Endocrinology Book

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Glucose Metabolism

Aka: Glucose Metabolism, Glycolysis, Embden-Meyerhoff Pathway, Gluconeogenesis, Blood Sugar Regulation, Citric Acid Cycle, Krebs Cycle, Kreb Cycle, Tricarboxylic Acid Cycle, TCA Cycle, Carbohydrate Metabolism, Energy Metabolism, Incretin, Acetyl Coenzyme A
  1. See Also
    1. Carbohydrate Metabolism
    2. High Energy Molecule (e.g. Adenosine Triphosphate, ATP)
  2. Definitions
    1. Glycolysis (Embden-Meyerhoff Pathway)
      1. glycolysis.png
      2. glycolyticPathMolecules.png
      3. Catabolic pathway to breakdown carbohydrates (Glucose, fructose) into pyruvate, without need for oxygen
      4. Represents only a small part of the overall energy generation from carbohydrates (2 net ATP and 1 NADH)
      5. Pyruvate may then be converted to acetyl-CoA (or, when oxygen is unavailable to Lactic Acid)
        1. Acetyl CoA enters TCA Cycle for energy generation (or is used to form Triglycerides)
      6. Triggered by Insulin, which lowers Glucose via both Glycolysis as well as increasing glycogen stores
    2. Acetyl Coenzyme A (Acetyl CoA)
      1. Synthesized from Coenzyme A and acetic acid
      2. Acetyl CoA is substrate in the biosynthesis of Fatty Acids, sterols and amino acids
      3. Serves as entry point of Citric Acid Cycle
        1. Feeds it substrate from Glucose (and other carbohydrate), amino acid and Fatty Acid catabolism
    3. Citric Acid Cycle (Krebs Cycle, Tricarboxylic Acid Cycle, TCA Cycle)
      1. glycolysis.png
      2. krebCycle.png
      3. Universal pathway seen across multicellular organisms, taking place in mitochondria in humans
      4. Generates energy from Acetyl CoA (3 NADH, 1 FADH, 1 GTP) derived primarily from Glucose
      5. Intermediate steps include oxaloacetate, isocitrate, a-Ketoglutarate, succinyl-CoA, Succinate, fumarate, malate
        1. Kreb Cycle intermediates also lead to other pathways (e.g. succinyl-CoA to heme synthesis pathways)
      6. With decreased Energy Intake or increased Energy Expenditure, Glucose reserves (e.g. glycogen) are exhausted
        1. In early starvation, Fatty Acids are catabolized to acetyl CoA (and glycerol), fueling the Krebs Cycle
        2. With longer starvation, amino acids are catabolized to enter the Krebs Cycle
    4. Gluconeogenesis
      1. gluconeogenesis.png
      2. Pathway forms Glucose from 3- or 4-carbon noncarbohydrate precursors (e.g. pyruvate, amino acids and glycerol)
      3. Process takes place in the Kidneys and liver and is triggered when Insulin levels are low and in starvation states
      4. The same triggers for Gluconeogenesis also trigger Lipolysis and Ketogenesis
  3. Physiology
    1. See Gastrointestinal Metabolism
    2. Images
      1. carbohydrateMetabolism.png
      2. gluconeogenesis.png
      3. glycolysis.png
      4. glycolyticPathMolecules.png
      5. krebCycle.png
    3. Blood Glucose
      1. Released from hepatic stores between meals
      2. Derived from ingested carbohydrates
        1. Postprandial Glucose >20 fold over hepatic release
    4. Insulin
      1. See Insulin
      2. General
        1. Insulin produced by pancreatic beta cells
        2. Insulin release stimulated by Blood Glucose
        3. Insulin response to Glucose is linear
          1. Insulin response is based on Glucose sensitivity
          2. Glucose sensitivity depends on Ambient Glucose
            1. Normal: Rapid Insulin release with a meal
            2. Fasting: Steeper rate of Insulin release
            3. Prolonged Hyperglycemia: Flattened response
        4. Overall Insulin effects
          1. Promotes Glucose uptake by liver and Muscle and for storage as glycogen
            1. Does not effect brain Glucose uptake (Glucose freely crosses blood brain barrier)
          2. Promotes cellular uptake of amino acids and protein synthesis
          3. Promotes hepatic synthesis of Fatty Acids, VLDL transport to adipose for Triglyceride storage
          4. Promotes Glycolysis for energy utilization
          5. Suppresses Gluconeogenesis
      3. Phase 1 Insulin Release
        1. Duration: 10 minutes
        2. Suppresses hepatic Glucose release
      4. Phase 2 Insulin Release
        1. Duration: 2 hours
