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BMC Cancer | Full text | A lactate shuttle system between tumour and stromal cells is a... - 0 views

shared by Nathan Goodyear on 12 Nov 14 - No Cached

Under hypoxic conditions, tumour cells primarily use glycolysis for energy, producing lactate, which is expelled to the tumour microenvironment, allowing tumours to continue their glycolytic activity
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Sonveaux et al. showed that lactate, which is generally considered a waste product, is preferred over glucose by oxidative tumour cells as their primary energy source
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MCT4 is a low-affinity transporter, which is abundant in highly glycolytic muscle cells and is one of the many target genes of hypoxia-inducible factor 1 alpha (HIF-1α)
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Other targets of HIF-1α include glucose transporter-1 (GLUT-1), the main transporter involved in glucose uptake [9,10]; lactate dehydrogenase V (LDHV), which is responsible for the conversion of pyruvate into lactate; pyruvate dehydrogenase kinase isozyme 1 (PDK1), which is responsible for the phosphorylation and consequent inactivation of pyruvate dehydrogenase (PDH); and carbonic anhydrase IX (CAIX), a hypoxia-related protein involved in pH regulation [11]. Alpha-methylacyl-CoA racemase (AMACR), pristanoyl-CoA oxidase (ACOX-3) and D-bifunctional protein (DBP), are also important fatty acid oxidation-related proteins in prostate cancer
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the essential role played by the cross-talk between stroma and epithelium in carcinogenesis and prostate cancer progression has been increasingly recognised
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strong membranous expression of MCT1 was consistently observed in cancer cells, suggesting a role for MCT1 in the transport of lactate into tumour cells from the acidic extracellular matrix, suggesting that lactate might be used as a fuel by oxidative cancer cells.
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Our hypothesis is in agreement with those of Fiaschi et al.[17], who describe the metabolic reprogramming of CAFs towards the Warburg phenotype as a result of contact with prostate cancer cells
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Using in vitro studies, they showed lactate production and efflux by de novo expressed MCT4 in CAFs and also demonstrated that, upon contact with CAFs, prostate cancer cells were reprogrammed towards aerobic metabolism, with an increase in lactate uptake via the lactate transporter MCT1.
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pharmacological inhibition of MCT1-mediated lactate uptake dramatically affected PCa cell survival and tumour outgrowth
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In this model, “energy transfer” or “metabolic coupling” between the tumour stroma and epithelial cancer cells fuels tumour growth and metastasis via oxidative mitochondrial metabolism in anabolic cancer cells
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the concomitant expression of MCT1 in tumour cells and MCT4 in fibroblasts in the same tissue is clinically significant, and associated with poor prognosis.
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Nathan Goodyear on 12 Nov 14

Study confirms the importance of the crosstalk between cancer cells and CAFs via MCTs in prostate cancer.

<div class="cArrow"> </div><div class="cContentInner">Study confirms the importance of the crosstalk between cancer cells and CAFs via MCTs in prostate cancer.</div>

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Mild Dehydration Affects Mood in Healthy Young Women - 0 views

jn.nutrition.org/...jn.111.142000.abstract dehydration water headaches mood energy

shared by Nathan Goodyear on 05 Jan 16 - No Cached

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High-Dose Vitamin C for Cancer Therapy - PMC - 0 views

