GLORIA

GEOMAR Library Ocean Research Information Access

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Hauppauge :Nova Science Publishers, Incorporated,
    Keywords: Fructose in human nutrition. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (180 pages)
    Edition: 1st ed.
    ISBN: 9781620811917
    Series Statement: Nutrition and Diet Research Progress
    Language: English
    Note: Intro -- FRUCTOSE -- FRUCTOSE -- CONTENTS -- PREFACE -- UNHEALTHY DIET INTAKE DURING THE PERI-NATAL AND ADULT PERIODS: DETRIMENTAL NEUROENDOCRINE AND METABOLIC EFFECTS -- ABSTRACT -- 1. INTRODUCTION -- 2. MATERIALS AND METHODS -- 2.1. Experimental Design I: Impact of FRD Consumption by the Lactating Mother on Metabolic and Neuroendocrine Functions in the First Male Offspring in the Adult Age -- 2.1.1. Animals and Diets -- 2.1.2. Studies Performed in Basal Condition -- 2.1.3. Glucose Tolerance Test (GTT) -- 2.1.4. Hypothalamic Sensitivity to Leptin -- 2.1.5. Morphological Characteristics of the AT -- 2.1.6. Isolation and Incubation of RPAT Cells -- 2.1.7. Measurement of Peripheral Biomarkers -- 2.1.8. Tissue RNA Isolation and Real-Time PCR -- 2.1.9. Medial Basal Hypothalamus: Western Blot Analysis -- 2.2. Experimental Design II: Impact of FRD Consumption by the Naive Adult Male Rat -- 2.2.1. Animals and Diets -- 2.2.2. Chemicals -- 2.2.3. Peripheral Metabolite Measurements -- 2.2.4. Glucose Tolerance Test (GTT) -- 2.2.5. Histological Studies in AAT -- 2.2.6. Enzymatic Antioxidant Activities and Lipid Soluble Antioxidants in AAT -- 2.2.7. Thiobarbituric acid Reactive Substances (TBARS) Measurement -- 2.2.8. Lipid Composition in AAT -- 2.2.9. Leptin Release by AAT -- 2.2.10. Gene Expression in AAT -- 3. STATISTICAL ANALYSIS -- 4. RESULTS -- 4.1. Experiment 1: FRD Administration to Normal Lactating Mothers: Neuroendocrine and Metabolic Impact on the First Adult Male Offspring -- 4.1.1. Body Weight, Energy Intake and Peripheral Metabolites in Lactating Mothers -- 4.1.2. Impact of FRD Administration to Lactating Mothers upon Offspring BW, Food Intake and Peripheral Biomarkers -- 4.1.3. Peripheral Adipokine Profile in 60 Day-old Male CD and FRD Rats -- 4.1.4. GTT in Adult Male Offspring from CD or FRD Lactating Mothers. , 4.1.5. Adult Offspring RPAT: Morphological Characteristics and Function -- 4.1.6. Hypothalamic Circuitry Controlling Food Intake in Adult Male Rats -- 4.1.7. Leptin Sensitivity in the CD and FRD Offspring -- 4.2. Experiment II: Effect of Short-Time FRD Administration to Naive Adult Male Rats -- 4.2.1. Dietary Intake, BW and Peripheral Biomarkers in Adult CD and FRD Male Rats -- 4.2.2. FRD-induced Modifications in AAT Mass and Adipocyte Characteristics -- 4.2.3. Impact of FRD on AAT FA Composition/Release and Redox State -- 4.2.4. Adipokines, IRS-1 and IRS-2 mRNAs Expressions in AAT Pads -- 4.2.5. In Vitro Leptin Secretion by Isolated Adipocytes from CD and FRD Rats -- 5. DISCUSSION -- 5.1. Detrimental Long-term Effect of Feeding Lactating Mothers with a FRD upon the Offspring's Health -- 5.2. FRD Administration to Adult Rats and Adiposity Dysfunction -- CONCLUSION -- ACKNOWLEDGMENT -- REFERENCES -- HIGH-FRUCTOSE CONSUMPTION AND METABOLIC DISEASES -- ABSTRACT -- INTRODUCTION -- BIOCHEMICAL CHARACTERISTICS -- SOURCES OF FRUCTOSE -- FRUCTOSE CONSUMPTION -- METABOLIC ASPECTS OF FRUCTOSE -- Intestinal absorption -- Hepatic Metabolism -- First