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Nathan Goodyear

Metformin Inhibits the Production of Reactive Oxygen Species from NADH:Ubiqui... - 0 views

www.jbc.org/20348

metformin LPS lipopolysaccharides IL-1beta inflammation

shared by Nathan Goodyear on 04 Oct 17 - No Cached
  • Nathan Goodyear on 04 Oct 17
     
    Metformin inhibits LPS induced IL-1beta stimulation.  Interesting that metformin is a inhibitor of complex I in the electron transport chain.
pharmacybiz

Walgreens Starts Strategic Review For Boots UK - 0 views

www.pharmacy.biz/-strategic-review-for-boots-uk

Walgreens-Boots-Alliance-uk Pharmacy-business pharmacy-news-uk Boots-news Walgreens-Boots-Alliance-news Walgreens-news-today

shared by pharmacybiz on 12 Jan 22 - No Cached
  • pharmacybiz on 12 Jan 22
     
    Walgreens Boots Alliance, the parent company of Boots UK, has begun a strategic review of its business in the United Kingdom, chief executive officer Rosalind Brewer said on Tuesday (January 11) - as the pharmacy chain tries to renew its focus on US healthcare. Boots has over 2,200 stores across the UK, which include pharmacies, health and beauty stores, among others, according to the chain's website. "This review is very much in line with our renewed priorities and strategic direction. In particular, our increased focus on US healthcare. While the process is at an exploratory stage, we do expect to move quickly," Brewer said at the JP Morgan Healthcare Conference. The review comes at a time when the company, which was formed in 2014 after the acquisition of stake in Alliance Boots by Walgreens, moves beyond its drugstores with its investments in two smaller healthcare providers, CareCentrix and VillageMD.
fitspresso

LeanBiome™ (Official) | Get Save UpTo $540 Today Only! - 0 views

usleanbiome.com

leanbiome us lean biome usa uk buy get does work discount 2022 australia legit weight loss bioma customer reviews review canada website ireland product

shared by fitspresso on 27 Sep 23 - No Cached
  • fitspresso on 27 Sep 23
     
    LeanBiome™ (Official) | Get Save UpTo $540 Today Only! usleanbiome.com LeanBiome™ Hurry Up! Offer Expires in: 00 HOUR 29 MINUTE 59 SECOND LeanBiome Attention! Get Special 84% Discount Today Faster fat burning and weight loss Healthy cholesterol and sugar levels Higher energy levels Regular price: $129 Only for: 39$ What Is LeanBiome? LeanBiome Lean for Good is a weight loss dietary supplement derived from scientifically researched ingredients and comprehensively developed to help people achieve sustainable weight control. The formula comes in a capsule format that is easy to take and is made with natural ingredients from plants and other sources to achieve its goals. The main ingredient in LeanBiome is piperine, which has been found to affect the body's ability to absorb micronutrients and other compounds more effectively. LeanBiome is a dietary supplement that claims to help weight management. It contains 100% natural ingredients that support healthy weight loss. It does not interfere with any natural process making it safe for use. It ranks among the top weight loss supplements that claim to provide a permanent solution. LeanBiome is made by a company named Lean for Good. It is made with natural and research-backed ingredients that help you lose excess fat without hassles. It is sold in capsule form. The company assures the composition is GMO, gluten, and soy-free. As for manufacturing standards, you need not fret. The company makes the supplement in a facility certified by the FDA. How Does LeanBiome Work? The starting period of the LeanBiome program includes a detoxification process that effectively removes any accumulated ree radicals, toxins, fand oxidative stress. This cleansing enables improved blood circulation, setting the stage for the body to initiate its own fat-burning mechanisms. To enhance metabolic activity, introducing the lean bacteria contained in LeanBiome to your gut microbiome is a beneficial approach. This activation triggers r
Nathan Goodyear

