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Nathan Goodyear

Human gut microbiota in obesity and after gastric bypass - 0 views

dl-web.dropbox.com/...PNAS-2009-Zhang-0812600106.pdf

obesity weight loss inflammation metabolic endotoxemia bariatric surgery gastric bypass probiotics firmicutes gut flora microbiota

shared by Nathan Goodyear on 26 Jan 12 - No Cached
  • Nathan Goodyear on 26 Jan 12
     
    It is proposed that the balance of bacteria in the gut play a critical role in energy utilization and obesity. This study showed that bypass surgery altered the gut bacteria to favor weight loss: decrease in firmicutes species. But, do we really need gastric bypass to do that? Of course not. Probiotics will do the same.
indiacardiacsurg

Totally Endoscopic Arterial Bypass Surgery (TECAB) Method Used by Dr. Naresh Trehan - 0 views

www.briefingwire.com/...ethod-used-by-dr-naresh-trehan

Dr. Naresh Trehan Dr.Trehan Cardiac Surgeon in Medanta Gurgaon Delhi Medanta Gurgaon Delhi

shared by indiacardiacsurg on 22 Feb 22 - No Cached
  • indiacardiacsurg on 22 Feb 22
     
    Dr. Naresh Trehan is the best in India offering specialized endoscopic surgery. Dr. Naresh Trehan accomplished the TECAB surgeries-a single bypass and a double bypass-through 4 keyholes (fingertip-size) incisions less than one centimeter long.
Nathan Goodyear

Gut microbiota after gastric bypass in human obesity: increased richness and associatio... - 0 views

ajcn.nutrition.org/...16.abstract

gastric bypass obesity gut microbiota microbiota inflammation WAT white adipose tissue dysbiosis gut

shared by Nathan Goodyear on 26 Jun 13 - No Cached
  • Nathan Goodyear on 26 Jun 13
     
    Not that I am proposing gastric bypass for weight loss.  IN my mind that is like a lobotomy for headache.  But, this study shows the link between gut bacteria and obesity.  This study documented an increase in the expression of certain bacteria types in the gut.   This was associated with increase in white adipose tissue gene expression.  Linking directly the gut and fat.
Nathan Goodyear

Variation in the 4q25 Chromosomal Locus Predicts Atrial Fibrillation After Coronary Art... - 0 views

circgenetics.ahajournals.org/...499.full

SNP AF atrial fibrillation coronary artery bypass cardiovascular disease 4q25

shared by Nathan Goodyear on 12 Sep 12 - No Cached
  • Nathan Goodyear on 12 Sep 12
     
    SNP in 4q25 associated with increased Atrial fibrillation post coronary artery bypass.
Nathan Goodyear

Gastric Bypass Surgery for Morbid Obesity Leads to an Increase in Bone Turnover and a D... - 0 views

jcem.endojournals.org/...1061

bypass gastric obesity surgery side effects bone loss

shared by Nathan Goodyear on 21 Mar 11 - No Cached
  • Nathan Goodyear on 21 Mar 11
     
    Gastric Bypass leads to bone loss; through malabsorption
Nathan Goodyear

Obesity Surgery, Volume 14, Number 2 - SpringerLink - 0 views

www.springerlink.com/...825740k3r2735308

Vitamin B B vitamins vitamin gastric bypass neuropathy peripheral neuropathy Bariatric surgery obesity

shared by Nathan Goodyear on 26 Jun 12 - No Cached
  • Nathan Goodyear on 26 Jun 12
     
    B vitamin deficiency following gastric bypass resulting in neuropathy.
Nathan Goodyear

Copper deficiency after gastric surgery: a reason ... [Am J Med Sci. 2009] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...19365170

deficiency copper gastric bypass

shared by Nathan Goodyear on 25 Jan 11 - No Cached
  • Nathan Goodyear on 25 Jan 11
     
    Copper deficiency present in gastric bypass patients: results in physiologic dysfunction in neurotransmitter synthesis
Nathan Goodyear

Impact of gastric bypass operation on survival: A population-based analysis - 0 views

www.journalacs.org/...abstract

gastric bypass impact weight loss obesity

shared by Nathan Goodyear on 11 May 11 - No Cached
  • Thirty-day mortality after gastric bypass is higher than previously reported and closely linked to surgeon inexperience
  • Nathan Goodyear on 11 May 11
     
