Feed-fast Flashcards
1
Q
Role of growth hormone and cortisol in blood glucose regulation
A
-counteract insulin action over long-term
2
Q
Main regulators of blood glucose
A
-insulin (down) and glucaon (up)
3
Q
Post-prandial
A
- refers to period 2-3 hours after a meal
- high blood insulin/glucagon ration
- insulin increases
- glucagon decreases
- blood glucose increases
- dietary monosaccharides are taken up by intestinal mucosal cells via SGLT-1 (glu and gal) and GLUT-5 (fru, high concentration glu), released into portal circulation via GLUT-2 (all 3)
- liver takes up sugars via GLUT-2; phosphorylated with glucokinase, galactokinase, and fructokinase respectively
- at very high blood glucose and following extensive glycolysis–>fatty acid and cholesterol de novo synthesis (high ATP–|IDH, PFK-1, citrate transported to cytosol inhibits PFK-1)
- Adipose cells move GLUT-4 to plasma membrane take in glucose, use glycerol-phosphate from glycolysis to do TAG synthesis
- Muscle cells move GLUT-4, do glycogen synthesis and protein synthesis
4
Q
Post-absorptive phase
A
•5-7 hrs after food intake and food absorption
- blood glucose levels have since postprandial phase
- insulin levels drop, glucagon rise, low insulin/glucagon
- glucagon stimulates glycogenolysis and gluconeogenesis and release of glucose into the blood by the liver, glycogen synthesis and glycolysis stop
- low insulin and elevated epinephrine and cortisol levels lead to mobilization of TAG stores in fat cells and release of free fatty acids into blood
- glycogen stores low after 4-6 hrs, and depleted after 1 day, only gluconeogenesis provides blood glucose
5
Q
Cortisol
A
- in responsee to stress pituitary releases ACTH which stimulates release of cortisol from adrenal cortex
- cortisol in medulla leasd to methylation of norepinepherine to epinepherine (PNMT, with SAM) and release of both into blood
- epinepherine inhibits insulin release and stimulates glucagon release
6
Q
Insulin
A
- signals high blood glucose, acts via insulin receptors in many tissues, favors degredation or storage of glucose, has general anabolic effect (proteins, fatty acids, TAGSs, Cholesterol), release VLDLs
- release inhibited by epinepherine and stimulated by glucose and amino acids (especially leucine (essential) and arg)
- activates protein phosphatases which dephospohrylate key enzymes
- induce glucokinase, PFK-1, pyruvate kinase, glucose 6-P dehydrogenase (PPP), acetyl-CoA carboxylase (FA synthesis), and HMG-CoA reductase (cholesterol synthesis)
- activate HMG-CoA reductase in liver
- Activate lipoprotein lipase in capillaries (TAG synthesis)
7
Q
Glucaon
A
- signals low glucose, acts at glucagon receptors found in liver
- rise in blood glucose from glycogenolysis and gluconeogesis
- degradation of fatty acis and ketogenesis
- release inhibited by glucose, stimulated by epinepherine adn amino acids (especially alanine (high in fasting because sent from muscle to glucose for gluconeogenesis) and arg
- activate adenylate cyclase to cAMP to active PKA that phosphorylate key enzymes
- induce pep carboxykinase, fructose-1, 6-bisphosphatase, adn glucose-6-phosphatase
8
Q
Liver
A
- glucagon: glycogen degradation and gluconeogenesis
- epinepherine-glycogen degredation (phosphorylation cascade)
- cortisol-induction of PEP carboxykinase–>gluconeogesis
9
Q
Effects of epinepherine
A
- glycogen degredation and glycolysis in muscle
- glycogen degredation in liver
- fatty acid degradation adn use of ketone bodies
- TAG degredation in fat cells and release of fatty acids and glycerol into blood
- degredation of proteins in muscle
- activate hormone sensitive lipase in fat cells
10
Q
Cortisol
A
- induce PEP carboxykinase
- help activate hormone-sensitive lipase
11
Q
muscle after meal
A
- high insulin/glucagon
- glucose uptake glut4
- glycogen synthesis
- glycolysis
- amino acid uptake, protein sythesis
- usage of branch-chain amino acids for energy metabolism (muscle has much more branced chain transaminase than liver)