Steps of Fructose and Glucose Metabolism -- Metabolic Fate of Triose-P from Fructose -- Endogenous Fructose Production -- Ectopic Lipid Deposition -- FRUCTOSE AND EXERCISE -- EFFECTS OF DIETARY FRUCTOSE -- Dyslipidemia -- Obesity and Fructose -- Uric acid and Fructose -- Hypertension and Fructose -- Metabolic Syndrome / Insulin Resistance / Diabetes -- CONCLUSION -- REFERENCES -- FRUCTOSE AND NON-ALCOHOLIC FATTY LIVER DISEASE -- ABSTRACT -- INTRODUCTION -- FRUCTOSE CATABOLISM IN THE LIVER -- FRUCTOSE CONSUMPTION AND ITS IMPACT ON BODY MASS -- EFFECT OF FRUCTOSE ON INSULIN SENSITIVITY: -- IMPACT OF FRUCTOSE ON LEPTIN SIGNALING -- IMPACT OF FRUCTOSE ON GHRELIN SECRETION. , Fructose Consumption and Hepatic Inflammation -- HIGH FRUCTOSE CONSUMPTION AND CARDIOVASCULAR DISEASE -- ASSOCIATION OF FRUCTOSE CONSUMPTION WITH NON-ALCOHOLIC FATTY LIVER DISEASE -- MECHANISTIC INSIGHT INTO FRUCTOSE-INDUCED FATTY LIVER DISEASE -- CONCLUSION -- ACKNOWLEGMENT -- REFERENCES -- DETRIMENTAL EFFECTS OF EXCESSIVE FRUCTOSE INGESTION ON MEMORY AND OTHER BRAIN FUNCTIONS -- ABSTRACT -- INTRODUCTION -- PERIPHERAL EFFECTS -- CENTRAL EFFECTS -- POSSIBLE MECHANISMS -- PHYSIOLOGICAL RELEVANCE -- CONCLUSION -- REFERENCES -- ROLE OF FRUCTOSE IN BODY FUNCTIONS: AN OVERVIEW -- ABSTRACT -- INTRODUCTION -- Fructose Synthesis -- SPECIFIC FUNCTION OF FRUCTOSE -- Health Implication of Fructose -- Fructose and Insulin Resistance -- Fructose and Diabetes Mellitus -- Fructose and Obesity -- Fructose and Non Alcoholic Fatty Liver (NAFLD) -- Fructose and Metabolic Syndrome -- Fructose and Uric Acid -- Fructose, Advanced Glycation End-Products, and Aging -- Functional Bowel Disturbances -- CONCLUSION -- REFERENCES -- FRUCTOSE FACILITATES ALCOHOL METABOLISM -- DEFINITION, DISCOVERY AND PROBLEMS OF ALCOHOL -- ALCOHOL PHARMACOKINETICS -- The Oxidative Metabolism of Ethanol -- BIOCHEMICAL BASIS OF THE METABOLIC CONSEQUENCES OF ALCOHOL -- ALCOHOLISM AND RELATED PROBLEMS -- Clinical Presentations of Alcoholism -- TREATMENT OF ALCOHOL-INDUCED PROBLEMS -- FRUCTOSE ACCELERATES BLOOD ETHANOL ELIMINATION RATE (BEER) -- Mechanisms of the Stimulatory Effect of Fructose on Blood Ethanol Elimination Rate (BEER) -- Challenges of the "Fructose Effect" -- HONEY AND ALCOHOL METABOLISM -- REFERENCES -- FRUCTOSE AND THE CONTROL OF FOOD INTAKE -- ABSTRACT -- INTRODUCTION -- Fructose and Obesity Animal Models -- Sugar Solution Access and the Control of Food Intake -- The 11 HSD Hypothesis and Fructose -- mRNA in Liver and Mesenteric Adipose 11β-HSD-1 mRNA. , Sugar Solutions and the Hypothalamus -- Do Different Sugars Affect the Controls of Intake Differently? -- CONCLUSION -- ACKNOWLEDGMENT -- REFERENCES -- ABBREVIATIONS -- EFFECT OF FRUCTOSE ON HEALTH -- ABSTRACT -- INTRODUCTION -- BENEFICIAL EFFECTS OF FRUCTOSE -- Lactulose Stimulates the Growth of Health-Promoting Bacteria in the Gastrointestinal Tract, and Inhibits Growth of Pathogenic Bacteria -- Dietary Fructooligosaccharides and Potential Benefits on Health -- Calcium Fructoborate Reduces Exacerbated Cellular Immune Responses Induced by Fusarium Toxins -- DELETERIOUS EFFECTS OF FRUCTOSE -- The Role of Fructose-Enriched Diets in Mechanisms of Nonalcoholic Fatty Liver Disease -- Fructose: A Highly Lipogenic Nutrient Implicated in Insulin Resistance, Hepatic Steatosis, and the Metabolic Syndrome -- Fructose-Induced Increase in Ethanol Metabolism and the