    Understand: surgery is surgery.  The death rate from weight loss surgeries is higher than reported as this large study shows.  Another thought: what are the long-term health implications.  I can tell you from the clients that I see, it is not good
Nathan Goodyear

Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and h... - 0 views

www.ncbi.nlm.nih.gov/...PMC1885574

vitamin C ascorbic acid Cancer

shared by Nathan Goodyear on 05 Mar 18 - No Cached
  • Proposed mechanism
  • The data show that pharmacologic ascorbate concentrations produced Asc•− selectively in extracellular fluid compared with blood and that H2O2 formation occurred when Asc•− concentrations were >100 nM in extracellular fluid.
  • These data validate the hypothesis that ascorbate is a prodrug for selective delivery of reactive species to the extravascular space
  • ...22 more annotations...
  • pharmacologic ascorbate as a prooxidant drug for therapeutic use.
  • Recently we reported that pharmacologic ascorbic acid concentrations produced H2O2 concentrations of ≥25 μM, causing cancer cell death in vitro
  • We found that H2O2 concentrations generated in vivo were those that caused cancer cell death in vitro
  • When ascorbate was given parenterally, Asc•−, the product of a loss of one electron from ascorbate, was detected preferentially in extracellular fluid compared with blood
  • Asc•− generation in extracellular fluid depended on the ascorbate dose and the resulting concentrations
  • With i.v. administration of ascorbate, Asc•− concentrations were as much as 12-fold greater in extracellular fluid compared to blood and approached 250 nM
  • In blood, such Asc•− concentrations were never produced and were always <50 nM
  • These data are all consistent with the hypothesis that pharmacologic ascorbate concentrations in vivo serve as a prodrug for selective delivery of H2O2 to the extracellular space
  • After oral ingestion, control of intracellular and extracellular ascorbate concentrations is mediated by three mechanisms: intestinal absorption, tissue transport, and renal reabsorption
  • intestinal absorption, or bioavailability, declines at doses >200 mg
    • Nathan Goodyear
      Nathan Goodyear on 05 Mar 18
       
      significant limitation of gut absorption of vitamin C--at 200 mg po.
  • corresponding to plasma concentrations of ≈60 μM
    • Nathan Goodyear
      Nathan Goodyear on 05 Mar 18
       
      equates to 0.06 mM.  Max blood levels found with po AA dosing has been 0.22 mM
  • at approximately this concentration, the ascorbate tissue transporter SVCT2 approaches Vmax, and tissues appear to be saturated
    • Nathan Goodyear
      Nathan Goodyear on 05 Mar 18
       
      SVCT2 Rc in gut reach max binding.
  • also at ≈60 μM, renal reabsorption approaches saturation, and excess ascorbate is excreted in urine
  • Parenteral administration bypasses tight control
  • When tight control is bypassed, H2O2 forms in the extracellular space
  • in vivo validation of ascorbate as a prodrug for selective H2O2 formation
  • Temporarily bypassing tight control with parenteral administration of ascorbate allows H2O2 to form in discrete time periods only, decreasing likelihood of harm, and provides a pharmacologic basis for therapeutic use of i.v. ascorbate
  • H2O2 formation results in selective cytotoxicity
  • Tumor cells are killed with exposure to H2O2 for ≤30 min
  • In vitro, killing is mediated by H2O2 rather than Asc•−
  • In addition to cancer treatment, another potential therapeutic use is for treatment of infections. H2O2 concentrations of 25–50 μM are bacteriostatic
  • virally infected cells may also be candidates
  • Nathan Goodyear on 05 Mar 18
     
    follow up invivo study to previous study from 2005.  Here, the authors prove their hypothesis that ascorbate is a prodrug for delivery of H2O2.
Nathan Goodyear

British Journal of Cancer - Role of glucose and ketone bodies in the metabolic control ... - 0 views

www.nature.com/...6601269a.html

glucose ketones cancer ketogenic diet ketogenic diet nutrition brain

shared by Nathan Goodyear on 03 Jul 13 - No Cached
  • Nathan Goodyear on 03 Jul 13
     
    Use of ketones to bypass the use of cancer cells of glucose as fuel.  This, selects out healthy cells and their adaptive metabolism versus the unadaptable metabolism of cancer cells.  
Nathan Goodyear

Nutrition & Metabolism | Full text | Targeting energy metabolism in brain cancer: revie... - 0 views

www.nutritionandmetabolism.com/...30

nutrition ketogenic diet ketogenic diet brain cancer

shared by Nathan Goodyear on 03 Jul 13 - Cached
  • Nathan Goodyear on 03 Jul 13
     
    Good review of the normal brain metabolism and then the benefits of the ketogenic diet to bypass glucose as the source of energy in states of cancer.
Nathan Goodyear

