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Fructose Intolerance • Too Much Fructose – Fructose-1-P Aldolase is rate-limiting – Depletion of P i – Reduction in [ATP] – Increase in glycolysis – Accumulation of lactate (acid) in blood • Fructose-1-P Aldolase Deficiency (Genetic Disease)
Metabolism of galactose • Source - lactose • Occures in the liver • Galactose is necessary for synthesis of lactose, glycolipids, protheoglycans, glycoprotheins or can converted to glucose • UDP-galactose is high energy molecules, galactose have ability bounded to other saccharides(-OH compound) and formed O- glycosidic bound (synthese glycosaminoglycanes, glycoproteines, glycolipides)
Page 1 and 2: Carbohydrate metabolism III
Page 3: Glycogen Catabolism Getting glucose
Page 6 and 7: Metabolism of Tissue Glycogen Diges
Page 9 and 10: Glycogen Phosphorylase (GP) • Pyr
Page 12 and 13: Debranching enzyme • Debranching
Page 14 and 15: • Glucose-6-P may enter Glycolysi
Page 16 and 17: Glycogen Synthesis • Uridine diph
Page 18 and 19: Glycogen Synthase Forms -(1 4) glyc
Page 20 and 21: Glycogen Synthase • Glycogen Synt
Page 23 and 24: Control of Glycogen Metabolism A hi
Page 25 and 26: Regulation of GP • Glycogen Synth
Page 27 and 28: Enzyme Cascades and GP/GS Hormonal
Page 29 and 30: Epinephrine and Glucagon The differ
Page 31: Hormonal Regulation of Glycogen Syn
Page 35 and 36: Other Substrates for Glycolysis Fru
Page 37 and 38: Sucrose (Table Sugar) O- -D-Glucopy
Page 39 and 40: Liver Metabolism of Fructose I (Lit
Page 41: Liver Metabolism of Fructose III
Page 45 and 46: Phosphorylation of Galactose
Page 47 and 48: Epimerization of UDP-Galactose Why
Page 49 and 50: The Role of Glucuronic acid • Uri
Page 51: Transformation of glucose-6-P fosfa

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