        2. Controls mealtime carbohydrates
      5. Basal Insulin Release
        1. Low continuous Insulin level
        2. Covers metabolic needs between meals
    5. Glucagon
      1. See Glucagon
      2. Endogenous polypeptide Hormone secreted by pancreatic alpha cells
      3. Opposite effect of Insulin
        1. While Insulin lowers Serum Glucose (glycogen storage, Glycolysis), Glucagon increases Serum Glucose
        2. However, both Insulin and Glucagon increase amino acid uptake from the liver
      4. Hypoglycemia effect (primary)
        1. Hypoglycemia Increases pancreatic secretion of Glucagon
        2. Glucagon stimulates Glucose release from glycogen (glycogenolysis)
        3. Glucagon also stimulates Glucose synthesis (Gluconeogenesis)
      5. Inhibitors of Glucagon release
        1. Hyperglycemia
          1. Inhibits pancreatic secretion of Glucagon
        2. GLP1 (Incretin)
          1. Secreted by Small Bowel
          2. Stimulates pancreatic beta cells and inhibits Glucagon
          3. See Incretin Mimetics (used in Type 2 Diabetes Mellitus)
      6. Amino Acid Excess Effect
        1. Increases pancreatic secretion of Glucagon
        2. Glucagon stimulates liver uptake of amino acids
          1. Both Insulin and Glucagon increase liver uptake of amino acids
      7. Acts at Catecholamine-independent receptors on cardiac cells
        1. Increases intracellular Calcium in cardiac cells
        2. Increases myocardial contractions
    6. Growth Hormone
      1. See Growth Hormone
      2. Polypeptide produced in the acidophil cells of the anterior pituitary
      3. Hypothalamus controls release when triggered by Hypoglycemia, decreased amino acids
        1. Growth Hormone Releasing Hormone (GHRH) stimulates release
        2. Somatostatin inhibits release
      4. Biochemistry
        1. Liver converts Growth Hormone to Insulin-like growth factor (IGF-1) and stimulates other growth factors
        2. Growth Hormone is a precursor to Testosterone
      5. Positive Function (stimulates or promotes the following activities)
        1. Bone and cartilage growth
        2. Protein synthesis
        3. Promotes Fatty Acid use as fuel instead of Glucose
          1. Lipid catabolism to Fatty Acids (for energy source)
          2. Hyperglycemia (from decreased cell utilization of Glucose) resulting in an increase of glycogen stores
    7. Cortisol
      1. See Cortisol
      2. Cortisol is synthesized in the Adrenal Cortex, derived from Cholesterol (See Cortisol Synthesis_
      3. Cortisol secretion is stimulated by Adrenocorticotropic Hormone (ACTH) in response to stress (See Pituitary Gland)
      4. Cortisol functionality
        1. Mobilizes available energy sources (Glucose, fats, amino acids)
          1. Increases Serum Glucose by stimulating liver Gluconeogenesis and glycogenolysis
          2. Increases serum Fatty Acids by promoting lipolysis of adipose Triglyceride stores
          3. Increases blood amino acids by breaking down proteins (outside liver)
            1. Within liver, Cortisol induces protein synthesis
        2. Antiinflammatory activity
          1. Inhibit histamine release
          2. Inhibit Lymphocyte production
          3. Stabilize MacrophageLysosomes
        3. Increases gastric acid production
    8. Epinephrine
      1. See Epinephrine
      2. Epinephrine has alpha-adrenergic effects (esp. alpha-2) specific to metabolism
        1. Increases Serum Glucose (Gluconeogenesis, Glycogenolysis)
        2. Increases Fatty Acids (Fat cell lipolysis of Triglycerides)
      3. Most of Epinephrine's primary effects are cardiopulmonary
        1. Alpha Adrenergic Agonist Effects
          1. Vasoconstriction (increased Systemic Vascular Resistance and Blood Pressure)
          2. Increases Vital Organ Perfusion (myocardial and cerebral perfusion)
          3. Decreases Non-Vital Organ Perfusion
            1. Decreases splanchnic and intestinal perfusion
            2. Decreases renal and skin perfusion
        2. Beta Adrenergic Agonist effects (Under 0.3 ug/kg/min)
          1. Increases myocardial contractility and Heart Rate
          2. Relaxes Bronchial Smooth Muscle (bronchodilation)
    9. Incretin
      1. Group of peptides
        1. Glucagon-Like Peptide-1 (GLP-1)
