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Nathan Goodyear

Targeting gut microbiota in obesity: effects of prebiotics and probiotics : Article : Nature Reviews Endocrinology - 0 views

www.nature.com/...nrendo.2011.126.html

LPS lipopolysaccharides gut microbiota dysbiosis inflammation obesity metabolic endotoxemia health probiotics

shared by Nathan Goodyear on 18 Jan 12 - No Cached
  • gut microbes have a role in the host's metabolic homeostasis
  • lipopolysaccharide (LPS)
  • Associations between circulating LPS level, consumption of a high-fat diet and the presence of obesity and type 2 diabetes mellitus have been confirmed in humans
  • ...8 more annotations...
  • high-fat diet induces metabolic endotoxemia in healthy individuals.
  • A link between energy intake (high-fat diet) and metabolic endotoxemia has also been described
  • associations have been proposed between high-fat diet, metabolic endotoxemia and levels of inflammatory markers (TLRs and SOCS3) in mononuclear cells
  • metabolic endotoxemia is associated with systemic and adipose tissue inflammation in pregnant women with obesity
  • A growing amount of evidence indicates that changes in the integrity of the intestinal barrier occur both in the proximal and the distal part of the gut, which can contribute to the entrance of LPS into the systemic circulation
  • intestinal endocannabinoid system
  • The low-grade systemic inflammation that characterizes the obese phenotype is controlled by peptides that are produced in the gut. These peptides are influenced by the presence or absence of the gut microbiota
  • these findings suggest that the gut microbiota modulates the biological systems that regulate the availability of nutrients, energy storage, fat mass development and inflammation in the host, which are all components of the obese phenotype
  • Nathan Goodyear on 18 Jan 12
     
    good look of how the the gut health, or lack there of, can influence energy homeostasis and contribute to obesity.  This article points to the presence of LPS playing a role in metabolic endotoxemia.  It does discuss the importance of the microbiota and their possible role in the low-grade systemic inflammation condition that is obesity.
Nathan Goodyear

The Journal of Nutritional Biochemistry - Record - 0 views

www.jnutbio.com/...ivp_10717323_13_1431

overweight obesity menopause peri-menopause hysterectomy weight gain

shared by Nathan Goodyear on 31 Jul 12 - No Cached
  • Nathan Goodyear on 31 Jul 12
     
    study shows that smoking cessation, physical inactivity, menopause, hysterectomy and energy intake associated with the perimenopause weight gain.  What is interesting about it is the energy imbalance is small that results in a big weight gain over time.  We need to look closely and be more frank with out clients about the risk that a hysterectomy poses for her health post surgery.
Nathan Goodyear

Oolong tea increases energy metabolism in Japan... [J Med Invest. 2003] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...13678386

weight-loss oolong tea energy expenditure metabolism

shared by Nathan Goodyear on 25 Nov 11 - No Cached
  • Nathan Goodyear on 25 Nov 11
     
    Oolong tea shown to improve energy expenditure, thus increase metabolism and increase weight loss
Nathan Goodyear

Cambridge Journals Online - Proceedings of the Nutrition Society - Fulltext - Extra-adrenal regeneration of glucocorticoids by 11β-hydroxysteroid dehydrogenase type 1: physiological regulator and pharmacological target for energy partitioning - 0 views

journals.cambridge.org/...displayFulltext

11-betaHSD1 metabolism obesity energy cortisol nutrition

shared by Nathan Goodyear on 08 Oct 13 - No Cached
  • Nathan Goodyear on 08 Oct 13
     
    Peripheral 11Beta-HSD1 plays critical role in fat metabolism and energy utilization.  Good discussion on the role that extra-adrenal 11Beta-HSD1 plays in metabolism
Nathan Goodyear

