Chapter 11 Flashcards
How is energy extracted from food?
via oxidation with carbon dioxide and water as the product
What are the 4 stages of energy extraction?
- metabolic fuels are hydrolyzed in the GI tract to glucose, amino acids, and fatty acids and absorbed
- building blocks degraded by various pathways in tissues to common metabolic intermediate=acetyl CoA
–energy in chemical bonds of acetyl-CoA and reducing NAD to NADH and FAD to FADH2
- citric acid cycle oxidizes acetyl-CoA to CO2
–energy released is conserved by reducing NAD to NADH and FAD to FADH2
- oxidative phosphorylation: energy of NADH and FADH2 is released via ETC anx used by ATP synthase to make ATP
–requires O2
What is the difference between type I and type II diabetes?
type I: beta cells don’t secrete enough insulin
type II: insulin receptor problem
–in obesity, there’s not enough of the insulin receptor put on the membrane
When do glucose levels peak and reach normal after a meal?
reach max at 45 minutes
back to normal at 90 minutes
normal concentration of glucose = 5 mM
How do glucose levels go back to normal?
inuslin and insulin independent cells (brain and erythrocytes)
What is the general pathway of extracting energy from metabolic fuels?
How is energy stored in the cell?
1) ATP: circulating form of energy; formed in catabolic pathways by phosphorylation of ADP
2) excess energy from diet is stored as fatty acids–reduced polymer of acetyl-CoA– and glycogen–polymer of glucose
3) proteins can also be mobilized for energy in prolonged fast
What is insulin and what are it’s target tissues?
anabolic hormone that promotes fuel storage
opposed by glucagon and epinephrine, cortisol, and growth hormone
–liver, muscle and adipose tissue
What is glucagon and what are it’s target tissues ?
responds rapidly to decreased blood glucose levels
–promotes synthesis and release of glucose into circulation
–target tissues= skeletal muscle, adipose tissue and liver
How are anabolic and catabolic pathways controlled?
1) allosteric inhibitors and activators of rate limiting enzymes
2) control of gene expression by insulin and glucagon
3) phsophorylation (glucagon) and dephosphorylation (insulin) of rate limiting enzymes
What happens during well-fed (absorptive) states?
immediately after a meal:
- blood glucose level rises and stimulates the release of insulin
- insulin promotes glycogen synthesis in liver and muscle
- after glycogen stores are full, liver converts excess glucose to fatty acids and triglycerides
- insulin promotes triglyceride syntehsis in adipose tissue and protein synthesis in muscle
–insulin promotes glucose entry into adipose tissue and muscle
–most energy needs of liver met by oxidative of excess amino acids
–brain and RBC are insenstiive to insulin; derive energy from oxidizing glucose to CO2 and water in well fed and normal fasting states
What energy do red blood cells utilize?
under all conditions, red blood cells use glucose anaerobically for all energy needs
What happens during postabsorptive states?
-glucagon and epinephrine levels rise during overnight fast
–in liver, glycogen degradation and release of glucose into blood are stimulated by glucagon
–hepatic gluconeogenesis is stimulated by glucagon; slower than glycogenolysis
–release of amino acids from skeletal muscle and fatty acids from adipose tissue stiulated by decrease in insulin and increase in epinephrine
–amino acids and faty acids are taken up by liver, where amino acids provide carbon skeletons and oxidation of fatty acids provide ATP necessary for gluconeogenesis
How is glucose transported?
polar so can’t enter cell by itself so uses GLUT transporters
–GLUT1,3: low Km, zero order kinetics; enters at steady pace; red blood cell and brain
–GLUT2: high Km, 1st order kinetics; liver
–insulin turns on GLUT4 at hormone level (via PI3K) in muscle and fat cells–insulin increases Vmax of GLUT4
–AMP actvated kinase only turns on GLUT4 in muscle
–as ATP decreases in muscle, AMP tells GLUT4 to go to the membrane
How are triglycerides transported?
can’t go through membrane becuase nonpolar
–so LPL is an enzyme in the adipose tissue membrane that breaks it down to fatty acid and glycerol
–insulin turns on LPL at gene level