        2. Glucose Dependent Insulinotropic Peptide (GIP) or Gastric inhibitory peptide
      2. Functions
        1. Triggers Insulin synthesis
        2. Inhibit Glucagon secretion
        3. Decreases gastric emptying
  4. Pathophysiology
    1. Lactic Acid
      1. Generated when oxygen is unavailable to allow for Krebs Cycle related Oxidative Phosphorylation
      2. Glycolysis generates 7 net ATP/Glucose (compared with 25 for Kreb Cycle) and does not require oxygen
      3. However, Glycolysis does use NAD+ (for glyceraldehyde 3-P to 1,3P2-glycerate)
        1. NAD+ is typically replenished in the Krebs Cycle related Oxidative Phosphorylation
        2. When oxygen is unavailable, pyruvate is metabolized to Lactic Acid, regenerating NAD+
  5. Pathophysiology: Insulin
    1. Insulin excess
      1. See Hypoglcemia
      2. See Insulin Shock (Insulin Overdose, Insulin Reaction)
    2. Insulin at low levels or deficiency
      1. Causes
        1. Low Insulin due to Diabetes Mellitus
          1. In Type I Diabetes, Insulin deficiency is key
          2. In Type II Diabetes, Insulin Resistance is key initially, but later Insulin deficiency results
        2. Low Insulin as a normal physiologic response to Hypoglycemia
      2. Low Insulin effects
        1. Gluconeogenesis and Glycogenolysis results in Hyperglycemia
        2. Lipolysis (Triglyceride breakdown to Fatty Acids)
          1. Further lysed into acetyl coA to be utilized in the Kreb Cycle (TCA Cycle, Citric Acid Cycle)
          2. Other Fatty Acids are diverted to Ketogenesis (Ketone formation)
            1. Occurs in Diabetic Ketoacidosis, Starvation Ketosis, Alcoholic Ketoacidosis
          3. Fatty Acids also form excess Cholesterol, Triglycerides within VLDL with increasing atherosclerosis
  6. Pathophysiology: Type I Diabetes
    1. See Type I Diabetes Mellitus
    2. See Maturity Onset Diabetes of the Young
    3. Deficiency of Insulin, with multiple underlying mechanisms
    4. Type 1A
      1. Environmental and genetic factors
      2. HLA-DR4 association
      3. Cell mediated pancreatic beta cell destruction
    5. Type 1B (uncommon)
      1. Primary Autoimmune Condition
      2. Associated with other Autoimmune Conditions
        1. Hashimoto's Thyroiditis
        2. Grave's Disease
        3. Myasthenia Gravis
      3. HLA-DR3 association
      4. Incidence highest in 30-50 year olds
    6. Secondary Diabetes Mellitus
      1. Cystic Fibrosis
  7. Pathophysiology: Type II Diabetes Mellitus
    1. See Type II Diabetes Mellitus
    2. Loss of Glucose sensitivity (see above)
      1. Loss of phase 1 Insulin response
      2. Insufficient phase 2 Insulin response
    3. Insulin production by beta cell
      1. First: Insulin increases to overcome Glucose toxicity
      2. Results in beta-cell exhaustion (Glucose Toxicity)
        1. Initially reversible beta cell exhaustion
        2. Permanent later as amyloid replaces beta cells
      3. Insulin levels decrease as beta cells fail
        1. Beta-cell function reduced to <50% by DM diagnosis
    4. Impaired Incretin action
      1. Incretins manage postprandial Glucose levels
        1. Incretin released from GI Tract following meals
      2. Endogenous Incretin effects
        1. Increases Glucose dependent Insulin secretion
        2. Delays gastric emptying
        3. Decreases food intake (improves satiety)
      3. Progressive Incretin reduced activity
        1. Glucagon-Like Peptide 1 (GLP-1) activity decreases
    5. Medications
      1. Increase Insulin sensitivity
        1. Metformin
        2. Thiazolidinediones
      2. Stimulate Insulin release from beta cells
        1. Meglitinides (act on phase 1 release)
        2. Sulfonylureas (act on phase 2 release)
      3. Replace Insulin
        1. See Insulin
      4. Increase Incretin levels (GLP-1)
        1. Exenatide (Byetta)
        2. Sitagliptin (Januvia)
  8. References
    1. Goldberg (2014) Clinical Physiology, Medmasters, Miami, p. 120-46

Acetyl Coenzyme A (C0001026)

Definition (NCI) The condensation product of coenzyme A and acetic acid which participates in the biosynthesis of fatty acids and sterols, in the oxidation of fatty acids and in the metabolism of many amino acids. In addition, Acetyl Coenzyme A acts as a biological acetylating agent.