Toll-like receptor signaling links dietary fatty acids to the metabolic syndrome - 0 views

www.ncbi.nlm.nih.gov/...PMC3099529

TLR toll-like receptors toll-like receptors fatty acids fat metabolic syndrome obesity overweight inflammation dietary

shared by Nathan Goodyear on 08 Oct 12 - No Cached
  • Activation of the innate immune system controls macronutrient metabolism
  • the innate immune response is the first line of defense against invading pathogens, wherein highly conserved pathogen-associated molecular patterns (PAMPs) are recognized by cognate pattern recognition receptors (PRRs
  • many studies have supported the idea that cytokine signaling directly promotes insulin resistance
  • ...10 more annotations...
  • innate immune system may be causally linked to obesity
  • adipose tissue contains a substantial population of macrophages, and macrophage-driven adipose inflammation contributes significantly to the pathogenesis of obesity
  • Collectively, activation of the innate immune system is strongly associated with ASCVD, insulin resistance, and obesity, and recent evidence suggests that much of this association can be traced to a unique family of PRRs known as TLRs
  • TLRs are a family of type I transmembrane receptors, currently thought to comprise at least 13 members in mammals, that specifically recognize a variety of microbial PAMPs and trigger host cellular responses
  • Free SFAs have indeed been demonstrated to elicit TLR4-dependent and TLR2-dependent responses in several cell types.
  • Endogenous SFAs released from adipocytes activate cocultured macrophages via TLR4 [18], indicating the potential for cellular crosstalk in adipose tissue. Collectively, there is a growing body of evidence that SFAs promote, whereas long chain PUFA antagonize, TLR4-dependent and TLR2-dependent signaling in multiple cell models
  • In an elegant study, Shi et al. [16] demonstrated that SFAs activate TLR4-dependent signaling in both macrophages and adipocytes, and mice lacking TLR4 are protected against insulin resistance driven by intravenous lipid infusion
  • In addition to effects in macrophages and adipocytes, SFAs can activate TLR4 in the hypothalamus, which triggers a central inflammatory response that results in resistance to anorexigenic signals
  • endogenous SFAs can indeed promote innate immunity and inflammatory disease
  • This finding strongly supports the work of Hwang and coworkers [19–22] demonstrating that ω-3 PUFAs can effectively counteract SFA-induced TLR4 activation in cultured macrophages and dendritic cells.
  • Nathan Goodyear on 08 Oct 12
     
    high dietary fatty acids linked to metabolic syndrome through TLR.
Nathan Goodyear

American College of Cardiology Foundation | Journal of the American College of Cardiolo... - 0 views

content.onlinejacc.org/article.aspx

mitochondria oxidative stress heart failure heart

shared by Nathan Goodyear on 19 Mar 13 - No Cached
  • Although currently no drugs that specifically target mitochondrial biogenesis in HF are available, acceleration of this process through adenosine monophosphate–activated kinase (AMPK), endothelial nitric oxide synthase (eNOS), and other pathways may represent a promising therapeutic approach
  • Mitochondrial biogenesis can be enhanced therapeutically with the use of adenosine monophosphate kinase (AMPK) agonists, stimulants of nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway (including phosphodiesteraes type 5 inhibitors), or resveratrol
  • metformin, a commonly used antidiabetic drug that activates AMPK signaling
  • ...10 more annotations...
  • Recent evidence suggests that the eNOS/NO/cGMP pathway is an important activator of mitochondrial biogenesis
  • BH4 (tetrahydrobiopterin) supplementation can prevent eNOS uncoupling and was found to reduce left ventricular hypertrophy
  • folic acid is known to replenish reduced BH4 and has been shown to protect the heart through increased eNOS activity
  • Both folate deficiency and inhibition of BH4 synthesis were associated with reduced mitochondrial number and function
  • Resveratrol, a polyphenol compound responsible for the cardioprotective properties of red wine, was recently identified as a potent stimulator of mitochondrial biogenesis
  • epidemiological studies reveal a reduced risk of cardiovascular disease in premenopausal, but not post-menopausal, women compared with men
  • post-menopausal women
    • Nathan Goodyear
      Nathan Goodyear on 19 Mar 13
       
      I would hypothesis that a change in the predominance of ER expression is one of ER beta to ER alpha: creating a more pro-inflammatory signal.
  • The majority of ROS in the heart appear to come from uncoupling of mitochondrial electron transport chain at the level of complexes I and III
  • Because the majority of ROS in HF comes from mitochondria, these organelles are the primary target of oxidative damage.
  • cardioprotective therapies such as angiotensin-converting enzyme inhibitors and ATII receptor blockers were shown to possess antioxidant properties, although it is not known whether they target mitochondrial ROS directly or indirectly
  • Nathan Goodyear on 19 Mar 13
     
    great review of mitochondrial biogenesis, oxidative stress and heart failure.  
Nathan Goodyear

