Metabolism overview Flashcards
Energy is extracted from food via
oxidation
4 stages of oxidation of food
- food is hydrolzyed in GI tract to monomeric building blocks
- building blocks degraded by various paths to make universal intermediate acetyl-CoA
- TCA cycle oxidizes acetyl-CoA to make CO2
- TCA cycle also makes 3 NADH and 1 FADH2 via dehydrogenases
- extraction of energy from food is ox. phosphorylation where energy of NADH and FADH2 released via ETC and used by ATP synthase to make ATP
What does mitochondria do
- FA oxidation (beta ox)
- acetyl-CoA production
- TCA
- ox. phosphorylation
- ketogenesis
what metabolism happens in cytoplasm
- glycolysis
- HMP shunt
- cholesterol synthesis (SER)
- protein synthesis (riubosomes, RER)
- FA’s
- nucleotides
What metabolic processes occur in both mitochondria and cytoplasm
- Heme synthesis
- Urea cycle
- Gluconeogenesis
When will sugars be used as source of acetyl-CoA to make ATP
when insulin is present
right after a meal
When is fat used as source of acetyl-CoA for ATP
inbetween meals when insulin is low
glucagon, cortisol, epinephrine are present
Fed state metabolism (after a meal)
- glycolysis
- aerobic respiration
- insulin stimulates storage of lipids, proteins, glycogen
Fasting (between a meal) metabolism
- hepatic glycogenolysis
- hepatic gluconeogenesis
- adippose release of FFA (minor)
- glucagon and epinephrine stimulate use of fuel reserves
Starvation (1-3 days) metabolism
blood glucose levels maintained by
- hepatic glycogenolysis
- adipose release FFA
- muscle and liver, shift fuel use from glucose to FFA
- hepatic gluconeogenesis from peripheral tissue lactate and alanine
- adipose tissue glycerol and propionyl CoA (from odd chain FFA)
Starvation after day 3
blood glucose levels maintained by
- adipose stores = ketone bodies main source for brain
- after adipose depleted, vital protein degradation accelerates = organ failure and death
- amount of excess stores determines survival time
when will Glycogen stores will be depleted
after day 1
What is Kwashiorkor
severe protein malnutrition
- skin lesions
- edema d/t decreased plasma oncotic pressure
- liver malfunction = fatty change
- small child with swollen abdomen
Kwashiorkor liver malfunction d/t
decreased apolipoprotein synthesis causes fatty change
Kwashiorkor MEALS mneumonic
Malnutrition
Edema
Anemia
Liver (fatty)
Skin lesions (hyperkeratosis, dyspigmentation)
What is Marasmus
malnutrition that does not cause edema
diet is deficient in calories, but no nutrients entirely absent
What does marasmus result in
muscle wasting
Rate determining enzyme of glycolysis
phosphofructokinase-1
PFK-1
- activated by: AMP, F-2,6-BP
- deactivated by: ATP, citrate
Rate determining enzyme of gluconeogenesis
Fructose-1,6-bisphosphatase
- activated by: citrate
- deactivated by: AMP, F-2,6-BP
Rate determining enzyme of TCA cycle
Isocitrate dehydrogenase
- activated by: ADP
- deactivated by: ATP, NADH
Rate determining enzyme of glycogenesis
glycogen synthase
- activated by: G6P, insulin, cortisol
- deactivated by: epinephrine, glucagon
Rate determining enzyme of glycogenolysis
Glycogen phosphorylase
- activated by: epinephrine, glucagon, AMP
- deactivated by: G6P, insulin, ATP
Rate determining enzyme of HMP shunt
G6PD
- activated by: NADP+
- deactivated by: NADPH
Rate determining enzyme of de novo pyrimidine synthesis
Carbamoyl phosphate synthetase II
- activated by: ATP, PRPP
- deactivated by: UTP