Definition (MSH) Acetyl CoA participates in the biosynthesis of fatty acids and sterols, in the oxidation of fatty acids and in the metabolism of many amino acids. It also acts as a biological acetylating agent.
Definition (CSP) participates in biosynthesis of fatty acids and sterols, fatty acid oxidation, metabolism of many amino acids, and acts as a biological acetylating agent.
Concepts Biologically Active Substance (T123) , Nucleic Acid, Nucleoside, or Nucleotide (T114) , Lipid (T119)
MSH D000105
SnomedCT 129915003
English Acetyl CoA, Acetyl Coenzyme A, CoA, Acetyl, Coenzyme A, Acetyl, acetyl coA, Coenzyme A, S-acetate, acetyl coenzyme A, acetyl CoA, Acetyl Coenzyme A [Chemical/Ingredient], acetyl coenzyme, acetyl coa, acetyl coenzyme a, ACETYL COENZYME A, Acetylcoenzyme A, Acetyl coenzyme A, Acetyl coenzyme A (substance), Acetyl-CoA
Swedish Acetyl-CoA
Czech acetylkoenzym A
Finnish Asetyylikoentsyymi A
Italian Acetyl-CoA, Acetyl CoA, Acetil-coenzima A
Russian ATSETIL-KOA, ATSETILKOENZIM A, ATSETILKOFERMENT A, АЦЕТИЛ-КОA, АЦЕТИЛКОФЕРМЕНТ A, АЦЕТИЛКОЭНЗИМ A
Polish Acetylo-koenzym A
Japanese アセチル-CoA, アセチルCoA, アセチルコエンザイムA, アセチルコエンチームA, アセチル補酵素A, アセチル-コエンザイムA
Norwegian Acetyl-koenzym A, Acetyl-coenzym A, Acetyl-CoA
Portuguese Acetilcoenzima A, Acetil CoA
Spanish acetilcoenzima A (sustancia), acetilcoenzima A, Acetil CoA, Acetilcoenzima A
French Acétyl-coA, Acétyl coenzyme A, Acétyl coA
German Acetyl-CoA, Acetyl-Coenzym A
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Citric Acid Cycle (C0008858)

Definition (GO) A nearly universal metabolic pathway in which the acetyl group of acetyl coenzyme A is effectively oxidized to two CO2 and four pairs of electrons are transferred to coenzymes. The acetyl group combines with oxaloacetate to form citrate, which undergoes successive transformations to isocitrate, 2-oxoglutarate, succinyl-CoA, succinate, fumarate, malate, and oxaloacetate again, thus completing the cycle. In eukaryotes the tricarboxylic acid is confined to the mitochondria. See also glyoxylate cycle. [ISBN:0198506732]
Definition (NCI_BioC) The Krebs cycle, also called the citric acid cycle, is a fundamental metabolic pathway involving eight enzymes essential for energy production through aerobic respiration, and, like glycolysis, arose early in evolution. This pathway is also an important source of biosynthetic building blocks used in gluconeogenesis, amino acid biosynthesis, and fatty acid biosynthesis. The Krebs cycle takes place in mitochondria where it oxidizes acetyl-CoA, releasing carbon dioxide and extracting energy primarily as the reduced high-energy electron carriers NADH and FADH2. NADH and FADH2 transfer chemical energy from metabolic intermediates to the electron transport chain to create a different form of energy, a gradient of protons across the inner mitochondrial membrane. The energy of the proton gradient in turn drives synthesis of the high-energy phosphate bonds in ATP, the common energy currency of the cell used to drive a huge variety of reactions and processes. An acetyl-CoA molecule (2 carbons) enters the cycle when citrate synthase condenses it with oxaloacetate (4 carbons) to create citrate (6 carbons). One source of the acetyl-CoA that enters the Krebs cycle is the conversion of pyruvate from glycolysis to acetyl-CoA by pyruvate dehydrogenase. Acetyl-CoA is a key metabolic junction, derived not only from glycolysis but also from the oxidation of fatty acids. As the cycle proceeds, the Krebs cycle intermediates are oxidized, transferring their energy to create reduced NADH and FADH2. The oxidation of the metabolic intermediates of the pathway also releases two carbon dioxide molecules for each acetyl-CoA that enters the cycle, leaving the net carbons the same with each turn of the cycle. This carbon dioxide, along with more released by pyruvate dehydrogenase, is the source of CO2 released into the atmosphere when you breathe. The Krebs cycle, like other metabolic pathways, is tightly regulated to efficiently meet the needs of the cell and the organism. The irreversible synthesis of