Intermediary metabolism of fructose. - 0 views

ajcn.nutrition.org/...754S.full.pdf+html

fructose metabolism

shared by Nathan Goodyear on 19 Sep 13 - No Cached
  • Nathan Goodyear on 19 Sep 13
     
    Good review on the metabolism of fructose.  Fructose is able to bypass the key regulatory step in glycolysis and promote Triglyceride synthesis without any negative feedback.
Nathan Goodyear

Fructose: A Key Factor in the Development of Metabolic Syndrome and Hypertension - 0 views

www.ncbi.nlm.nih.gov/...PMC3677638

fructose phosphofructokinase MetS metabolic syndrome metabolic syndrome insulin resistance ATP mitochondria uric acid

shared by Nathan Goodyear on 01 Oct 13 - No Cached
  • Nathan Goodyear on 01 Oct 13
     
    Fructose intake increases MetS and hypertension.  The high fructose intake upregulates phosphofructokinase which increases triglyceride production, bypassing central regulation.  This results in ATP depletion with reduced capacity to recover.  Thus attempts by the cells to increase ATP through AMP deaminase results in uric acid production.
Nathan Goodyear

Free triiodothyronine: a novel predictor of postoperative atrial fibrillation -- Cerill... - 0 views

ejcts.ctsnetjournals.org/...487

triiodothyronine free T3 atrial fibrillation CABG cardiovascular disease

shared by Nathan Goodyear on 01 Feb 11 - No Cached
  • Nathan Goodyear on 01 Feb 11
     
    Conclusions: Low basal fT3 concentration can reliably predict the occurrence of postoperative Atrial Fibrillation in Coronary-bypass patients
Nathan Goodyear

Plasma Ghrelin Levels after Diet-Induced Weight Loss or Gastric Bypass Surgery - NEJM - 0 views

www.nejm.org/...NEJMoa012908

diet weight loss overweight weight-loss surgery ghrelin bypass

shared by Nathan Goodyear on 26 Oct 11 - No Cached
  • Nathan Goodyear on 26 Oct 11
     
    "diets" and weight-loss surgery effect ghrelin diferently
Nathan Goodyear

Inhibition of tumor angiogenesis as a strategy to circumvent acquired resista... - 0 views

onlinelibrary.wiley.com/...bies.950130106

chemotherapy angiogenesis

shared by Nathan Goodyear on 25 Sep 20 - No Cached
  • Nathan Goodyear on 25 Sep 20
     
    Even with cancer chemoresistance to chemo, the move to inhibit angiogenesis i.e. via lower dose, allows a bypass of the resistance to another means of action.
indian-health

Top 12 Cardiologists in Bangalore Leaders in the Treatment of Coronary Artery Disease - 0 views

www.briefingwire.com/...ent-of-coronary-artery-disease

best cardiologist in bangalore top 10 cardiologist in bangalore Top 12 Cardiologists in Bangalore top cardiologist in bangalore best heart hospital in bangalore cardiologist bangalore best heart specialist in bangalore heart specialist bangalore

shared by indian-health on 02 Mar 22 - No Cached
  • indian-health on 02 Mar 22
     
    Best cardiac surgery hospitals Bangalore recently received the coveted three-star rating from the Society of Thoracic Surgeons (STS) for its patient care and outcomes in isolated coronary artery bypass grafting (CABG) procedures.
indiacardiacsurg

High apoplexy Reduction with No-Touch Beating Heart Bypass Surgery - 0 views

www.briefingwire.com/...h-beating-heart-bypass-surgery

Dr. Naresh Trehan heart specialist India Best Cardiac Surgeon in Medanta Gurgaon Delhi Medanta Gurgaon Delhi

shared by indiacardiacsurg on 07 Feb 22 - No Cached
  • indiacardiacsurg on 07 Feb 22
     
    The no-touch beating heart technique completed "without aortic manipulation, at the same time as achieved best by a minority of surgeons, has an essential place within the risk patient undergoing CABG," commented Dr. Naresh Trehan heart specialist India. Email id: - nareshtrehan@indiacardiacsurgerysite.com Call: - +91-9370586696
Nathan Goodyear