Metabolic management of brain cancer - 0 views

www.sciencedirect.com/...S0005272810006857

brain cancer

shared by Nathan Goodyear on 17 Jun 13 - No Cached
  • Glutamine is a major metabolic fuel for both brain tumor cells and tumor-associated macrophages (TAMs)
  • the malignant phenotype of brain tumor cells that survive radiotherapy is often greater than that of the cells from the original tumor.
  • Conventional chemotherapy has faired little better than radiation therapy for the long-term management of malignant brain cancer
  • ...37 more annotations...
  • most conventional radiation and brain cancer chemotherapies can enhance glioma energy metabolism and invasive properties, which would contribute to tumor recurrence and reduced patient survival [34].
  • We contend that all cancer regardless of tissue or cellular origin is a disease of abnormal energy metabolism
  • complex disease phenotypes can be managed through self-organizing networks that display system wide dynamics involving oxidative and non-oxidative (substrate level) phosphorylation
  • As long as brain tumors are provided a physiological environment conducive for their energy needs they will survive; when this environment is restricted or abruptly changed they will either grow slower, growth arrest, or perish [8] and [19]
  • New information also suggests that ketones are toxic to some human tumor cells and that ketones and ketogenic diets might restrict availability of glutamine to tumor cells [68], [69] and [70].
  • The success in dealing with environmental stress and disease is therefore dependent on the integrated action of all cells in the organism
  • Tumor cells survive in hypoxic environments not because they have inherited genes making them more fit or adaptable than normal cells, but because they have damaged mitochondria and have thus acquired the ability to derive energy largely through substrate level phosphorylation
  • Cancer cells survive and multiply only in physiological environments that provide fuels (mostly glucose and glutamine) subserving their requirement for substrate level phosphorylation
  • Integrity of the inner mitochondrial membrane is necessary for ketone body metabolism since β-hydroxybutyrate dehydrogenase, which catalyzes the first step in the metabolism of β-OHB to acetoacetate, interacts with cardiolipin and other phospholipids in the inner membrane
  • the mitochondria of many gliomas and most tumors for that matter are dysfunctional
  • Cardiolipin is essential for efficient oxidative energy production and mitochondrial function
  • Any genetic or environmental alteration in the content or composition of cardiolipin will compromise energy production through oxidative phosphorylation
  • The Crabtree effect involves the inhibition of respiration by high levels of glucose
  • the Warburg effect involves elevated glycolysis from impaired oxidative phosphorylation
  • the Crabtree effect can be reversible, the Warburg effect is largely irreversible because its origin is with permanently damaged mitochondria
  • The continued production of lactic acid in the presence of oxygen is the metabolic hallmark of most cancers and is referred to as aerobic glycolysis or the Warburg effect
  • We recently described how the retrograde signaling system could induce changes in oncogenes and tumor suppressor genes to facilitate tumor cell survival following mitochondrial damage [48].
  • In addition to glycolysis, glutamine can also increase ATP production under hypoxic conditions through substrate level phosphorylation in the TCA cycle after its metabolism to α-ketoglutarate
  • mitochondrial lipid abnormalities, which alter electron transport activities, can account in large part for the Warburg effect
  • targeting both glucose and glutamine metabolism could be effective for managing most cancers including brain cancer
  • The bulk of experimental evidence indicates that mitochondria are dysfunctional in tumors and incapable of generating sufficient ATP through oxidative phosphorylation
  • Cardiolipin defects in tumor cells are also associated with reduced activities of several enzymes of the mitochondrial electron transport chain making it unlikely that tumor cells with cardiolipin abnormalities can generate adequate energy through oxidative phosphorylation
  • The Crabtree effect involves the inhibition of respiration by high levels of glucose
  • Warburg effect involves elevated glycolysis from impaired oxidative phosphorylation
  • TCA cycle substrate level phosphorylation could therefore become another source of ATP production in tumor cells with impairments in oxidative phosphorylation
  • Caloric restriction, which lowers glucose and elevates ketone bodies [63] and [64], improves mitochondrial respiratory function and glutathione redox state in normal cells
  • DR naturally inhibits glycolysis and tumor growth by lowering circulating glucose levels, while at the same time, enhancing the health and vitality of normal cells and tissues through ketone body metabolism
  • DR is anti-angiogenic
  • DR also reduces angiogenesis in prostate and breast cancer
  • We suggest that apoptosis resistance arises largely from enhanced substrate level phosphorylation of tumor cells and to the genes associated with elevated glycolysis and glutaminolysis, e.g., c-Myc, Hif-1a, etc, which inhibit apoptosis
  • Modern medicine has not looked favorably on diet therapies for managing complex diseases especially when well-established procedures for acceptable clinical practice are available, regardless of how ineffective these procedures might be in managing the disease
  • More than 60 years of clinical research indicates that such approaches are largely ineffective in extending survival or improving quality of life
  • The process is rooted in the well-established scientific principle that tumor cells are largely dependent on substrate level phosphorylation for their survival and growth
  • Glucose and glutamine drive substrate level phosphorylation
  • targeting the glycolytically active tumor cells that produce pro-cachexia molecules, restricted diet therapies can potentially reduce tumor cachexia
  • It is important to recognize, however, that “more is not better” with respect to the ketogenic diet
  • Blood glucose ranges between 3.0 and 3.5 mM (55–65 mg/dl) and β-OHB ranges between 4 and 7 mM should be effective for tumor management
  • Nathan Goodyear on 17 Jun 13
     
