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Nathan Goodyear

Ghrelin-Induced Food Intake Is Mediated via the Orexin Pathway - 0 views

endo.endojournals.org/...1506.long

ghrelin orexin orexins appetite

shared by Nathan Goodyear on 28 May 13 - No Cached
  • Ghrelin, a peptide produced in the stomach and hypothalamus, stimulates feeding and GH secretion
  • Centrally administered ghrelin exerts an orexigenic activity through the neuropeptide Y (NPY)
  • though ghrelin is predominantly produced in endocrine cells of the stomach (17, 18), it is also synthesized in the hypothalamic arcuate nucleus (1, 19), a critical region for feeding
  • Nathan Goodyear on 28 May 13
     
    ghrelin stimulates feeding through orexin signaling.
Nathan Goodyear

International Journal of Obesity - Breast-feeding and childhood obesity[mdash]a systema... - 0 views

www.nature.com/...0802758a.html

Breast-feeding childhood obesity

shared by Nathan Goodyear on 23 Aug 11 - No Cached
  • Nathan Goodyear on 23 Aug 11
     
    breast feeding appears to reduce obesity rates in children
Nathan Goodyear

Inhibitory effect of breast milk on inf... [Pediatr Infect Dis J. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20442687

vaccine vaccination Breast-feeding

shared by Nathan Goodyear on 23 Jan 12 - No Cached
  • Nathan Goodyear on 23 Jan 12
     
    absolutely crazy recommendation from authors of study from CDC: delay breast-feeding to improve effectiveness of rotavirus vaccine.  This was because the study proposed that the IgA from the mother's breast milk reduced the potency of the vaccine.  
Nathan Goodyear

Gut microbiota of healthy Canadian infants: profiles by mode of delivery and infant die... - 0 views

www.cmaj.ca/385

gut flora dysbiosis microbiota Cesarean delivery C_S breast feeding children pediatrics infants

shared by Nathan Goodyear on 17 Feb 14 - No Cached
  • Nathan Goodyear on 17 Feb 14
     
    Cesarean delivery and lack of breast feeding significantly alter gut flora.  This has potential significant metabolic consequences--diabetes, asthma, obesity...The urge to deliver at convenient times may lay the foundation for our metabolic crisis in the US.
Nathan Goodyear

Duration of Breastfeeding and Risk of Overweight: A Meta-Analysis - 0 views

aje.oxfordjournals.org/...397.abstract

breast feeding obesity overweight pediatrics children GI bifidobacteria

shared by Nathan Goodyear on 25 Aug 11 - No Cached
  • Nathan Goodyear on 25 Aug 11
     
    the longer breast feeding occurs, the lower the risk of obesity/overweight in the child.  One role is the resultant GI colonization with bifidobacteria.
Nathan Goodyear

Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Re... - 0 views

pharmrev.aspetjournals.org/...162.full

orexin orexins sleep energy

shared by Nathan Goodyear on 02 Jan 13 - No Cached
  • Nathan Goodyear on 02 Jan 13
     
    great read on orexins!  Orexins play a role in feeding and in sleep/wake cycle. Orexins interact with the limbic system to play a role in reward.
Nathan Goodyear

Glioblastoma Cells Require Glutamate Dehydrogenase to Survive Impairments of Glucose Me... - 0 views

cancerres.aacrjournals.org/...7986.full.pdf

cancer Glioblastoma EGCG glutamine glucose

shared by Nathan Goodyear on 29 Jun 13 - No Cached
  • Nathan Goodyear on 29 Jun 13
     
    This article describes how important glutamine is as an alternative energy source in Glioblastoma. Cancer is a substrate-level dependent energy production disease. If one disrupts glycolysis as a source of energy, then many cancers will use glutamine through glutaminolysis. The cancer cells will do this through glutamate dehydrogenase and glutamate production. This will increase alpha-ketoglutarate which will then feed the substrate-level phosphorylation through the TCA cycle. This study mentioned that EGCG is a way to naturally inhibit glutamate dehydrogenase.
Nathan Goodyear

Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up - 0 views

endo.endojournals.org/...4109.full

inflammation obesity overweight hypothalamus HPA

shared by Nathan Goodyear on 04 Oct 12 - No Cached
  • Leptin, secreted by adipocytes in proportion to body fat mass
  • The saturated fatty acid palmitate (16:0) induces NF-κB signaling through a TLR4-dependent mechanism
  • 18:0 (stearic) and longer saturated fatty acids as well as linolenic acid (18:3) increased proinflammatory cytokines, ER stress markers, and TLR4 activation
  • ...6 more annotations...
  • (SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling
  • IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding
  • the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule
  • , serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]
  • and stimulating anorexigenic neurons
  • signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids
  • Nathan Goodyear on 04 Oct 12
     
    great read on the current understanding of how obesity and resultant inflammation disrupts hypothalamic function.
Nathan Goodyear

Ketone bodies as a fuel for the brain during starvation - Owen - 2005 - Biochemistry an... - 0 views

onlinelibrary.wiley.com/...full

ketones ketone bodies brain nutrition diet ketogenic diet ketogenic

shared by Nathan Goodyear on 17 Nov 16 - No Cached
  • Nathan Goodyear on 17 Nov 16
     
    Ketones, acetoacetate, beta-hydroxybutyrate, and acetone, feed the brain independent of glucose.
Nathan Goodyear

