Chapter 12: Glycolysis and Pyruvate Dehydrogenase
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danielrampar on November 14, 2011
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19 terms
Terms | Definitions |
|---|---|
 What is the function of the PI-3 Kinase? | Is responsable for openning up vesicles that have GLUT-4 inside to allow GLUT-4 be put onto the surface on the adipocyte or the muscle cells. (Pag. 139 and 170) |
| What is Insulin doing regarding the uptake of glucose in the adipocyte or muscle cell; Is it increasing or decreasing the Km or Glucose uptake or increasing or decreasing the Vmax of Glucose uptake? | Increasing in Glucose rate uptake which means increase Vmax. Insulin has not effect on teh Km. (Pag. 125 and 170) |
| Effect of Insulin in Liver? | Increase Glycogen synthesis Increase Fatty acids synthesis Increase Cholesterol synthesis |
| Effect of Insulin in Adipocyte? | Induce Lipoprotein lipase: release Fatty acids from Lipoproteins to be taken by the adipocyte to make FAT (Triglycerides) (pag. 162, 165 and 171) |
| Functions of GLUT 2 | In Liver: uptake glucose In Pancreatic B-cells: glucose sensor |
| Function of Hexokinase? and why it´s so important? | Transform Glucose into Glucose-6P (G6P) This enzyme is highly regulated by the product (G6P), that means that G6P inhibit this enzyme. If G6P is not used the increase of G6P inhibits this enzyme. (Pag 172) |
| What does the Glucokinase? | The same function of the Hexokinase but only in the Liver. |
| Relation between Glycolisis and Methehemoglobinemia? | The RBC has active transporters in it´s membrane, so has to undergo Glycolisis to obtain energy for itself. Furthermore they need not only the ATP of the Glycolisis but also the NADH to transform MetHb (Methehemoglobina) into Hb. The MetHb has a higher affinity for O2 so it can not realese bound oxygen. (Pag 172) |
| 3 most important enzymes in Glycolisis? | Hexokinase - Glucokinase (Liver) PFK-1 (Phosphofrcutokinase) Pyruvate Kinase (Pag. 172) |
| Pyruvate Kinase (PK) deficiency? | Hemolytic Anemia Increased 2,3 BPG (Bisphosphoglycerate) NOOOO Heinz Bodies (Pag 172) |
| Whisch is the most common cause of Hemolitic anemia? and the second most common cause? | Most common cause G6PD deficiency 2° common cause: Pyruvate Kinase Deficiency The difference between these two are that G6PD deficiency has Heinz Bodies (Pag. 172) |
| Relation between Glucokinase and Proteins glycosylation? | In Diabetics the Insulin doesn´t work so the Glucokinase is not going to be activated by the Insulin. Therefore the Glucokinase is not going to phosphorylate glucose to be trapped in the Liver. So glucose goes out again to the blood and produce hyperglycemia that is going to generate protein glycosylation. (Pag. 168 and 172) |
| Relation between 2,3 biphosphoglycerate (2,3-BPG) and Hb | The 2,3-BPG has affinity for the B-protein of the Hb, it produces that the Oxygen that is carrying the Hb can be given to the tissue. If 2,3-BPG doesn´t exit the Hb would have a greater affinity to the O2 and not unload ot to the tissues. |
| Who activates the Pyruvate Kinase? | Pyruvate Kinase is activated by Fructose 1,6-bisphosphate (feedforward activation) (Pag. 174) |
| The most important enzymes in Galactose Metabolism and there function? | There are two: 1. Galactokinase: Transform Galactose in Galactose 1-P 2. Gal 1-P uridyl transferase: Transform Galactose 1-P in Glucosa 1-P (PAG. 177) |
| Deficit of Galactokinase? and why? | Cataracts early in life Because Galactose is accumulated and is converted in Galactilol by the enzyme Aldose reductase. Galactilol is Osmotic, attracts water, producing swelling and the Cataracts (PAG. 177) |
| Deficit in Galactose 1-P? | Cataracts in early life Vomiting, diarrhea following lactose ingestion Lethargy Liver damage, hyperbilirrubinemia Mental retardation All this features because it accumulates in Liver, Brain and Other tissues (PAG. 177) |
| What is Aldolase B? and symptoms of their deficiency? | Aldolase B is an enzyme in the Fructose Metabolism that converts Fructose 1-P in DHAP and Glyceraldehyde. Their deficiency causes: (all the symptoms begin after weaning-destete) +Lethargy, vomiting +Liver damage, hyperbilirrubinemia Hypoglycemia Hyperuricemia Renal proximal tubule defect (Fanconi) (Pag. 179) |
| What is the relation between Fanconi syndrome and Deficiency of Aldolase B? | The proximal tubule can take Fructose and with the enzyme Fructokinase can transform it in Fructose 1-P. In the other hand has the enzyme Aldolase B to transform Fructose 1-P in DHAP and Glyceraldehyde. If the person has Aldolase B deficiency (HEREDITARY FRUCTOKINASE INTOLERANCE) the Fructokinase is going to accumulate in the renal cells of the proximal tubule and cause damage. (Fanconi Syndrome) (Pag. 179) |
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