researchers showed how estrogen receptors located in the hypothalamus serve as a master switch to control food intake, energy expenditure and body fat distribution.
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Revealing Estrogen's Secret Role In Obesity - 0 views
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When estrogen levels in the VMN dipped, the animals' metabolic rate and energy levels also plummeted
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The findings suggested that the ER-alpha in this region plays an essential role in controlling energy balance, body fat distribution and normal body weight.
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α-Lipoic acid increases energy expenditure by enhancing adenosine monophospha... - 0 views
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Inborn-like errors of metabolism are determinants of breast cancer risk, clinical respo... - 0 views
www.ncbi.nlm.nih.gov/...PMC6114970
cancer metabolism breast cancer glutamine glutamate aspartate oncogenes
shared by Nathan Goodyear on 24 Sep 18
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We now recognize that human cancers evolve in an environment of metabolic stress. Rapidly proliferating tumor cells deprived of adequate oxygen, nutrients, hormones and growth factors up-regulate pathways that address these deficiencies to overcome hypoxia (HIF), vascular insufficiency (VEGF), growth factor deprivation (EGFR, HER2) and the loss of hormonal support (ER, PR, AR) all to enhance survival and proliferation
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The results suggest that breast cancer could be preceded by systemic subclinical disturbances in glucose-insulin homeostasis characterized by mild, likely asymptomatic, IEM-like biochemical changes
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The process would include variable periods of hyperinsulinemia with the consequent systemic MYC activation of glycolysis, glutaminolysis, structural lipidogenesis and further exacerbation of hypoglycemia, the result of MYC's known role as an inhibitor of liver gluconeogenesis
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The metabolic changes we describe in breast cancer arise in concert with IEM-like changes in oxidative phosphorylation as detected by increased values of the ratio lactate/pyruvate (Supplementary Table 2A, 2B) characteristic of Ox/Phos deficiency [25]. In our study, 76% (70/92) of the European breast cancer patients had lactate/pyruvate ratios values higher than the normal value of 25.8
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four-fold higher frequency of cancer (including breast) in patients with energy metabolism disorders
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growing recognition that cancer cells differ from their normal counterparts in their use of nutrients, synthesis of biomolecules and generation of energy
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glutamine concentrations in the cancer patients were reduced to nearly 1/8 of the levels observed in the normal population
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blood concentrations of aspartate (p = 1.7e-67, FDR = 8.3e-67) (Figure (Figure1E)1E) and glutamate (p = 6.4e-96, FDR = 6.2e-95) (Figure (Figure1F)1F) were nearly 10 fold higher than the normal ranges of 0–5 μM/L and 40 μM/L, respectively
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glutamine consumption associated with parallel increases in glutamate and aspartate (Figure (Figure1A1A red arrows) is considered a hallmark of MYC-driven “glutaminolysis”
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Gln/Glu ratio inversely correlates with i- late stage metabolic syndrome and with ii- increased chance of death
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changes in glutamine consumption, reflected by the Gln/Glu ratio could provide a metabolic link between breast cancer initiation and diabetes, reflective of a systemic metabolic reprogramming from glucose to glutamine as the preferred source of precursors for biosynthetic reactions and cellular energy
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the metabolic dependencies of cancer characterized by excessive glycolysis, glutaminolysis and malignant lipidogenesis, previously considered a consequence of local tumor DNA aberration [23] could, instead, represent a systemic biochemical aberration that predates and very likely promotes tumorigenesis
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accumulation of very long chain acylcarnitines such as C14:1-OH (p = 0.0, FDR = 0.0), C16 (p = 0.0, FDR = 0.0), C18 (p = 0.0, FDR = 0.0) and C18:1 (p = 1.73e-322, FDR = 1.16-321) and lipids containing VLCFA (lysoPC a C28:0) (p = 1.14-e95, FDR = 1.65e-95) in the blood of breast and colon cancer patients
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Among the most powerful metabolic equations for MYC-activation is that which links the widely used MYC-driven desaturation marker ratio of SFA/MUFA to the MYC glutaminolysis-associated ratio of (Asp/Gln)
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liver dysfunction shares many features with both IEM and cancer suggesting a role for hepatic dysfunction in carcinogenesis
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cancer “conscripts” the human genome to meet its needs under conditions of systemic metabolic stress
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ScienceDirect.com - Physiology & Behavior - The effects of a high-energy diet on hippoc... - 0 views
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Statin-Associated Myopathy with Normal Creatine Kinase Levels - 0 views
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statins statin muscle cells mitochondria CoQ10 energy myopathy necrosis
shared by Nathan Goodyear on 28 Apr 12
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Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslip... - 0 views
www.nutritionandmetabolism.com/...5
fructose metabolic syndrome metabolic syndrome insulin resistance obesity nutrition metabolism
shared by Nathan Goodyear on 16 Sep 13
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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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Electric Wheelchair For Increased Independence foot rests and four wheels large wheels at the back strengths and environment propelled by a motor comfortable and functional stretching abdominal muscle
shared by wheelchairindia9 on 14 May 15
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When it comes to wheelchairs, young children have a different set of needs than adults. Aesthetically, devices designed for kids are often sleek and colorful, and functionally, they are typically lightweight and adjustable. As any parent knows, young people don't stay the same size for long and since a wheelchair is a major purchase don't want a simple growth spurt to render it useless. That's why kids wheelchair category offers models that feature seat width and depth adjustability, elevating legrests, and other versatile features. Pediatric walkers differ from adult walkers in several ways. For one, walking aids for children are usually adjustable, taking growth patterns into account; but many models also provide gait training and postural correction. Those caring for kids in their formative years must be concerned about more than just the young person's mobility, they must also consider their development. Cerebral Palsy Wheelchair: Cerebral Palsy Wheelchair Description: The model designed for cerebral palsy child only. Ultra light weight aluminium alloy frame Seat Width 38 cms (15") Net Weight: 18.5 kgs Epoxy powder coated frame Detachable arm rest & foot rest provided Elevated and swinging foot rest Elevated foot rest provided to elevate leg angle Height adjustable and detachable head rest Hydraulic reclining high back for a comfortable posture Hydraulic adjustable seat angle Detachable back and seat pad Extra cushion upholstery provided to under arm, head & calg Foldable Lever and paddle brakes provided Safety belt provided Maintenance free rear solid wheels Cloth look like water proof upholstery Anti wheels for better safety and stability Extra cushion upholstery provided to under arm, head & leg Folding action Lever and paddle brakes provided Safety belt provided Maintenance free rear solid wheels Cerebral Palsy Wheelchair Recline system: Recline system provides kids with the most comfortable resting environme
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Branched-chain amino acids as a protein- and energy-source in liver cirrhosis. - PubMed... - 0 views