acetyl-CoA from pyruvate by pyruvate dehydrogenase is one important regulatory step, and is inhibited by high concentrations of ATP that indicate abundant energy. Citrate synthase, alpha-ketoglutarate dehydrogenase and isocitrate dehydrogenase are all key regulatory steps in the cycle and are each inhibited by abundant energy in the cell, indicated through high concentrations of ATP or NADH. The activity of the Krebs cycle is closely linked to the availability of oxygen, although none of the steps in the pathway directly use oxygen. Oxygen is required for the electron transport chain to function, which recycles NADH back to NAD+ and FADH2 back to FADH, providing NAD+ and ADH required by enzymes in the Krebs cycle. If the oxygen supply to a muscle cell or a yeast cell is low, NAD+ and FADH levels fall, the Krebs cycle cannot proceed forward, and the cell must resort to fermentation to continue making ATP. Some Krebs cycle enzymes require non-protein cofactors for activity, such as thiamine, vitamin B1. Insufficient quantities of this vitamin in the diet leads to decreased activity of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, and a decrease in the ability of the Krebs cycle to meet metabolic demands, causing the disease beriberi. Although the elucidation of the Krebs cycle remains one of the landmarks of biochemistry, aspects of the Krebs cycle and its enzymes are still actively researched in the modern proteomic era.
Definition (CSP) series of reactions involving oxidation of a two-carbon acetyl unit to carbon dioxide and water with the production of high-energy phosphate bonds by means of tricarboxylic acid intermediate.
Definition (MSH) A series of oxidative reactions in the breakdown of acetyl units derived from GLUCOSE; FATTY ACIDS; or AMINO ACIDS by means of tricarboxylic acid intermediates. The end products are CARBON DIOXIDE, water, and energy in the form of phosphate bonds.
Concepts Molecular Function (T044)
MSH D002952
SnomedCT 129911007, 88521006
English Citric Acid Cycle, Citric Acid Cycles, Cycle, Citric Acid, Cycle, Krebs, Cycle, Tricarboxylic Acid, Cycles, Citric Acid, Cycles, Tricarboxylic Acid, Krebs Cycle, Tricarboxylic Acid Cycle, Tricarboxylic Acid Cycles, Krebs' cycle, tricarboxylic acid cycle, TCA cycle, citric acid cycle, Krebs cycle, Krebs cycle pathway, function, Krebs cycle pathway -RETIRED-, cycles krebs, tca cycle, cycle krebs, cycle kreb, krebs cycle, acid citric cycle, kreb cycle, The Krebs Cycle, The Citric Acid Cycle, TCA Cycle, Szent-Gyorgyi-Krebs Cycle, Krebs cycle pathway (substance), Krebs cycle pathway, Citric acid cycle pathway, Krebs cycle pathway, function (observable entity), Tricarboxylic acid cycle pathway, Krebs cycle pathway (function)
Swedish Citronsyracykel
Czech Krebsův cyklus, citrátový cyklus
Portuguese Ciclo do Ácido Cítrico, Ciclo de Krebs, Ciclo do Ácido Tricarboxílico
Finnish Sitruunahappokierto
French Cycle de Krebs, Cycle des acides tricarboxyliques, Cycle de l'acide citrique
Russian TSIKL TRIKARBONOVYKH KISLOT, LIMONNOI KISLOTY TSIKL, KREBSA TSIKL, TSIKL KREBSA, КРЕБСА ЦИКЛ, ЛИМОННОЙ КИСЛОТЫ ЦИКЛ, ЦИКЛ КРЕБСА, ЦИКЛ ТРИКАРБОНОВЫХ КИСЛОТ
Italian Ciclo dell'acido tricarbossilico, Ciclo di Krebs, Ciclo dell'acido citrico
Polish Cykl kwasu cytrynowego, Cykl Krebsa
Japanese クエン酸サイクル, Krebs回路, TCA回路, くえん酸サイクル, くえん酸回路, クエン酸回路, クレブス回路, トリカルボン酸回路, 枸櫞酸サイクル
Spanish vía de ciclo de Krebs (sustancia), vía de ciclo de Krebs - RETIRADO -, vía de ciclo de Krebs - RETIRADO - (concepto no activo), vía del ciclo de Krebs, vía del ciclo del ácido cítrico (entidad observable), vía del ciclo del ácido cítrico (función), vía del ciclo del ácido cítrico, vía del ciclo del ácido tricarboxílico, Ciclo de Krebs, Ciclo del Ácido Cítrico, Ciclo del Ácido Tricarboxílico
German Citratzyklus, Krebs-Zyklus, Tricarboxylsäurezyklus
Dutch Citroenzuurcyclus, Cyclus, citroenzuur-, Krebs-cyclus
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Energy Metabolism (C0014272)

Definition (MSH) The chemical reactions involved in the production and utilization of various forms of energy in cells.
