22460832
Descripción
Fichas por Evian Chai, actualizado hace más de 1 año
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Creado por Evian Chai
hace alrededor de 4 años
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| Pregunta | Respuesta |
| W | 2-4 hours after a meal |
| In the fed state, there is a high ...to... ratio There is an increase in ..., ..., and .... There is synthesis of ..., ..., and ... | Insulin: glucagon ratio Blood glucose, amino acids, chylomicrons Glycogen, TAG, protein |
| In the liver during the fed state, ... and .... occur | Glycolysis turns glucose to acetyl CoA for lipid synthesis Glycogen synthesis |
| When glycogen synthase/phosphorylase is not phosphorylated, what is activated/inactivated? What does this lead to? | Glycogen synthase activated, phosphorylase inactivated Leads to synthesis of glycogen |
| What happens to fat metabolism during the fed state? How is fatty acid oxidation lowered? | 1. Acetyl CoA carboxylase is activated 2. Fatty acid/TAG synthesis Malonyl CoA from FA synthesis inhibits carnitine transferase, which is essential for FA oxidation |
| Glucose transport in the RBC/Brain is .... because they rely on glucose for fuel | Insulin independent |
| What transporters are increased during the fed state in muscles? What is activated? What uptake also increases to increase protein synthesis? | GLUT 4 glucose transporters Glycogen synthase activated Amino acid |
| What occurs in adipose tissue during the fed state? | 1. Lipoprotein lipase activated to increase breakdown of TAG for resynthesis into TAG in storage 2. Increased GLUT4 |
| Alpha cells in the islets of langerhans secrete... This is stimulated by.... | Glucagon Low blood glucose, Increased AA in blood (fine tuning), adrenaline |
| What are the effects of glucagon in terms of: 1. Fuel 2. Blood glucose 3. Liver usage of glucose/AA 4. Adipose tissue/FA oxidation | 1. Mobilise fuel 2. Maintain blood glucose 3. Increase cAMP to activate gluconeogenesis/glycogenolysis/increase AA uptake in liver 4. Increase FA release in adipose tissue+activate FA oxidation/ketone body formation in liver |
| What do B cells secrete? What is this regulated by? What is this stimulated by? | 1. Insulin 2. High insulin causes down regulation of receptors (-tive feedback) 3. Rise in AA in blood, Increase in blood glucose, Glucagon (fine tuning), Gut hormones |
| How is insulin created and secreted from the B cell? | 1. Rise in blood glucose/AA leads to increased ATP in B cell 2. K+ channel closes 3. Ca2+ channel opens 4. Ca2+ causes exocytosis of insulin 5. Proinsulin cleaved to insulin+C peptide |
| What are the effects of insulin in terms of: 1. Food storage 2. AA 3. Glycogen/glucose 4. FA 5. Cellular effects | 1. Up Food storage 2. AA uptake/synthesis 3. Glycogen synthesis (dephosphorylates glucagon phosphorylase/synthase) 4. FA synthesis 5. Activate Akt |
| What type of receptor is Akt? | Tyrosine kinase receptor |
| What are the effects of Akt? | 1. Translocate GLUT4 to increase glucose transport to muscle/adipose 2. Inhibit glycogen synthase kinase, which normally inactivates glycogen synthase by phosphorylating it 3. Inhibits lipolysis by phosphorylating phosphodiesterase so PKA ISNT activated=no lipase activation 4. Activates RAS which is phosphorylated to MEK kinase-->MAPK-->gene expression changes |
| What causes changes in metabolism? | 1. Changes in enzymes synthesis 2. Covalent modification of enzymes 3. Amount of substrate available 4. Allosteric effects on enzymes (eg. phosphorylation) |
| Which are the 4 HYPERglycaemic hormones? (increase blood glucose levels) | 1. Glucagon 2. Growth hormone 3. Cortisol 4. Adrenaline |
| What is the only HYPOglycaemic hormone? | Insulin |
| What does adrenaline do in terms of: 1. Fuel 2. Glucose/glycogen 3. FA | 1. Mobilise fuel 2. Increase glycogenolysis in the liver 3. FA release from adipose |
| What does cortisol do in terms of: 1. AA 2. Glucose/glycogen 3. FA | Long term effects on 1. Increase AA mobilisation in muscle 2. Increase gluconeogenesis 3. Increase FA release from adipose tissue |
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