    Dr Seyfriend presents his metabolic approach to the treatment of brain cancer.
Nathan Goodyear

International Journal of Obesity - The role of short chain fatty acids in appetite regu... - 0 views

www.nature.com/...ijo201584a.html

SCFA gut gut health obesity appetite energy

shared by Nathan Goodyear on 09 Nov 16 - No Cached
  • Nathan Goodyear on 09 Nov 16
     
    SCFA
Nathan Goodyear

Ketogenic Diet - Nutrition and Traumatic Brain Injury - NCBI Bookshelf - 0 views

www.ncbi.nlm.nih.gov/...NBK209323

ketones ketone bodies ketogenic ketogenic diet brain brain injury TBI concussion MCT medium chain triglycerides nutrition B

shared by Nathan Goodyear on 16 Nov 16 - No Cached
  • Nathan Goodyear on 16 Nov 16
     
    good review of the impact of ketones on TBI.  The authors conclude that precursors to ketones may be the right approach to treatment.  This would be MCT's and ketones.
Nathan Goodyear

Marked Seizure Reduction after MCT Supplementation - 0 views

www.ncbi.nlm.nih.gov/...PMC3870649

MCT medium chain triglycerides MCTs seizures

shared by Nathan Goodyear on 21 Nov 16 - No Cached
  • Nathan Goodyear on 21 Nov 16
     
    Case study: MCT reduced frequency of seizures.
Nathan Goodyear

Effects of exogenous ketone supplementation on blood ketone, glucose, triglyceride, and... - 0 views

www.ncbi.nlm.nih.gov/...PMC4743170

ketones ketone bodies ketone salts BHB Beta-hydroxybutyrate MCT MCTs medium chain triglycerides

shared by Nathan Goodyear on 21 Nov 16 - No Cached
  • Nathan Goodyear on 21 Nov 16
     
    animal study finds increased BHB after ketone salt supplementation.  A resultant decrease in glucose was found.  The use of ketone salts was with concomitant MCT.  The effect was in 30-60 minutes and sustained, significantly for 8 hours.  Weight loss was also seen.  No change in cholesterol and triglycerides was seen.
Nathan Goodyear

Dietary fiber and the short-chain fatty acid acetate promote resolution of neutrophilic... - 0 views

www.jleukbio.org/...275.abstract

SCFA fiber diet nutrition inflammation gout gut bacteria gut gut flora gut microbiome gut microbiota

shared by Nathan Goodyear on 09 Jan 17 - No Cached
  • Nathan Goodyear on 09 Jan 17
     
    new animal study finds that high fiber diet intake increases gut flora SCFA production that reduces inflammation in gout
Nathan Goodyear

International Journal of Obesity - The type and quantity of dietary fat and carbohydrat... - 0 views

www.nature.com/...ijo201233a.html

carbohydrates diet indued obesity DIO fats fat dietary metabolic syndrome obesity

shared by Nathan Goodyear on 09 Sep 13 - No Cached
  • Nathan Goodyear on 09 Sep 13
     
    Diet intake effects gut bacterial balance which effects metabolism and obesity risk.
Nathan Goodyear