Telomerase at the intersection of cancer and aging - 0 views

www.ncbi.nlm.nih.gov/...PMC3896987

telomere telomeres telomerase telomerase activator aging disease cancer

shared by Nathan Goodyear on 18 May 16 - No Cached
  • The anti-aging role of telomerase has been demonstrated to be largely mediated by its canonical role in elongating telomeres, which prevents the accumulation of critically short telomeres and loss of tissue homeostasis
  • Short telomeres, and subsequent DDR activation, could occur both in cancer and aging
  • increased abundance of short telomeres correlates with higher genomic instability and decreased longevity in various organisms, including mice, zebrafish, and yeast
  • ...15 more annotations...
  • mice deficient for telomerase or for telomere binding proteins are characterized by accelerated age-related defects
  • In humans, short telomeres are considered good indicators of an individual’s health status and correlate with both genetic and environmental factors
  • Although recent findings strongly support the idea that short telomeres drive several age-related diseases 38 we cannot exclude the possibility that in some situations short telomeres may be a consequence of the disease itself.
  • the current view is that telomerase deficiency may contribute to the early steps of cancer development by fueling chromosomal instability, while subsequent activation of telomerase may be necessary to allow tumor growth and tumor progression towards more malignant states
  • telomerase activation can be an early event in cancer, it is not necessary for cancer initiation
  • telomerase can stimulate tumor progression by ensuring maintenance of telomeres above a critically short length, thus preventing induction of cellular senescence or apoptosis
  • Almost all human cancers present activation of telomerase as a hallmark, most likely as a mechanism to allow unlimited cell proliferation of tumor cells
  • recent evidence demonstrated that short telomeres alone could lead to genomic instability and cancer
  • Getting rid of telomerase can also be problematic; the lack of telomerase could lead to increased chromosomal instability, which in turn could be at the basis for cancer initiation when tumor suppressor barriers are bypassed
  • telomerase activation is a potential therapeutic strategy for the treatment of age-related diseases
  • telomerase activation in adult or old mice by means of a gene therapy strategy was shown to be sufficient to improve metabolic fitness, neuromuscular capacity, and prevent bone loss, as well as significantly increase both median and maximum longevity, without increased cancer incidence
  • These studies suggest that telomerase expression could be considered a feasible approach to reverse tissue dysfunction and extend healthy lifespan without increasing cancer incidence
  • humans almost completely lose telomerase activity from somatic tissues in the adulthood
  • a change of paradigm seems to be occurring in telomerase biology, with a switch from viewing telomerase as fueling cancer to reversing aging
  • Telomerase expression in a background of high levels of tumor suppressors or in aged organisms seems to prevent its expected pro-cancer activity and yet it still functions as an anti-aging factor
  • Nathan Goodyear on 18 May 16
     
    Telomerase activity and longer telomere length is shown to correlated inversely with many chronic diseases of aging.  In contrast, telomerase activity is found to be involved in carcinogenesis.  Increased carcinogenic potential of telomerase activity has not borne out in studies.  In addition, increased CD8 cell activity as a result of telomerase activation will actually decrease carcinogenic potential via NK activation.
Nathan Goodyear

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 - Cached
  • For thousands of years humans consumed fructose amounting to 16–20 grams per day
  • daily consumptions amounting to 85–100 grams of fructose per day
  • 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
  • ...29 more annotations...
  • 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]).
  • Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
  • 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.
  • A prolonged elevation of TG was also seen in the high fructose subjects
  • 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
  • Chronic fructose consumption reduces adiponectin responses, contributing to insulin resistance
  • A definite relationship has also been found between metabolic syndrome and hyperhomocysteinemia
  • 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
  • Fructose stimulates TG production, but impairs removal, creating the known dyslipidemic profile
  • the effects of fructose in promoting TG synthesis are independent of insulinemia
  • 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
  • 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
  • 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
  • Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
  • fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
  • Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
  • 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
  • High fructose diets can have a hypertriglyceridemic and pro-oxidant effect
  • Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
  • Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
  • LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
  • Fructose has also been implicated in reducing PPARα levels
  • PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
  • decreased PPARα expression can result in reduced oxidation, leading to cellular lipid accumulation
  • fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
  • LDL particle size has been found to be inversely related to TG concentration
  • 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
  • High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
  • 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
  • Nathan Goodyear on 16 Sep 13
     
    Fructose and metabolic syndrome.  Good discussion of the impact of high fructose intake and metabolic dysfunction.  This study also does a great job of highlighting the historical change of fructose intake.
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