Definition (NCI) Any subcellular or molecular event, process, or condition concerned with storing and generating metabolic energy.
Definition (PSY) Expenditure of mental or physical effort.
Concepts Physiologic Function (T039)
MSH D004734
SnomedCT 251833007
English Energy Expenditure, Energy Expenditures, Energy Metabolisms, Expenditure, Energy, Expenditures, Energy, Metabolism, Energy, Metabolisms, Energy, ENERGY METAB, energy metabolism, Energy Metabolism, metabolism energy, energy expenditure, Energy Metabolism Process, Energy metabolism, Energy expenditure, Energy expenditure (observable entity)
Spanish Gasto de Energía, gasto energético (entidad observable), gasto energético, Metabolismo Energético
Swedish Energiomsättning
Czech energie - výdej, energetický metabolismus, energetický výdej, spotřeba energie (metabolismus)
Finnish Energia-aineenvaihdunta
French Dépense énergétique, Métabolisme énergétique
Italian Dispendio energetico, Metabolismo energetico
Russian BIOENERGETIKA, POTREBLENIE ENERGII, ENERGETICHESKII OBMEN, ENERGII RASKHOD, БИОЭНЕРГЕТИКА, ПОТРЕБЛЕНИЕ ЭНЕРГИИ, ЭНЕРГЕТИЧЕСКИЙ ОБМЕН, ЭНЕРГИИ РАСХОД
Japanese 生体エネルギー学, エネルギー消費, エネルギー代謝
Croatian ENERGIJA, METABOLIZAM
Polish Przemiana energii, Metabolizm energetyczny
Norwegian Not Translated[Energy Metabolism]
German Energiestoffwechsel, Energieumsatz, Energieverbrauch
Dutch Stofwisseling
Portuguese Gasto Energético, Metabolismo Energético
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Gluconeogenesis (C0017715)

Definition (GO) The formation of glucose from noncarbohydrate precursors, such as pyruvate, amino acids and glycerol. [MetaCyc:GLUCONEO-PWY]
Definition (NCI_NCI-GLOSS) The process of making glucose (sugar) from its own breakdown products or from the breakdown products of lipids (fats) or proteins. Gluconeogenesis occurs mainly in cells of the liver or kidney.
Definition (NCI) The biosynthesis of new glucose as opposed to that generated by the metabolism of glycogen. Gluconeogenesis occurs mainly in the liver or kidneys, and involves the biosynthesis of glucose from 3-carbon or 4-carbon non-carbohydrate precursors such as amino acids or fats.
Definition (CSP) biosynthesis of glucose from 3-carbon precursors, including aminoacids (this is the basis of protein breakdown during starvation).
Definition (MSH) Biosynthesis of GLUCOSE from nonhexose or non-carbohydrate precursors, such as LACTATE; PYRUVATE; ALANINE; and GLYCEROL.
Concepts Molecular Function (T044)
MSH D005943
English Gluconeogenesis, glucose biosynthesis, glucose biosynthetic process, gluconeogenesis, Gluconeogenic Process
Swedish Glukoneogenes
Czech glukoneogeneze
Finnish Glukoneogeneesi
French Gluconéogenèse, Néoglucogenèse, Glyconéogenèse, Néoglycogenèse
Russian GLIUKONEOGENEZ, ГЛЮКОНЕОГЕНЕЗ
Croatian GLUKONEOGENEZA
Polish Glukoneogeneza
Portuguese Neoglucogênese, Gliconeogênese, Neoglicogênese, Gluconeogênese
German Gluconeogenese, Glukoneogenese
Italian Gluconeogenesi
Dutch Gluconeogenese
Spanish Gluconeogénesis
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Glycolysis (C0017952)

Definition (GO) The chemical reactions and pathways resulting in the breakdown of a carbohydrate into pyruvate, with the concomitant production of a small amount of ATP. Glycolysis begins with the metabolism of a carbohydrate toe generate products that can enter the pathway and ends with the production of pyruvate. Pyruvate may be converted to ethanol, lactate, or other small molecules, or fed into the TCA cycle. [GOC:bf, GOC:dph, ISBN:0201090910, ISBN:0716720094, ISBN:0879010479, Wikipedia:Glycolysis]
Definition (NCI) A series of anaerobic chemical reactions that cells utilize to produce energy. Glycolysis is a biochemical pathway in which glucose is catabolized into lactate or pyruvate via enzymatic reactions to generate ATP.