Randomized controlled trial of maternal omega-3 long-chain PUFA supplementation during ... - 0 views

ajcn.nutrition.org/...ajcn.113.069203.abstract

pregnancy n-3 omega-3 omega 3 DHA docosahexaenoic acid attention memory

shared by Nathan Goodyear on 27 Feb 14 - No Cached
  • Nathan Goodyear on 27 Feb 14
     
    randomized study finds no difference in attention, memory in children born to mothers supplementing with DHA.  Good randomized design, but several problems.  First, did these women need supplementation.  No testing was done to determine need.  They may have needed more or none at all--the standard throw a dart on the wall and hope it sticks paradigm.  Second, Neurologcial development starts from day one, so do properly determine effect, the authors need to start support at conception or even better- before.  This follows that logic that women desiring conception should start extra folic acid 3 months prior. The literature is moving in the right direction, but they are still limiting themselves.  
Nathan Goodyear

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

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • 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
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • 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
  • ...56 more annotations...
  • 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
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • 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
  • 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
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • 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
  • 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
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • 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
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • 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.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • 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
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • 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
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • 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
  • 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
  • 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
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • 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
  • 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
  • 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
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • 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
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • 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
  • 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
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
wheelchairindia9

Hand Driven Tricycle India - 0 views

www.wheelchairindia.com/...ard-Single-Hand-Drive-Tricycle

Various Types Of Tricycle For Handicapped tricycle for handicapped children special needs tricycles strength and coordination hand driven tricycle india

shared by wheelchairindia9 on 18 Apr 15 - No Cached
  • wheelchairindia9 on 18 Apr 15
     
    Tricycle is also better and will enable the rider to make sharper turns on roads. Every time a person needs to be seated in a conventional tricycle or disembark from it, the needs help. But attached footrests to help the rider. With a bigger seat and stronger tyres, the vehicle will also help vendors. And every part of the cycle can be dismantled too, which makes it easier to transport. Although tricycles are often associated with toddlers, they are also widely ridden by adults. 'Trikes' are often ridden by older adults or people with disabilities who prefer the extra balance offered by a third wheel. Characteristics of Tricycles: Three wheels. Easily balanced. Brakes. Gears. Often have a storage basket at the rear. Can buy electric powered tricycles. In tricycles distinct types of pedal-driven motion. The tricycle was conceived and produced especially for children from the outset, however bicycles for children were derived by a simple reduction of the scale of the adult counterpart. Standard Single Hand Drive Tricycle: Frame : Made by E.R.W. Tubes 22.22 mm- 18 G. Seat & Back : MS, CRC Sheet Seat Size 18"x 16" Wheel Size : Wheel Diameter 28"x 1 1/2" Tyre and Tube Standard Company. Parts : Standard Quality Color : Black Painted Brake : Front Wheel liver System Drive : Rear Wheel Right Side Tricycle with rear wheel chain-driven transmission and a diamond shaped frame, it quickly entered into widespread use for transportation, work, and leisure purposes. Tricycles are available to accommodate a vast array of special needs. Hand-pedaled recumbent tricycles make it possible for those without the use of their legs. Children, teens and adults with cerebral palsy and similar disorders can select tricycles specially designed to increase strength and coordination. Caregivers to autistic children can ride with their child on tandem special needs tricycles built to accommodate one adult and one child rider.
wheelchairindia9

Tricycle Manufacturers - 0 views

www.wheelchairindia.com/...TRICYCLE

Comfortable Ergonomics For Wheelchair Users lightweight frames and seats Tricycle Manufacturers increase strength and coordination durability and safety Karman Ergonomic Wheelchair upper body strength

shared by wheelchairindia9 on 13 May 15 - No Cached
  • wheelchairindia9 on 13 May 15
     