Risk of Syndrome X -- Metabolic and Behavioural Effects of Sucrose and Fructose/Glucose Drinks -- Fructose and Changes in Triglyceride or Body Weight -- A High-Fructose Diet Worsens Eccentric Left Ventricular Hypertrophy in Experimental Volume Overload -- Fructose and Hypertension -- Nutrition and Alzheimer's Disease: The Detrimental Role of a High Carbohydrate Diet -- Increased Fructose Intake as a Risk Factor for Dementia -- Aqueous Extract of Globularia Alypum Decreases Hypertriglyceridemia and Ameliorates Oxidative Status of the Muscle, Kidney, and Heart in Rats Fed a High-Fructose Diet -- Grape Seed Extract Supplementation Prevents High-Fructose Diet-Induced Insulin Resistance in Rats By Improving Insulin and Adiponectin Signalling Pathways -- Effects of a Maternal Diet Supplemented with Chocolate and Fructose Beverage during Gestation and Lactation on Rat Dams and their Offspring. , Maternal Fructose Intake during Pregnancy and Lactation Alters Placental Growth and Leads to Sex-Specific Changes in Fetal and Neonatal Endocrine Function -- DISCUSSION -- REFERENCES -- MAMMALIAN TRIOKINASE AND DIHYDROXYACETONE KINASE ARE THE SAME ENZYME -- ABSTRACT -- INTRODUCTION: FRUCTOSE METABOLISM -- THE REPORTED PROPERTIES OF TRIOKINASE -- DIHYDROXYACETONE KINASE -- "TRIOKINASE" IS THE SAME ENZYME AS DIHYDROXYACETONE KINASE -- CONCLUSION -- REFERENCES -- INDEX.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 92 (2005), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Neuroinflammation is associated with a variety of CNS pathologies. Levels of tumor necrosis factor-alpha (TNF-α), a major proinflammatory cytokine, as well as extracellular ATP, are increased following various CNS insults. Here we report on the relationship between ATP/P2 purinergic receptor activation and lipopolysaccharide (LPS)-induced TNF-α release from primary cultures of rat cortical astrocytes. Using ELISA, we confirmed that treatment with LPS stimulated the release of TNF-α in a concentration and time dependent manner. ATP treatment alone had no effect on TNF-α release. LPS-induced TNF-α release was attenuated by 1 mm ATP, a concentration known to activate P2X7 receptors. Consistent with this, 3′-O-(4-Benzoyl)benzoyl-ATP (BzATP), a P2X7 receptor agonist, also attenuated LPS-induced TNF-α release. This reduction in TNF-α release was not due to loss of cell viability. Adenosine and 2-chloroadenosine were ineffective, suggesting that attenuation of LPS-induced TNF-α release by ATP was not due to ATP breakdown and subsequent activation of adenosine/P1 receptors. Interestingly, treatment of astrocyte cultures with 10 µm or 100 µm ATP potentiated TNF-α release induced by a submaximal concentration of LPS. UTP and 2methylthioADP (2-MeSADP), P2Y receptor agonists, also enhanced this LPS-induced TNF-α release. Our observations demonstrate opposing effects of ATP/P2 receptor activation on TNF-α release, i.e. P2X receptor activation attenuates, whereas P2Y receptor activation potentiates TNF-α release in LPS-stimulated astrocytes. These observations suggest a mechanism whereby astrocytes can sense the severity of damage in the CNS via ATP release from damaged cells and can modulate the TNF-α mediated inflammatory response depending on the extracellular ATP concentration and corresponding type of astrocyte ATP/P2 receptor activated.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...