Revealing Estrogen's Secret Role In Obesity - 0 views

www.sciencedaily.com/...070820145348.htm

estrogen obesity

shared by Nathan Goodyear on 07 Jun 11 - No Cached
  • researchers showed how estrogen receptors located in the hypothalamus serve as a master switch to control food intake, energy expenditure and body fat distribution.
  • This research seems to support a link between estrogen and regulation of obesity
  • ventromedial nucleus or VMN, is a key center for energy regulation.
  • ...2 more annotations...
  • When estrogen levels in the VMN dipped, the animals' metabolic rate and energy levels also plummeted
  • 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.
  • Nathan Goodyear on 07 Jun 11
     
    estrogen plays role in obesity in menopausal women.
Nathan Goodyear

α-Lipoic acid increases energy expenditure by enhancing adenosine monophosphate-activated protein kinase-peroxisome proliferator-activated receptor-γ coactivator-1α signaling in the skeletal muscle of aged mice - 0 views

www.metabolismjournal.com/...abstract

alpha lipoic acid ALA

shared by Nathan Goodyear on 07 May 11 - No Cached
  • LA improves skeletal muscle energy metabolism
  • LA increases lean mass loss
  • Nathan Goodyear on 07 May 11
     
    alpha lipoic acid improves energy production, lean mass and weight loss
Nathan Goodyear

Inborn-like errors of metabolism are determinants of breast cancer risk, clinical response and survival: a study of human biochemical individuality - 0 views

www.ncbi.nlm.nih.gov/...PMC6114970

cancer metabolism breast cancer glutamine glutamate aspartate oncogenes

shared by Nathan Goodyear on 24 Sep 18 - No Cached
  • 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
  • RAS, PI3K, TP53 and MYC
  • 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
  • ...16 more annotations...
  • 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
  • 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
  • four-fold higher frequency of cancer (including breast) in patients with energy metabolism disorders
  • growing recognition that cancer cells differ from their normal counterparts in their use of nutrients, synthesis of biomolecules and generation of energy
  • glutamine concentrations in the cancer patients were reduced to nearly 1/8 of the levels observed in the normal population
  • 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
  • glutamine consumption associated with parallel increases in glutamate and aspartate (Figure ​(Figure1A1A red arrows) is considered a hallmark of MYC-driven “glutaminolysis”
  • Gln/Glu ratio inversely correlates with i- late stage metabolic syndrome and with ii- increased chance of death
  • 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
  • lower Gln/Glu ratios inversely correlated with insulin resistance and the risk of diabetes
  • 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
  • these metabolic disturbances would be expected to remain extant after therapeutic interventions
  • 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
  • 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)
  • liver dysfunction shares many features with both IEM and cancer suggesting a role for hepatic dysfunction in carcinogenesis
  • cancer “conscripts” the human genome to meet its needs under conditions of systemic metabolic stress
  • Nathan Goodyear on 24 Sep 18
     
    Breast cancer is a metabolic disease.  Now, where have I heard that cancer is a metabolic disease?
Nathan Goodyear

ScienceDirect.com - Physiology & Behavior - The effects of a high-energy diet on hippocampal-dependent discrimination performance and blood-brain barrier integrity differ for diet-induced obese and diet-resistant rats - 0 views

www.sciencedirect.com/...S0031938412002028

obesity overweight hippocampus brain diet

shared by Nathan Goodyear on 10 Oct 12 - No Cached
  • Nathan Goodyear on 10 Oct 12
     
    We have known that diet and brain inflammation were linked.  This study shows a link between, what they call High energy diet (better known as  high calorie, high fat, high carb...), and altered hippocampus brain function.
Nathan Goodyear

Cell Metabolism - The Ubiquitin Ligase Mul1 Induces Mitophagy in Skeletal Muscle in Response to Muscle-Wasting Stimuli - 0 views

www.cell.com/...S1550413112004056

muscle wasting mitochondria energy metabolism

shared by Nathan Goodyear on 02 Jan 13 - No Cached
  • Nathan Goodyear on 02 Jan 13
     
    loss of mitochondria leads to muscle wasting.  Kind of makes sense.  The muscles lose the ability to make energy and thus the muscle cells die and waste.  Thus, preserve mitochondrial function and you will slow muscle wasting.
Nathan Goodyear

Coming Full Circle: Contributions of Central and Peripheral Oxytocin Actions to Energy Balance - 0 views

endo.endojournals.org/...589.abstract

oxytocin anorexin appetite weight loss

shared by Nathan Goodyear on 13 Feb 13 - No Cached
  • Nathan Goodyear on 13 Feb 13
     
    oxytocin shown to inhibit appetite as an anorexigen.  As a hormone, prolactin, regulates energy balance
Nathan Goodyear

Nutrition & Metabolism | Full text | Targeting energy metabolism in brain cancer: review and hypothesis - 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.
arunaraayala