www.ncbi.nlm.nih.gov/...PMC9231292 vitamin C cancer

shared by Nathan Goodyear on 27 Jul 22 - No Cached

diabetes [8], atherosclerosis [9], the common cold [10], cataracts [11], glaucoma [12], macular degeneration [13], stroke [14], heart disease [15], COVID-19 [16], and cancer.
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1–5% of the Vit-C inside the human cells
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interaction between Fe(II) and H2O2 produces OH− through the Fenton reaction
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metabolic activity, oxygen transport, and DNA synthesis
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Iron is found in the human body in the form of haemoglobin in red blood cells and growing erythroid cells.
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macrophages contain considerable quantities of iron
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iron is taken up by the majority of cells in the form of a transferrin (Tf)-Fe(III) complex that binds to the cell surface receptor transferrin receptor 1 (TfR1)
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excess iron is retained in the liver cells
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the endosomal six transmembrane epithelial antigen of the prostate 3 (STEAP3) reduces Fe(III) (ferric ion) to Fe(II) (ferrous ion), which is subsequently transferred across the endosomal membrane by divalent metal transporter 1 (DMT1)
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labile iron pool (LIP)
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LIP is toxic to the cells owing to the production of massive amounts of ROS.
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DHA is quickly converted to Vit-C within the cell, by interacting with reduced glutathione (GSH) [45,46,47]. NADPH then recycles the oxidized glutathione (glutathione disulfide (GSSG)) and converts it back into GSH
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Fe(II) catalyzes the formation of OH• and OH− during the interaction between H2O2 and O2•− (Haber–Weiss reaction)
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Ascorbate can efficiently reduce free iron, thus recycling the cellular Fe(II)/Fe(III) to produce more OH• from H2O2 than can be generated during the Fenton reaction, which ultimately leads to lipid, protein, and DNA oxidation
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Vit-C-stimulated iron absorption
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reduce cellular iron efflux
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high-dose Vit-C may elevate cellular LIP concentrations
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ascorbate enhanced cancer cell LIP specifically by generating H2O2
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Vit-C produces H2O2 extracellularly, which in turn inhibits tumor cells immediately
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tumor cells have a need for readily available Fe(II) to survive and proliferate.
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Tf has been recognized to sequester most labile Fe(II) in vivo
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Asc•− and H2O2 were generated in vivo upon i.v Vit-C administration of around 0.5 g/kg of body weight and that the generation was Vit-C-dose reliant
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free irons, especially Fe(II), increase Vit-C autoxidation, leading to H2O2 production
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iron metabolism is altered in malignancies
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increase in the expression of various iron-intake pathways or the downregulation of iron exporter proteins and storage pathways
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Fe(II) ion in breast cancer cells is almost double that in normal breast tissues
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macrophages in the cancer microenvironment have been revealed to increase iron shedding
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Advanced breast tumor patients had substantially greater Fe(II) levels in their blood than the control groups without the disease
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increased the amount of LIP inside the cells through transferrin receptor (TfR)
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Warburg effect, or metabolic reprogramming,
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Warburg effect is aided by KRAS or BRAF mutations
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Vit-C is supplied, it oxidizes to DHA, and then is readily transported by GLUT-1 in mutant cells of KRAS or BRAF competing with glucose [46]. DHA is quickly converted into ascorbate inside the cell by NADPH and GSH [46,107]. This decrease reduces the concentration of cytosolic antioxidants and raises the intracellular ROS amounts
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increased ROS inactivates glyceraldehyde 3-phosphate dehydrogenase (GAPDH)
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ROS activates poly (ADP-ribose) polymerase (PARP), which depletes NAD+ (a critical co-factor of GAPDH); thus, further reducing the GAPDH associated with a multifaceted metabolic rewiring
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Hindering GAPDH can result in an “energy crisis”, due to the decrease in ATP production
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high-dose Vit-C recruited metabolites and increased the enzymatic activity in the pentose phosphate pathway (PPP), blocked the tri-carboxylic acid (TCA) cycle, and increased oxygen uptake, disrupting the intracellular metabolic balance and resulting in irreversible cell death, due to an energy crisis
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mega-dose Vit-C influences energy metabolism by producing tremendous amounts of H2O2
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Due to its great volatility at neutral pH [76], bolus therapy with mega-dose DHA has only transitory effects on tumor cells, both in vitro and in vivo.
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Testosterone, the male hormone connection: treating diabetes and heart disease. - 0 views

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Diabetes - 0 views

sehatobat.blogspot.com/...es-alami-solusi-mengatasi.html obesity hormones disease

shared by obat sehat on 04 Dec 12 - No Cached

obat sehat on 04 Dec 12

Insulin is a hormone produced by the pancreas to control blood sugar. Diabetes can be caused by too little insulin, resistance to insulin, or both. To understand diabetes, it is important to first understand the normal process by which food is broken down and used by the body for energy. Several things happen when food is digested: A sugar called glucose enters the bloodstream. Glucose is a source of fuel for the body. An organ called the pancreas makes insulin. The role of insulin is to move glucose from the bloodstream into muscle, fat, and liver cells, where it can be used as fuel. People with diabetes have high blood sugar because their body cannot move sugar into fat, liver, and muscle cells to be stored for energy. This is because either: Their pancreas does not make enough insulin Their cells do not respond to insulin normally Both of the above There are two major types of diabetes. The causes and risk factors are different for each type: Type 1 diabetes can occur at any age, but it is most often diagnosed in children, teens, or young adults. In this disease, the body makes little or no insulin. Daily injections of insulin are needed. The exact cause is unknown. Type 2 diabetes makes up most diabetes cases. It most often occurs in adulthood. However, because of high obesity rates, teens and young adults are now being diagnosed with it. Many people with type 2 diabetes do not know they have it. Gestational diabetes is high blood sugar that develops at any time during pregnancy in a woman who does not have diabetes. Diabetes affects more than 20 million Americans. Over 40 million Americans have pre-diabetes (which often comes before type 2 diabetes).

<div class="cArrow"> </div><div class="cContentInner">Insulin is a hormone produced by the pancreas to control blood sugar. Diabetes can be caused by too little insulin, resistance to insulin, or both. To understand diabetes, it is important to first understand the normal process by which food is broken down and used by the body for energy. Several things happen when food is digested: A sugar called glucose enters the bloodstream. Glucose is a source of fuel for the body. An organ called the pancreas makes insulin. The role of insulin is to move glucose from the bloodstream into muscle, fat, and liver cells, where it can be used as fuel. People with diabetes have high blood sugar because their body cannot move sugar into fat, liver, and muscle cells to be stored for energy. This is because either: Their pancreas does not make enough insulin Their cells do not respond to insulin normally Both of the above There are two major types of diabetes. The causes and risk factors are different for each type: Type 1 diabetes can occur at any age, but it is most often diagnosed in children, teens, or young adults. In this disease, the body makes little or no insulin. Daily injections of insulin are needed. The exact cause is unknown. Type 2 diabetes makes up most diabetes cases. It most often occurs in adulthood. However, because of high obesity rates, teens and young adults are now being diagnosed with it. Many people with type 2 diabetes do not know they have it. Gestational diabetes is high blood sugar that develops at any time during pregnancy in a woman who does not have diabetes. Diabetes affects more than 20 million Americans. Over 40 million Americans have pre-diabetes (which often comes before type 2 diabetes).</div>

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