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CARBOHYDRATE TOLERANCE

CARBOHYDRATE TOLERANCE. Glucose tolerance is the ability to regulate the blood glucose concentration after the administration of a test dose of glucose (normally 1 g/kg body weight) Diabetes Mellitus decrease glucose tolerance.

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CARBOHYDRATE TOLERANCE

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  1. CARBOHYDRATE TOLERANCE Glucose tolerance is the ability to regulate the blood glucose concentration after the administration of a test dose of glucose (normally 1 g/kg body weight) Diabetes Mellitus decrease glucose tolerance. Normal blood glucose levels are 50-100 mg per desi liter (500/180 - 1000/180 mmol / l). Depend on the intake of food before the test. Patients do not febrile, not in stress.

  2. 500 8 Glucose 400 6 300 4 200 2 Insulin 100 0 0 noon 8 am 6 pm midnight 8 am Blood glucose levels are relatively constant Plasma glucose (mmol/l) Plasma insulin (pmol/l) meals Time of day

  3. There is also an opinion that under the normal curve160 mg/100 ml one hour and120 mg/100 ml two hours after administration of glucose.

  4. BLOOD GLUCOSE LEVELS Sources:1) Food2) Gluconeogenesis3) Glycogenolysis Maintenance of blood glucose by the liver with glycogenolysis and gluconeogenesis, is under hormonal control (glucagon or if blood glucose drops very promptly  epinephrine)

  5. Coordination between organs is needed to control blood glucose levels Glycogen Food consumption Gluconeogenesis Glucose muscle adipocytes liver

  6. 55% Oxidation 45% Brain 75% Glycogenolysis 10% Muscle Glucose 20% Glycolysis (muscle) 25% Gluconeogenesis 25% Re-uptake (liver, gut) 60% from lactate Carbohydrate metabolism Glucose turnover (basal state)

  7. If blood glucose ↓ pancreatic glucagon released, glucagon activates adenylyl cyclase, an enzyme catalyzes formation of cAMP from ATP, cAMP activates the cAMP-dependent protein kinase, which in turn will converts phosphorylase kinase b to phosphorylase kinase a (ATP as phosphate donors). Active phosphorylase kinase catalyzes phosphorylase b to phosphorylase a. Phosphorylase a break down glycogen and generate G 1P. With glucantransferase and debranching enzyme glycogenolysis will proceed until the liver depleted with glycogen. G-1P converted to G-6P and G-6Pase splits the phosphate. Glucose then enters the circulation.

  8. Glycogenn Glycogenn -1 + G-1P  G-6P  G ( in the Liver )

  9. Other hormones (in addition to glucagon and epinephrine)affecting blood glucose levels:InsulinGHACTHCortisolThyroid

  10. INSULIN • Secreted in inactive formProinsulin C peptide + insulin C peptide is more easily measuredSubstances or chemicals which stimulates insulin secretion:glucose, amino acids, free fatty acids, ketone bodies, glucagon, tolbutamide and secretine.In contrast epinephrine inhibits Insulin secretion • Insulin entrance of G into cells except liver, erythrocytes and neuronal cells.

  11. Insulin MW 5808 PC2 (PC3) PC3 Proinsulin C peptide Ca2+-dependent endopeptidases A Chain B Chain

  12. Growth Hormone: Growth hormone may affect levels    blood glucose by activating    Hormone Sensitive Lipase. The resulting fatty acids, and derivatives (acetyl-CoA and ketone compounds) causes inhibition of glucose consumption by peripheral tissues

  13. ACTH (Adreno Cortico Tropic Hormone) • Affect the metabolism of carbohydrates together with GH increase gluconeogenesis Cortisol: enhance gluconeogenesis

  14. Renal function in Carbohydrate Metabolism • As a “safety clap“. If blood glucose ↑ , some will be excreted through the kidneys (renal threshold)Renal threshold: 170 - 180 mg / dl.Glucosuria occurredTubule reabsorption capability350 mg / min.

  15. 55% Oxidation 45% Brain 75% Glycogenolysis 10% Muscle → Glucose 20% Glycolysis (muscle) 25% Gluconeogenesis 25% Re-uptake (liver, gut) 60% from lactate Carbohydrate metabolism Glucose turnover (basal state)

  16. Biomedical importance • Normal metabolism: hunger if not prolonged, sports, pregnancy and lactation • Abnormal metabolism: lack of certain foodstuffs, as well as enzyme deficiencies or because of abnormal hormone secretion. The most interesting disease to study is diabetes mellitus ( DM ).

  17. Glycolysis: Pyruvate kinase enzyme  hemolytic anemia.Malignant tumor ↑ lactic acidHeart can not tolerance unaerobic glycolysis Oxidation of pyruvic acid: vitamin deficiency vit. B1 beri-beri Glycogen: abnormal accumulation of I  VIII MP Shunt: G6PD deficiency  hemolytic Fructose: Essential Fructosuria, "hereditary"                  fructose intoleranceSorbitol: ↑ peristalsis Diabetes Mellitus: ↓ glucose utilization

  18. Hemolytic can be caused by deficiency of thefollowing enzymes:PFK-1 (phosphofructo kinase-1)Pyruvate kinaseG6PD (glucose 6 phosphate dehydrogenase) High dietary fructose or fructose infusioncan cause:↓ inorganic phosphate (Pi) ↓ ATP synthesisDecreases in inhibition of Purine synthesisby ATP  ↑ Uric acid (uric acid)

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