Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Bruno Sopko Introduction Macronutrients ◦ Aminoacids, proteins ◦ Carbohydrates ◦ Fatty acids, cholesterol Regulation of macronutrient uptake Micronutriets ◦ Fat-soluble vitamins ◦ Water-soluble vitamins ◦ Minerals Energy and nutrition homeostasis ◦ ◦ ◦ ◦ Exogenous Inputs–Environmental Signals Metabolic Signals Endocrine Signals Neural Signals Genes and Gene–Environment Interactions Aminoacids, proteins Carbohydrates Fatty acids, cholesterol Fiber Digestion, absorption of the proteins Protein turnover Essential aminoacids Interorgan cooperation AA transport into the cell Regulation of AA metabolism - anabolic Regulation of AA metabolism - catabolic Effect of AA on glucagon and insulin secretion Nitrogen balance Glucagon activates phenylalanine hydroxylase by an adenosine 3′5′-cyclic monophosphate (cAMP)-dependent mechanism. Glucagon activates glutaminase and the glycine cleavage enzyme, although the mechanism of these effects remains obscure. Glucagon and glucocorticoids induce the synthesis of a number of amino acid catabolising enzymes. Carbohydrates – intake Carbohydrates - regulation Adipose tissue hormones ◦ Leptin Panecreatic hormones GIT hormones Glucagon Insulin Pancreatic Polypeptide ◦ Reduces apetite by unknown mechanism Amylin ◦ Reduces food intake Ghrelin (produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas) ◦ appetite-regulating hormone (leptin antagonist) ◦ growth hormone secretagogue Peptide YY (ileum and colon) ◦ potential proabsorptive hormone ◦ reduce appetite Incretins : Glucagon -Like Peptides (GLP-1,2) and Glucose -Dependent Insulinotropic Peptide (gut) Oxyntomodulin (Parietal cells - stomach epithelial cells that secrete gastric acid (HCl) and intrinsic factor) ◦ suppress appetite Cholecystokinin (I-cells in the mucosal epithelium) Bombesin - like Peptides Apo A-IV (intestine) Enterostatin (intestine by pancreatic procolipase) Obestatin (produced from the same prohormon as ghrelin) ◦ release of digestive enzymes and bile from the pancreas and gallbladder ◦ hunger suppressant ◦ inducing drug tolerance to opioids ◦ gastrin-releasing peptide (GRP) ◦ Neuromedin B (NMB) ◦ activate lecithin-cholesterol acyltransferase and cholesterylester transfer protein in vitro; ◦ play a role in the regulation of appetite and satiety in rodent models; ◦ display anti-oxidant and anti-atherogenic properties in vitro and in rodent models; ◦ modulate the efficiency of enterocyte and hepatic transcellular lipid transport in vitro. ◦ reduction of insulin secretion ◦ increase in sympathetic drive to brown adipose tissue ◦ stimulation of adrenal corticosteroid secretion ◦ initiates a sensation of fullness of stomach ◦ antagonise growth hormone secretion and food intake induced by ghrelin Lipid soluble vitamins ◦ Vitamin A Water soluble vitamins Minerals hydrophobic compounds, absorbed efficiently with lipids, transport in the blood in lipoproteins or attached to specific binding proteins, more likely to accumulate in the body, more likely to lead to hypervitaminosis Retinol Biologically active forms retinoids: retinol, retinal, retinoid acid. Major vit. A precursors (provitamins) → plants carotenoids. Foodstaf of animals origin contain most of vit. A in the form of esters (retinylpalmitates) – retinol and long fatty acid Cyklohexan ring and isoprenoid chain Retinol esters → hydrolysis by pancreatic enzymes to retinol. b-caroten is cleaved to retinal by bcarotene 15,15´ dioxygenase (cofactors iron and bile salts). Intestinal cells → esterification of retinol → transported in chylomicrons. Remnants of chylomicrons → liver→ esterification (if the concentration exceeds 100 mg, esters are stored ). Transport of retinol to target organs tightly bound to retinolbinding protein, RBP. Transcription and cell differentiation Retinoic acid regulates the transcription of genes - acts through nuclear receptors (steroid-like receptors). Retinol retinal Retinol dehydrogease retinoic acid Retinaldehyde dehydrogenasa By binding to various nuclear receptors, vit. A stimulates (RAR – retinoid acid receptor) or inhibits (RXR- retinoid „X“ receptor) transcription of genes transcription. All-trans-retinoic acid binds to RAR and 9-cis-retinoic acid binds to RXR. Retinoic acid is necessary for the function and maintenance of epithelial tissues. Vision Gene transcription Immune function Embryonic development and reproduction Bone metabolism Haematopoieis Skin health Antioxidant activity cod liver oil meat egg milk dairy products carrot broccoli spinach papaya apricots Calciol, vitamin D2 (cholecalciferol) → precursor of calcitriol, D3 (1,25-dihydroxycalciferol). Regulates with PTH calcium and phosphate level (absorption, reabsorption, excretion). Synthesis in the skin (7-dehydrocholesterol) UV → further transformation in the liver and kidneys . In addition to sunbathing: various fish species (salmon, sardines and mackerel, tuna, catfish, eel), fish oil, cod liver eggs, beef liver, mushrooms Absorbed with the food fats and is dependent on the presence of the bile salts (any disease which resulted in an impairment of fat absorption likewise resulted