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MBC - Lecture 51
Glucose Homeostasis (Mock)
| Question | Answer |
|---|---|
| Lecture 51 | Glucose Homeostasis |
| Inadvertent starvation causes: | Poverty/neglect/abuse, anorexia nervosa, GI disease |
| Iatrogenic starvation causes: | Pre-op, bowel rest, weight loss |
| Subcutaneous adipose tissue accounts for approximately ___ of fuel reserve. | 2/3 |
| Skeletal muscle accounts for approximately ___ of fuel reserve. | 1/3 |
| During starvation, blood glucoses ___. | decreases |
| During starvation, plasma insulin ___. | decreases |
| During starvation, plasma glucagon ___. | increases |
| After ___ hours of starvation, liver glycogen is used up. | 12-24 hours |
| During starvation, ketogenesis is ___. | increased |
| During starvation, plasma free fatty acids ___. | increases (become main source of energy) |
| Under normal circumstance BUN level is ___. | constant/stable (regardless of protein intake) |
| BUN goes up during ___ failure. | renal failure (inability to excrete nitrogen) |
| Glucagon ___ G-6-Pase, F-1,6-Bpase, and PEPCK. | up-regulates |
| Insulin ___ G-6-Pase, F-1,6-Bpase, and PEPCK. | down-regulates |
| Ethanol is metabolized to ___. | acetaldehyde |
| Ethanol metabolism converts and traps ___. | NAD+/NADH |
| Trapping of NADH impairs ___. | Gluconeogenesis (blocked lactate to glucose) and OAA tied up as malate (malate dehydrogenase) |
| Ethanol potentiates ___. | insulin |
| Postprandial state is similar to ___ induced state. | insulin |
| During overnight fast, the liver and muscle is running on ___. | glycogen |
| During overnight fast, ___ is used (even though glycogen is not all gone). | fat |
| During overnight fast, glycerol from TG breakdown is used in ___. | gluconeogenesis |
| During overnight fast, ketosis is turned ___. | on |
| Glucose-Alanine Cycle | Transport alanine from muscle to the liver for gluconeogenesis |
| Cori Cycle | “Glucose-lactate” cycle, transport lactate from muscle to the liver for gluconeogenesis |
| During prolonged fasting, glycogen is ___. | depleted |
| During prolonged fasting, ___ is the major source of energy. | fatty acid (from TG breakdown) |
| During prolonged fasting, ___from fat breakdown is glucose sparing. | ketogenesis |
| High glucose inhibits ___. | glucose-6-phosphate dehydrogenase |
| Fructose-2,6-bisphosphate is an allosteric activator of ___. | PFK-1 |
| Malonyl-CoA inhibits ___ in B-oxidation. | CPT I |
| Excess citrate is converted to ___ for fatty acid and cholesterol synthesis. | acetyl-CoA |
| Phosphorylation signaled by glucagon: | GPCR, adenylate cyclase, cAMP, PKA |
| Dephosphorylation signaled by insulin: | RTK, protein phosphatase (targets PKA activated enzymes), cAMP phosphodiesterase |
| Phosphorylation by glucagon ___ glycogen synthase. | inactives (decrease glycogen synthesis) |
| Phosphorylation by glucagon ___ glycogen phosphorylase and its kinase. | activates (increase G1P release) |
| Phosphorylation by glucagon ___ PFK-2. | inactivates (decrease glycolysis) |
| Phosphorylation by glucagon ___FBPase-2. | activates (increase gluconeogenesis) |
| Phosphorylation by glucagon ___ PK. | inactivates (increase gluconeogenesis) |
| Phosphorylation by glucagon ___ ACC. | inactivates (decrease malonyl-CoA) |
| Dephosphorylation by insulin ___ protein phosphatase 1. | activates |
| Dephosphorylation by insulin ___ glycogen synthase. | activates (increase glycogenesis) |
| Dephosphorylation by insulin ___ glycogen phosphorylase and its kinase. | inactivates (decrease G1P release) |
| Dephosphorylation by insulin ___ glut2 and glucokinase. | activates |
| Dephosphorylation by insulin ___ PFK-2. | activates (increase glycolysis) |
| Dephosphorylation by insulin ___ FBPase-2. | inactivates (decreases gluconeogenesis) |
| Dephosphorylation by insulin ___ ACC. | activates (increase FA synthesis) |
| Normal blood glucose level: | 60 to 110 |
| Low blood glucose level (hypoglycemic): | <45 |
| High blood glucose level (diabetes mellitus): | >120 |
| Fasting Oral Glucose Load | Standard dose of glucose is given then read 2 hours later, normal levels are <8 mmol/L, diabetic levels are > 11 mmol/L |
| Impaired glucose tolerance (“pre-diabetic”) is the area between ___ and ___. | diabetic and normal |
| Hb A1c levels: | >7% poor control of diabetes, ~6% is minimal risk, >5% increased risk for hypoglycemia |
| Lag effect in Hb A1c test is due to: | the lifespan of erythrocytes (120 days) |
| DM Type 1 – Onset | Usually <20 years old |
| DM Type 1 – Insulin Synthesis | Absent or reduced (immune destruction) |
| DM Type 1 – Plasma Insulin Concentration | Low or absent |
| DM Type 1 – Islet Cell Antibodies | Yes |
| DM Type 1 – Genetic | Inheritance associated with HLA antigens |
| DM Type 1 – Obesity | Uncommon |
| DM Type 1 – Ketoacidosis | Yes |
| DM Type 2 – Onset | Usually <40 years old |
| DM Type 2 – Insulin Synthesis | Preserved, combination of impaired production and insulin resistance |
| DM Type 2 – Plasma Insulin Concentration | Low, normal, or high |
| DM Type 2 – Islet Cell Antibodies | No |
| DM Type 2 – Genetic | Polygenic, not associated with HLA |
| DM Type 2 – Obesity | Common |
| DM Type 2 – Ketoacidosis | Uncommon |
Created by:
emyang
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