Definition (NCI_NCI-GLOSS) A process in which glucose (sugar) is partially broken down by cells in enzyme reactions that do not need oxygen. Glycolysis is one method that cells use to produce energy. When glycolysis is linked with other enzyme reactions that use oxygen, more complete breakdown of glucose is possible and more energy is produced.
Definition (CSP) called the Embden-Meyerhoff or glycolytic pathway in which glucose is anaerobically catabolized into the simpler compounds lactic acid or pyruvic acid, resulting in energy stored in the form of ATP.
Definition (MSH) A metabolic process that converts GLUCOSE into two molecules of PYRUVIC ACID through a series of enzymatic reactions. Energy generated by this process is conserved in two molecules of ATP. Glycolysis is the universal catabolic pathway for glucose, free glucose, or glucose derived from complex CARBOHYDRATES, such as GLYCOGEN and STARCH.
Definition (MSH) An old term for glycolysis. Often it is used to describe anaerobic glucose catabolism that includes the further conversion of PYRUVIC ACID to LACTIC ACID or ETHANOL.
Concepts Molecular Function (T044)
MSH D006019
SnomedCT 129909003, 50476007
English Glycolysis, Embden-Meyerhof pathway, function, Embden-Meyerhof pathway -RETIRED-, anaerobic glycolysis, glycolyse, glycolysis, Glycolytic Process, Embden Meyerhof pathway, Embden-Meyerhof pathway (substance), Embden-Meyerhof-Parnas pathway, glycolytic process, Embden-Meyerhof pathway, Embden-Meyerhof pathway, function (observable entity), Embden-Meyerhof pathway (function), Embden Meyerhof Parnas Pathway, Embden Meyerhof Pathway, Embden-Meyerhof Pathways, Embden-Meyerhof Pathway, Embden-Meyerhof-Parnas Pathway, Pathway, Embden-Meyerhof-Parnas, Pathway, Embden-Meyerhof, Pathways, Embden-Meyerhof
Swedish Glykolys
Czech glykolýza
Finnish Glykolyysi
French Voie d'Embden-Meyerhof, Voie d'Embden-Meyerhof-Parnas, Glycolyse
Russian GLIKOLIZ, ГЛИКОЛИЗ
Japanese 解糖, 解糖作用
Croatian GLIKOLIZA
Polish Glikoliza
Spanish vía de Embden - Meyerhof - RETIRADO -, vía de Embden - Meyerhof (sustancia), Glicólisis, vía de Embden - Meyerhof (entidad observable), vía de Embden - Meyerhof (función), vía de Embden - Meyerhof - RETIRADO - (concepto no activo), vía de Embden - Meyerhof, Glucólisis
Norwegian Glykolyse, Embden-Meyerhof-Parnas-stoffskifteveien
German Glycolyse
Italian Glicolisi
Dutch Glycolyse
Portuguese Glicólise
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Carbohydrate Metabolism (C0302820)

Definition (ICF) Functions involved in the process by which carbohydrates in the diet are stored and broken down into glucose and subsequently into carbon dioxide and water.
Definition (ICF-CY) Functions involved in the process by which carbohydrates in the diet are stored and broken down into glucose and subsequently into carbon dioxide and water.
Definition (GO) The chemical reactions and pathways involving carbohydrates, any of a group of organic compounds based of the general formula Cx(H2O)y. Includes the formation of carbohydrate derivatives by the addition of a carbohydrate residue to another molecule. [GOC:mah, ISBN:0198506732]
Definition (NCI) Processes concerned with the synthesis, breakdown, and oxidation of carbohydrates in the tissues.
Definition (CSP) sum of chemical changes that occur within the tissues of an organism consisting of anabolism (biosynthesis) and catabolism of carbohydrates; the buildup and breakdown of carbohydrates for utilization by the organism.
Definition (MSH) Cellular processes in biosynthesis (anabolism) and degradation (catabolism) of CARBOHYDRATES.