Putin and Modi agreed to sign energy deals ahead of BRICS - Locality News - 0 views

www.localitynews.com/gn-energy-deals-ahead-of-brics

BRICS SUMMI T GOA ENERGY DEAL NARENDRA MODI VALDIMIR PUTIN

shared by arunaraayala on 17 Oct 16 - No Cached
  • arunaraayala on 17 Oct 16
     
    Putin is seeking to seal deals with India in a shot to assist resuscitate Russia's recession-hit eco...
Nathan Goodyear

Effects of dietary polyphenols on neuroregulatory factors and pathways that mediate food intake and energy regulation in obesity - Panickar - 2012 - Molecular Nutrition & Food Research - Wiley Online Library - 0 views

onlinelibrary.wiley.com/...abstract

polyphenols nutrition leptin insulin diet obesity

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    review article of polyphenols positive effect on neuroregulatory factors involved in food intake and energy balance.  Only abstract available here.
Nathan Goodyear

Statin-Associated Myopathy with Normal Creatine Kinase Levels - 0 views

www.annals.org/...581.full.pdf+html

statins statin muscle cells mitochondria CoQ10 energy myopathy necrosis

shared by Nathan Goodyear on 28 Apr 12 - No Cached
  • Nathan Goodyear on 28 Apr 12
     
    Statins shown to damage the cells ability to make energy and resultant muscle damage occurs.
Nathan Goodyear

Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslipidemia - 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.
wheelchairindia9

Wheelchair Pediatric - 0 views

www.wheelchairindia.com/...CP-PEDIATRIC-WHEELCHAIR

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 - No Cached
  • wheelchairindia9 on 14 May 15
     
    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
Nathan Goodyear

Branched-chain amino acids as a protein- and energy-source in liver cirrhosis. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...14684176

BCAA branched chain amino acids liver cirrhosis hepatitis ammonia

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    BCAA for liver cirrhosis to improve ammonia clearance.  Increased glutamine is a means to compensate for the decreased ammonia clearance as well as a means to improve energy balance often present in these clients.  Night time dosing prevents fasting catabolic exacerbations.
Nathan Goodyear

Branched Chain Amino Acid Supplementation for Patients with Cirrhosis | Clinical Correlations - 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 - No Cached
  • low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
  • 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
  • oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
  • ...35 more annotations...
  • malnutrition progressing to cachexia is another common manifestation of cirrhosis
  • Malnutrition can be mitigated with BCAA supplementation
  • 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
  • Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
  • BCAAs metabolites inhibit proteolysis
  • Patients with cirrhosis have both insulin deficiency and insulin resistance
  • 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
  • Coadministration of BCAAs and glucose has been found to be particularly useful
  • BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
  • Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
  • another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
  • 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
  • BCAA administration has also been shown to have a positive effect on liver regeneration
  • 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
  • BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
  • Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
  • 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
  • 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
  • Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
  • patients taking BCAA supplementation report improved quality of life
  • BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
  • BCAAs make up 20-25% of the protein content of most foods
  • 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
  • In addition to BCAAs from diet, oral supplements of BCAAs can be used
  • 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
  • Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
  • Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
  • the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
  • 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
  • Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
  • hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia
  • 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
  • patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
  • Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
  • the serum BCAA concentration is strongly correlated with the serum albumin level
  • Nathan Goodyear on 05 Oct 15
     
    great review of cirrhosis and BCCA supplementation.
Nathan Goodyear

Neurodegenerative disorders: clues from glutamate ... [Crit Rev Neurobiol. 1996] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...8971131

neurodegenerative disease

shared by Nathan Goodyear on 07 Feb 11 - No Cached
  • 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.
  • Nathan Goodyear on 07 Feb 11
     
    Magnesium and Zinc improve neurodegenerative disease via glutamate blockade; Poor energy production at foundation of neurodegenerative disease
Nathan Goodyear

A mitochondrial paradigm for degenerative diseases... [Novartis Found Symp. 2001] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...11280029

mitochondrial paradigm

shared by Nathan Goodyear on 08 Feb 11 - No Cached
  • the decline of mitochondrial energy production resulting in increased oxidative stress and apoptosis does play a significant role in degenerative diseases and ageing.
  • Nathan Goodyear on 08 Feb 11
     
    oxidative stress leads to decreased mitochondrial energy production, which results in cell death, and thus aging.
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