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MBC - Lecture 51

Glucose Homeostasis (Mock)

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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