Concepts Molecular Function (T044)
MSH D050260
Russian УГЛЕВОДОВ МЕТАБОЛИЗМ, UGLEVODNYI OBMEN, METABOLIZM KARBOGIDRATNYI, UGLEVODOV METABOLIZM, МЕТАБОЛИЗМ КАРБОГИДРАТНЫЙ, УГЛЕВОДНЫЙ ОБМЕН
English carbohydrate metabolic process, Carbohydrate metabolism, carbohydrate metabolism, carbohydrates metabolism, metabolism carbohydrate, Carbohydrate Metabolic Process, Carbohydrates--Metabolism, Metabolism, Carbohydrates/Storage/Polysaccharides, Carbohydrate Metabolism, Metabolism, Carbohydrate
Czech sacharidy - metabolismus
Finnish Hiilihydraattiaineenvaihdunta
French Métabolisme glucidique, Métabolisme des glucides, Métabolisme hydrocarboné
Japanese 炭水化物代謝, 代謝-糖, 糖代謝, 代謝-炭水化物
Swedish Kolhydratmetabolism
Croatian Not Translated[Carbohydrate Metabolism]
Polish Metabolizm węglowodanów
Norwegian Not Translated[Carbohydrate Metabolism]
Portuguese Metabolismo do Carbo-Hidrato, Metabolismo dos Carbo-Hidratos, Metabolismo do Carboidrato, Metabolismo dos Carboidratos
German Kohlenhydratstoffwechsel, Stoffwechsel, Kohlenhydrat-
Italian Metabolismo dei carboidrati
Spanish Metabolismo de los Carbohidratos, Metabolismo de los Hidratos de Carbono
Sources
Derived from the NIH UMLS (Unified Medical Language System)


glucose metabolism (C0596620)

Definition (GO) The chemical reactions and pathways involving glucose, the aldohexose gluco-hexose. D-glucose is dextrorotatory and is sometimes known as dextrose; it is an important source of energy for living organisms and is found free as well as combined in homo- and hetero-oligosaccharides and polysaccharides. [ISBN:0198506732]
Definition (CSP) sum of chemical changes that occur within the tissues of an organism consisting of anabolism (biosynthesis) and catabolism of glucose; the buildup and breakdown of glucose for utilization by the organism.
Concepts Molecular Function (T044)
English glucose metabolic process, cellular glucose metabolic process, glucose metabolism, Glucose Metabolism
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Incretins (C1562292)

Definition (CSP) insulinotropic peptides released by the gastrointestinal tract in response to food; stimulates insulin secretion and inhibits glucagon secretion.
Definition (MSH) Peptides which stimulate INSULIN release from the PANCREATIC BETA CELLS following oral nutrient ingestion, or postprandially.
Concepts Hormone (T125) , Amino Acid, Peptide, or Protein (T116) , Pharmacologic Substance (T121)
MSH D054795
SnomedCT 417524005
English Glucose Dependent Insulin Releasing Hormone, Insulin-Releasing Hormone, Glucose-Dependent, Hormone, Glucose-Dependent Insulin-Releasing, Glucose-Dependent Insulin-Releasing Hormone, Incretin, incretin hormone, incretin, incretins, Incretins, Incretin (substance)
Portuguese Incretinas, Hormônio Liberador de Insulina Dependente de Glucose, Efeito Incretina
Spanish Incretinas, Hormona Liberadora de Insulina Dependiente de Glucosa, Efecto Incretina, incretina (sustancia), incretina
Finnish Inkretiinit
French Gluco-incrétines, Incrétines, Incrétine, Hormones incrétines, Hormones insulinotropes
German Glukoseabhängiges insulinfreisetzendes Hormon, Inkretine, Glucoseabhängiges insulinfreisetzendes Hormon, Inkretin
Italian Incretina, Incretine
Russian ИНКРЕТИНЫ, GLIUKOZO-ZAVISIMYI INSULIN-RILIZING GORMON, INKRETINY, ГЛЮКОЗО-ЗАВИСИМЫЙ ИНСУЛИН-РИЛИЗИНГ ГОРМОН, ИНСУЛИН-ВЫСВОБОЖДАЮЩИЙ ГЛЮКОЗА-ЗАВИСИМЫЙ ГОРМОН, INSULIN-VYSVOBOZHDAIUSHCHII GLIUKOZA-ZAVISIMYI GORMON
Japanese インクレチン, 腸膵島ホルモン
Swedish Inkretiner
Czech inkretiny
Polish Inkretyny, Hormon uwalniający insulinę glukozozależną
Sources
Derived from the NIH UMLS (Unified Medical Language System)


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