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Branched Chain Amino Acid Supplementation for Patients with Cirrhosis | Clinical Correl... - 0 views
www.clinicalcorrelations.org/?p=3544
BCCA branched chain amino acids liver cirrhosis hepatitis amino acids
shared by Nathan Goodyear on 05 Oct 15
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low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
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supplementation of BCAAs is thought to facilitate ammonia detoxification by supporting synthesis of glutamine, one of the non-branched chain amino acids, in skeletal muscle and in the brain as well as diminishing the influx of AAAs across the blood-brain barrier
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oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
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Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease
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Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
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BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization
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BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
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Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
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another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
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BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves
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A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells
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BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
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Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
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long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding
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The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation
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Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
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BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
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Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran
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Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy
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Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
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Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
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the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
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A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs
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Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
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BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver
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patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
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Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
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Neurodegenerative disorders: clues from glutamate ... [Crit Rev Neurobiol. 1996] - PubM... - 0 views
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glutamate antagonists or agents that improve energy metabolism may slow the degenerative process and offer a therapeutic approach for temporarily retarding the progression of these disabling disorders.
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A mitochondrial paradigm for degenerative diseases... [Novartis Found Symp. 2001] - Pub... - 0 views
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the decline of mitochondrial energy production resulting in increased oxidative stress and apoptosis does play a significant role in degenerative diseases and ageing.
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Leptin serves body as energy signal | Harvard Gazette - 0 views
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replacing leptin to physiologically normal levels during fasting fully restored testosterone to baseline, indicating that leptin regulates the hypothalamic-pituitary- gonadal axis that controls the release of testosterone and estrogen
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Determinants of intramyocellular triglyceride turnover: implications for insulin sensit... - 0 views
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Mitochondrial Fission Induces Glycolytic Reprogramming in Cancer-Associated Myofibrobla... - 0 views
www.ncbi.nlm.nih.gov/...PMC3478457
warburg effect Cancer cancer associated fibroblasts CAFs reverse warburg effect lactate aerobic glycolysis mitochondria oxidative stress ROS H2O2
shared by Nathan Goodyear on 11 Nov 14
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L-lactate functions as an onco-metabolite, stimulating mitochondrial biogenesis and OXPHOS in adjacent cancer cells, directly providing energy for tumor growth
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Oxidative stress in stromal fibroblasts then induces their metabolic conversion into cancer-associated fibroblasts. Such oxidative stress drives the onset of autophagy, mitophagy, and aerobic glycolysis in fibroblasts, resulting in the local production of high-energy mitochondrial fuels (such as L-lactate, ketone bodies, and glutamine). These recycled nutrients are then transferred to cancer cells, where they are efficiently burned via oxidative mitochondrial metabolism (OXPHOS)
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stromal L-lactate serves as a high-energy mitochondrial “fuel” for cancer cells. We have termed this new model of cancer metabolism “Two-Compartment Tumor Metabolism”, where two opposing metabolic compartments co-exist, side-by-side, with stromal glycolysis fueling OXPHOS in cancer cells
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Reverse Warburg Effect”, is that catabolic fibroblasts should promote tumor growth, without any increases in angiogenesis
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when cancer cells use L-lactate as a mitochondrial fuel source, this metabolic phenotype is a predictor of lethal cancer metabolism
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mitochondrial dysregulation is likely the “root cause” of several human disease(s), and especially epithelial cancers
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Both in vitro and in vivo studies have now provided convincing evidence that “activated” stromal fibroblasts, a.k.a., myofibroblasts, may play a critical role in initiating tumor recurrence, via paracrine interactions with adjacent tumor epithelial cells
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A new hypothesis is that cancer is not a cell autonomous disease, but rather a disease of the tumor microenvironment
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cancer cells behave as metabolic parasites, by inducing oxidative stress in adjacent normal fibroblasts
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recent experimental evidence indicates that cancer-associated fibroblasts have a catabolic phenotype, and undergo autophagy and mitophagy, resulting in the onset of glycolytic metabolism, driving L-lactate production, and its release into the tumor microenvironment
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oncogenic mutations in cancer cells lead to ROS production and the “secretion” of hydrogen peroxide species
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A good discussion of what is proposed the Reverse Warburg effect. A process by which the local environment dictates tumor progression. The cancer cells release ROS primarily in the form of H2O2 and this leads to Cancer Associated Fibroblasts (CAFs) in the stroma. The altered stromal environment increases ROS further and promotes ocogenic metabolites through the classic Warburg effect. This high lactate production from the CAFs then is used by the cancer cells via classic oxidative phosphorylation. Complex, beautiful and still an the understanding is a work in progress. This study/article points to the importance of oxidative stress in some cancer development through CAFs.