Sugar in Children's Cereals | Environmental Working Group - 0 views

breakingnews.ewg.org/...sugar_in_childrens_cereals

breakfast cereal healthy sugar children

shared by Nathan Goodyear on 08 Dec 11 - No Cached
  • Nathan Goodyear on 08 Dec 11
     
    great resource to make healthy breakfast cereal choices for your family.  You would never think to feed your family twinkies for breakfast, but the sugar content of many cereals is doing just that.
Nathan Goodyear

ingentaconnect The Role of Orexin System in Antipsychotics Induced Weight Gain - 0 views

www.ingentaconnect.com/...art00002

orexin eating feeding weight-loss overweight obesity weight gain

shared by Nathan Goodyear on 02 Dec 11 - No Cached
  • The orexins modulate feeding behavior, some metabolic processes and arousal.
  • Nathan Goodyear on 02 Dec 11
     
    antipsychotics are associated with significant weight gain.  One proposed mechanism is the increased activation of orexin neurons in the areas of the brain (lateral hypothalamus and perifornical area) that regulate eating.  Amphetamines stimulate the same, just a drastically reduced levels
Nathan Goodyear

TO EAT OR TO SLEEP? OREXIN IN THE REGULATION OF FEEDING AND WAKEFULNESS - Annual Review... - 0 views

www.annualreviews.org/...annurev.neuro.24.1.429

orexin sleep narcolepsy eating feeding overweight weight-loss obesity

shared by Nathan Goodyear on 02 Dec 11 - No Cached
  • Nathan Goodyear on 02 Dec 11
     
    orexin: neuropeptide involved in regulation of sleep and eating.  Effected by stress. Suprise, suprise
Nathan Goodyear

Gut Microbiota, Low-grade Inflammation, and Metabolic Syndrome. - ResearchGate - 0 views

www.researchgate.net/...mmation_and_Metabolic_Syndrome

gut inflammation metabolic syndrome microbiota dysbiosis

shared by Nathan Goodyear on 17 Feb 14 - No Cached
  • Nathan Goodyear on 17 Feb 14
     
    Gut dysbiosis can be the cause of chronic inflammation that results in metabolic syndrome.  This can be, in part, precipitated by delivery, breast feeding, and diet.
Nathan Goodyear

Reduced breast cancer incidence in women treated with subcutaneous testosterone, or tes... - 0 views

www.maturitas.org/...abstract

Testosterone aromatase breast cancer anastrazole women female hormone hormones

shared by Nathan Goodyear on 20 Mar 14 - No Cached
  • Nathan Goodyear on 20 Mar 14
     
    Study finds that Testosterone with or with the aromatase inhibitor anastrazole as a pellet reduced breast cancer risk.  This conclusion should be taken with caution.  It is well know that abnormal breast tissue, breast cancer, highly expresses aromatase activity which would increase Testosterone to estradiol production.  This would feed any growing tumor.  But, this study finds protection.  The failure of this study is the measurement of hormone levels.
Nathan Goodyear

Endogenous Steroid Hormone Concentrations and Risk of Breast Cancer Among Premenopausal... - 0 views

jnci.oxfordjournals.org/...1406.long

hormone hormones Testosterone free total estradiol breast cancer women female

shared by Nathan Goodyear on 21 Mar 14 - No Cached
  • Nathan Goodyear on 21 Mar 14
     
    Prospective study finds that elevated total and free Estradiol levels in the follicular phase and elevated total and free Testosterone levels in both the follicular and luteal phase are associated with increased breast cancer in women.  The risk is for pre menopause in this study.  This and several other studies point to serious questions about the massive dosing of Testosterone via pellets, injections, and topicals for libido.  We appear to be following the same patter as seen with premarin, provera, now Testosterone in men and this may be the next ball to drop.  Is the Testosterone therapy merely producing an environment that feeds breast cancer?
Nathan Goodyear

Metabolic syndrome as a prognostic factor for breast cancer recurrences - Pasanisi - 20... - 0 views

onlinelibrary.wiley.com/...full

Testosterone women metabolic syndrome metabolic syndrome breast cancer

shared by Nathan Goodyear on 12 Mar 14 - No Cached
  • Nathan Goodyear on 12 Mar 14
     
    Women with metabolic syndrome have increased recurrence of breast cancer after initial therapy.  Likewise, Increasing Testosterone was associated with increasing risk of metabolic syndrome.  This is the opposite of men.  One wonders what this massive doping of Testosterone that is underway is doing to women?  Are we merely feeding disease?
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.
Nathan Goodyear

Metformin Use and All-Cause and Prostate Cancer-Specific Mortality Among Men With Diabetes - 0 views

jco.ascopubs.org/...JCO.2012.46.7043.abstract

prostate diabetes cancer mortality metformin

shared by Nathan Goodyear on 13 Aug 13 - No Cached
  • Nathan Goodyear on 13 Aug 13
     
    Study out of Canada finds that Metformin reduces mortality rates for all-cause and due to prostate cancer in those with diabetes.  The key point here is glucose.  Metformin is going to inhibit gluconeogenesis and this limit hepatic glucose production feeding the cancer.  This is just the abstract and several questions come to mind: what was the glucose control like in these patients?  What dietary changes if any were these patients following?  A better study would be to compare the effects of a ketogenic diet with restriction of glutamine versus the metformin.
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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