Metabolism Flashcards
ATPs produced from anaerobic glycolysis
2
ATPs produced from aerobic glycolysis
5or7(6or8)
ATPs produced from each molecule of FADH2 in TCA
1.5 (2)
ATPs produced from each molecule of NADH in TCA
2.5 (3)
ATPs produced from complete oxidation of glucose
30or32(36or38)
ATPs produced from complete oxidation of palmitate
106 (129)
ATPs required to create 1 molecule of urea
3 ATPs but 4 high- energy bonds
ATPs required to activate fatty acids (i.e., attach CoA)
2 ATP equivalents (ATPàAMP)
ATPs required to convert ribose-5P to PRPP
2 ATP equivalents (ATPàAMP)
ATPs required to attach one amino acid to the growing polypeptide chain during translation
4
redominant hormone in the well fed state
INSULIN
Hormone that helps maintain blood glucose levels during starvation
GLUCAGON
Exert effects similar to glucagon
EPINEPHRINE, CORTISOL, GROWTH HORMONE
Ratio of carbon dioxide produced/oxygen consumed
RESPIRATORY QUOTIENT
Main metabolic fuel of neurons and erythrocytes
GLUCOSE
Main metabolic fuel of heart muscle
FATTY ACIDS
Main fuel of the skeletal and heart muscle, and alternative fuel of the brain during a fast
KETONE BODIES
Percentage of the brain’s energy requirement that can be met by ketone bodies
20%
Product of aerobic glycolysis Product of glycogenolysis in muscle
PYRUVATE
Product of anaerobic glycolysis
LACTATE
Product of glycogenolysis in liver
GLUCOSE
Product of glycogenolysis in muscle
GLUCOSE-6- PHOSPHATE
Building block of fatty acids and cholesterol
ACETYL COA
Main substrate used for gluconeogenesis during a fast
GLUCOGENIC AMINO ACIDS
Intermediate that can never be used for gluconeogenesis
ACETYL COA
After 24 hours of starvation, which pathway is mainly responsible for maintaining blood glucose levels? Percentage of gluconeogenesis that occurs in the kidney during a prolonged fast
GLUCONEOGENESIS 40%
Hours of fasting before glycogen stores are exhausted
18 hours
Cause of death in prolonged starvation
CATABOLISM OF ESSENTIAL AMINO ACIDS
Metabolic effects of acute alcohol intoxication
HYPOGLYCEMIA LACTIC ACIDOSIS KETOACIDOSIS
Massive increase of this molecule leads to metabolic effects of alcohol intoxication
NADH
Intermediate in alcohol metabolism that causes flushing, tachycardia, hyperventilation, and nausea
ACETALDEHYDE
Ketoacidosis with hyperglycemia
DIABETIC KETOACIDOSIS
Ketoacidosis with hypoglycemia
PROLONGED STARVATION ALCOHOL INTOXICATION
Critical intermediate necessary to maintain TCA cycle activity usually depleted in prolonged starvation and alcohol intake
OXALOACETATE
TCA intermediate that is depleted during hyperammonemia
α-KETOGLUTARATE
TCA intermediate that links it to the urea cycle
FUMARATE
Formula for BMI computation
WEIGHT IN KG HEIGHT IN M2
On ketogenic diet, these pathways that remain active in the liver even during the fed state
GLUCONEOGENESIS KETOGENESIS