between insulin resistance and inflammation in nonalcoholic fatty live... - 0 views
link.springer.com/...s12944-017-0572-9
liver inflammation IL-6 TNF-alpha insulin resistance insulin NF-KappaB NAFLD
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Body Fat Distribution and Cortisol Metabolism in Healthy Men: Enhanced 5β-Red... - 0 views
jcem.endojournals.org/...4924.long
cortisone cortisol obesity overweight men 11-betaHSD type 1 5-alpha reductase metabolism
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Specific Contribution of Methionine and Choline in Nutritional Nonalcoholic Steatohepat... - 0 views
www.ncbi.nlm.nih.gov/...PMC2881778
SAMe methylation GSH glutathione NASH nonalcoholic steatohepatitis NAFLD non-alcoholic fatty liver
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Polycystic Ovary Syndrome with Hyperandrogenism Is Characterized by an Increased Risk o... - 0 views
jcem.endojournals.org/...jc.2012-1382.abstract
PCOS NAFLD obesity insulin resistance polycystic ovarian syndrome ovary syndrome non-alcoholic fatty liver
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Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views
www.ncbi.nlm.nih.gov/...PMC3314172
metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation
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Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
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intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
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the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
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Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
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a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
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Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
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there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
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To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
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intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
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intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
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mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
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Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
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ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
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under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
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intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
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prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
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TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
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overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
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Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
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hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
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overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
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these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
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circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
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significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
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entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
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Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
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both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
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In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
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IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
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Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
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it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
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this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
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evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
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In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
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intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
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overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
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excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
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oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
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central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
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overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
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chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
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recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
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when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
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autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
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The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
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Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
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Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
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TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
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these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
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TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
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central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
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cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
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central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
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the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
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Resveratrol up-regulates hepatic uncoupling protein... [Nutr Res. 2012] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...23084643
resveratrol inflammation NAFLD non-alcoholic fatty liver high fat diet fat diet
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Obstructive Sleep Apnea Predisposes to Nonalcoh... [Endocr Pract. 2013] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...24246334
sleep apnea NAFLD Testosterone women non-alcoholic fatty liver PCOS polycystic ovarian syndrome
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The clinical efficacy of the adipocyte-derived hor... [Arch Physiol Biochem. 2006] - Pu... - 0 views
www.ncbi.nlm.nih.gov/...16931453
leptin glucose metabolism dyslipidemia fatty liver elevated cholesterol
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In hypoleptinemic patients with lipodystrophy, there is a dramatic improvement in glucose metabolism, dyslipidemia and hepatic steatosis
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The major green tea polyphenol, (-)-epigallocatech... [J Nutr. 2008] - PubMed result - 0 views
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Our results indicate that long-term EGCG treatment attenuated the development of obesity, symptoms associated with the metabolic syndrome, and fatty liver. Short-term EGCG treatment appeared to reverse preexisting high-fat-induced metabolic pathologies in obese mice. These effects may be mediated by decreased lipid absorption, decreased inflammation, and other mechanisms.