in an impairment of vitamin D absorption) Absorption is a passive process which is influenced by the composition of the gut contents. Absorbed with the long-chain fatty acids and is present in the chylomicrons of the lymphatic system. Vitamin E is a famil of a-, b-, g-, d- tocopherols and corresponding tocotrienols izomers. They are formed from chroman ring and hydrofobic fytyl side chain. The highest biological activity has a-tokoferol. Absorbtion from the small intestine (50 %) Its absorption is dependent on the presence of lipids in the diet. Associated with plasma lipoproteins → liver uptake through receptors for apolipoprotein E. a-tocopherol is bind to a-tocopherol transport protein (a-TTP) → transported to the target organs (the excess is stored in adipocytes, in muscle, liver). b-, g- a d-tocopherols are transferred into the bile and degraded. fortified cereals seeds and seed oils, like sunflower nuts and nut oils, like almonds and hazelnuts green leafy vegetables, broccoli cabbage celery Vitamin K is a group of lipophilic, hydrophobic vitamins. They are needed for the postranslation modification of proteins required for blood coagulation, They are involved in metabolism pathways, in bone mineralisation, cell growth, metabolism of blood vessel wall. Vitamin K1 Vitamin K1 (phylloquinon) – plant origin Vitamin K2 (menaquinon) – normally produced by bacteria in the large intestine K1 a K2 are used differently in the body Vitamin K2 ◦ K1 – used mainly for blood clothing ◦ K2 – important in noncoagulation actions - as in metabolism and bone mineralization, in cell growth, metabolism of blood vessel walls cells. Synthetic derivatives of Vit.K Green leafy vegetables vegetable oil broccoli Cereals The absorption of K1 and K2 analogs occurs via an active, energy-dependent transport process, whereas K3 (menadione) analogs are absorbed by passive diffusion. Vitamin C Vitamin C is a water-soluble vitamin. Almost all animals and plants synthesize their own vitamin C, not man. Vitamin C was first isolated in 1928 and in 1932 it was proved to be the agent which prevents scurvy. Vitamin C Vitamin C is a weak acid, called ascorbic acid or its salts “ascorbates”. It is the L-enantiomer of ascorbic acid. The D-enantiomer shows no biological activity. Absorbed in the small intestine, primarily the ileum, by an active transport system - both sodium dependent and energy dependent. Cytochrome P450 oxidases (several) Dopamine-β-monooxygenase Peptidyl glycine α-amidating monooxygenase Cholesterol 7-α-hydroxylase 4 Hydroxyphenylpyruvate oxidase Homogentisate 1,2-dioxygenase Proline hydroxylase Procollagen-proline 2-oxoglutarate-3-dioxygenase Lysine hydroxylase γ-Butyrobetaine, 2-oxoglutarate-4-dioxygenase Trimethyllysine-2-oxoglutarate dioxygenase Deficiency of vitamin C Fatigue, personality changes, decline in psychomotor performance and motivation. Vitamin C deficiency over 3-5 months results in symptomatic scurvy. Scurvy leads to the formation of liver spots on the skin, spongy gums, and bleeding from all mucous membranes. In advanced scurvy there are open, suppurating wounds and loss of teeth. Severe scurvy may progress to neuritis, jaundice, fever, dyspnea, and death. Absorption Place B1-thiamine specific active transport mechanism small intestine B2-riboflavin active carrier and is energy and sodium dependent jejunum B3-niacin simple diffusion and facilitated diffusion small intestine B5-panthotenic acid facilitated diffusion small intestine B6 facilitated diffusion may exist small intestine B7-biotin facilitated diffusion jejunum B9-folic acid carrier-mediated, pHdependent jejunum B12-cobalamin B12 is bound to a carrier protein called intrinsic factor distal portion of the ileum Choline Carnitine Inositol Pyrroloquinoline Quinone Ubiquinone Orotic Acid Para-Aminobenzoic Acid (PABA) Lipoic Acid Bioflavinoids Pseudovitamins Sodium ◦ Transported with other compounds Potasium ◦ Passive transport Chloride ◦ Passive transport Calcium (20% - 50 %) ◦ Vitamin D dependent ◦ Passive diffusion Phosphorus ◦ Active, saturable, sodium-dependent mechanism (vitamin D) Magnesiun (30 % - 70 %) ◦ Passive diffusion ◦ Active diffusion Iron Zinc Copper Selenium Iodine Molybdenum Manganese Cobalt ◦ Haem bound ◦ Free ◦ Lactoferrin ◦ passive ◦ diffusion while the latter may involve the zinc-binding metallothionein protein and/or a cysteinerich ◦ intestinal protein ◦ Active diffusion ◦ Selenocysteine ◦ Iodide ion, diffusion ◦ Diffusion ◦ Unknown ◦ interfere with the absorption of iron and in fact can completely block iron uptake ◦ cobalamin Pyruvate carboxylase Acetyl CoA carboxylase Isocitrate dehydrogenase Mitochondrial superoxide dismutase Arginase Glucokinase Galactose transferrase Hydroxymethyl transferase Superoxide dismutase Literature Thomas M. Devlin ed. Textbook of biochemistry with clinical correlations, Fourth edition (1997), Wiley and sons. Christos S. Mantzoros, NUTRITION AND METABOLISM, Underlying Mechanisms and Clinical Consequences (2009), Humana Press, a part of Springer Science+Business Media Carolyn D. Berdanier (1998), ADVANCED NUTRITION, Micronutrients Others are cited directly on the pages