Anatomy Exam III: Text pt 2
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48 terms
Terms | Definitions |
|---|---|
 Define glycogenesis | Gynthesis of glycogen from glucose |
| What are the four factors insulin exerts on carbohydrates? | (1) Facilitates glucose transport into most cells (2) Stimulates glycogenesis (3) Inhibits glycogenolysis (4) Decreases hepatic output by inhibiting gluconeogenesis. |
| What is the plasma membrane carrier transports glucose between the blood and cells? | GLUT (glucose transporter) |
| What happens to glucose immediately upon entering the cell? | physphorylation into glucose-6-phosphate |
| Purpose of GLUT-1 | Transport glucose across blood-brain barrier |
| Purpose of GLUT-2 | Transfers into the adjeacent bloodstream the glucose that has entered the kidney and intestinal cells by means of sodium and glucose cotransporter (SGLT) |
| Purpose of GLUT-3 | Main transporter of glucose into neurons |
| Purpose of GLUT-4 | Majority of glucose uptake by most cells |
| What hormone allows for GLUT-4 action? | Insulin binding is required for GLUT-4 action |
| T/F all GLUT carriers respond to insulin | False (GLUT-4 only) |
| T/F GLUT-4 is always present on the plasma memebrane | False (absent w/o insulin) |
| How does insulin promote GLUT-4 expression? | Insulin binds its receptor which signals intracellular vesicles containing GLUT-4 to bind with cell membrane, inserting the GLUT-4 |
| T/F GLUT-4 is degraded after glucose transport | False (recycled via endocytosis) |
| T/F The brain, working muscles, and the liver are not insulin dependent for glucose update | TRUE |
| T/F Glucose permeability to the brain via GLUT-1, GLUT-3, GLUT-4 | False (GLUT-1, GLUT-3) |
| T/F Skeletals muscles always require insulin for glucose uptake | False (Only at rest, not during exercise) |
| T/F Insulin stimulates insertion of GLUT-4 in skeletal muscles during exercise | False (muscle contractions trigger insertion of GLUT-4) |
| T/F The liver does not require GLUT-4 | TRUE |
| T/F Insulin enhances glucose metabolism in the liver | TRUE |
| What are the four effects of insulin on fat? | (1) Enhances entry of fatty acids into adipose tissue (2) Increases transport of blusoe into adipose tissue (GLUT-4 recruitment) (3) Promotes triglyceride synthesis (indirectly) (4) Inhibits lipolysis |
| What are the three actions of insulin on protein? | (1) Promostes active transport of aa from blood into muscles and other tissue (2) Increases rate of aa incorporation into protein (3) Inhibits protein degradation |
| T/F Insulin is essential for normal growth | True (glucose -> anabolic effect on protein) |
| What is the primary stimulus for increased insulin secrtion? | Increase in blood glucose concentration |
| Via what mechanism does glucose stiulate insulin secretion? | excitation-secretion coupling process: changes B cell's membrane potential->insulin secretion |
| Glucose stimulation of insulin: Step 1 | Glucose enteres B cell via GLUT-2 |
| Glucose stimulation of insulin: Step 2 | Glucose phosphorylated to glucose-6-phosphate |
| Glucose stimulation of insulin: Step 3 | Glucose-6-phosphate oxidized by to yield ATP |
| Glucose stimulation of insulin: Step 4 | ATP closes ATP-sensitive K+ channel on binding |
| Glucose stimulation of insulin: Step 5 | Decrease K+ permeability leads to depolarization of B cell |
| Glucose stimulation of insulin: Step 6 | Depolarization cause volatage-gated Ca++ channels to open |
| Glucose stimulation of insulin: Step 7 | Ca++ enters cell through open channels |
| Glucose stimulation of insulin: Step 8 | Ca++ entry triggers exocytosis of secretory vesicles containing insulin |
| Glucose stimulation of insulin: Step 9 | Insulin is secreted |
| How does aa level affect insulin release? | Elevated aa levesl directly simulates the B cells to increase insulin secretion. ++Insulin enhances the entry of these aa into the cell, lowering blood aa levels and promoting protein synthesis |
| What mechanism causes aa to simtulate insulin release? | Same pathway as glucose: aa oxidation -> ATP production and start of cascade |
| What are incretins? | They increase insulin secrtion by increasing cAMP, enhancing Ca++ induced relesae of insulin |
| What are the two incretins? | GIP (glucose-dependent insulinotropic peptide), GLP (glucagon-like peptide) |
| T/F The gastrointestinal incretins work via negative feedback to regulate insulin | False (feedforward: anticipatory release prior to actual nutrient absorption) |
| T/F Parasympathetic activity inhibits insulin release | False (stimulates) |
| T/F Sympathetic stimulation increases epinephrine and inhibits insulin secretion | True |
| Why would sympathetic stimulation inhibit insulin secretion? | Decreased insulin increases blood glucose concentration availablity for fight/flight response or increased muscle activity |
| What is the most common endocrine disorder? | Diabetes mellitus |
| What is the most prominent feature of diabetes mellitus? | hyperglycemia |
| What is the key characteristic of both diabetes mellitus and diabetes insipidus? | polyuria (large urine volume) |
| Key character of DM Type I | lack of insulin secretion |
| Key character of DM Type II | insulin resistance (normal (or increased) insulin secretion but reduced sensitivity) |
| What are the two gross contributors of death due to insulin deficiency? | (1) effects of hyperglycemia (2) ketosis toxicity (acidosis) |
| Why does hyperglycemia lead to death? | Hyperglycemia -> polyuria -> dehydration -> (1) CNS failure (2) Low peripheral cirulation (a) low cerebral flow (b) renal failure -> death |
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