    Tricycles make cycling accessible to all, whatever personal challenges. There are a wide range of disability cycles that suit people with a variety of learning and physical disabilities, as well as health issues. Tricycles have 3 wheels, which means that the rider does not need to be able to balance. This is particularly useful for people with learning disabilities, such as Dyspraxia, and those recovering from illnesses. Tricycles can be fitted with foot plates to make it easier for riders to rotate the pedals and they come in upright or recumbent (horizontal sitting position). For adults and children with balance issues, stabilisers can also be fitted to standard bikes, which makes them more like tricycles. Tricycles come in a variety of accessible styles for people of all abilities including many persons with spinal cord injury disabilities. Tricycles is a great upper body workout and can provide a great sense of freedom for persons with disabilities. While the high cost prevents many from enjoying Tricycles they are steadily growing in popularity. Tricycle Deluxe Double Hand Drive: Frame : Made by E.R.W. Tubes 38.0 mm-16 G. 25.4 mm & 22.22 mm- 18 G. Seat & Back: M S, C.R.C. Sheet. Seat Size 18"x 16" Wheel Size: Wheel Diameter 24"x 1 1/2" Tyre and Tube Standard Company. Parts: Standard Quality. Color: Black Painted. Brake: Front Wheel liver System Drive: Rear Wheel Right Side. Hand powered cycles work along the same principle as standard cycles. The pedals are replaced with handles that also steer, and riders use their arms to push the handles around to drive the chain and wheels. Most hand cycles have 3 wheels, although some have 4 wheels. 4-wheel cycles may have power assistance instead of the rider turning handles,or they may be built for going down hill, in which case gravity powers the bike. As with tricycles, hand cycles can have upright seats or low down recumbent seats. Specialist 'clip on' cycles are also available that can be attached
Nathan Goodyear

The effect of long-term supplementation with branched-chain amino acid granules in pati... - 0 views

www.ncbi.nlm.nih.gov/...23090049

BCAA amino acids HCV hepatitis hepatitis C liver disease cancer hepatocellular

shared by Nathan Goodyear on 20 May 15 - No Cached
  • Nathan Goodyear on 20 May 15
     
    BCAA improve overall survival in HCV related liver cancer.
Nathan Goodyear

Clinical significance of therapy using branched-chain amino acid granules in patients w... - 0 views

onlinelibrary.wiley.com/...full

hepatitis C hepatitis BCAA amino acids liver disease cancer hepatocellular

shared by Nathan Goodyear on 20 May 15 - No Cached
  • Nathan Goodyear on 20 May 15
     
    BCAA reduces incidence of hepatocellular cancer in patients with HCV.
Nathan Goodyear

Oral supplementation with branched-chain amino acid granules prevents hepatocarcinogene... - 0 views

www.ncbi.nlm.nih.gov/...23607436

BCAA amino acids liver disease cancer HCV hepatitis C hepatocellular cirrhosis hepatitis

shared by Nathan Goodyear on 20 May 15 - No Cached
  • Nathan Goodyear on 20 May 15
     
    Study finds 12 g/day BCAA reduced the incidence of hepatocellular carcinoma in those patients with HCV.
Nathan Goodyear

Metabolic Effects of Dietary Fiber Consumption and Prevention of Diabetes - 0 views

jn.nutrition.org/...439.long

soluble insoluble fiber dietary diet nutrition diabetes

shared by Nathan Goodyear on 22 Oct 13 - No Cached
  • DF are highly complex substances that can be described as any nondigestible carbohydrates and lignins not degraded in the upper gut
  • Commonly, DF are classified according to their solubility in water, even though grading according to viscosity, gel-forming capabilities, or fermentation rate by the gut microbiota might be physiologically more relevant
  • Main sources of soluble DF are fruits and vegetables
  • ...8 more annotations...
  • n increased intake of total DF was inversely associated with markers of insulin resistance in several studies
  • consumption of insoluble DF increased whole body glucose disposal independent of changes in body weight in both short-term and more prolonged studies
  • Short-chain fatty acids (SCFA) such as acetate, propionate, and butyrate are produced by bacterial fermentation of indigestible DF polysaccharides in the colon
  • increased production of SCFA is assumed to be beneficial by reducing hepatic glucose output and improving lipid homeostasis
  • a high DF diet (oligofructose) reduced gram-negative bacterial content and body weight, whereas a high fat diet increased the proportion of a gram-negative bacterial lipopolysaccharides (LPS) containing microbiota in humans
  • Prospective cohort studies indicate that diets high in insoluble cereal DF and whole grains might reduce diabetes risk
  • soluble DF (i.e., pectin, inulin, and β-glucans)
  • cereal DF (i.e., cellulose and hemicelluloses)
  • Nathan Goodyear on 22 Oct 13
     
    Good discussion of dietary fiber intake and Diabetes.  
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