BC 23 Metabolism Concepts Flashcards
metabolism
highly coordinated and directed, not random
catabolism: break down for energy and building blocks (net energy producing)
- glycolysis: breakdown monosacch
- glycogenolysis: breakdown glycogen
- fatty acid B oxidation: breakdown FA
anabolism: use energy to drive biosynthesis from building blocks (net energy consuming)
- gluconeogenesis: synthesis of monosacc
- glycogenesis: synth of glycogen
- lipogenesis: synth of FA
Metabolism regulation
4 types all controlled by enzyme activity and concentration
- allosteric change: effector molecule directly binds outside active site: rapid/concentration dependant
- covalent modification: phos/dephos: rapid, until opposing enz acts
- transcription: increase or decrease in mRNA prod: slow, long lasting
- compartmentalization: physical separation: constant unless overflow
fed/fasting state
Absorptive phase (fed state): just eaten, actively absorbing nutrients from the gut
post absorptive phase: fasting state, gut has emptied so most tissues must use stored or manufactured fuels
-hormone control, insulin in fed stat, glucagon/epi in fasting state
insulin
Liver/adipose/muscle
RTK receptor
RTK phosphorylation, signal cascade, dephosphorylated state of covalently regyulated met enz. altered Gene expression
Glucagon
liver only
Gs coupled receptor, Galpha s
cAMP increased activity PKA
overall phosphorylated state of cov met enz
altered GE
Epinephrine
Liver, adipose muscle
Gs coupled receptor Galpha s
cAMP increased activity of PKA
overall phosphorylated state of cov reg met enz
altered GE
Two regulatory considerations
- feul source(fed/fast)
- energy level: need or surplus , doe we have enough ATP
- allosteric modifiers,
- AMP activated protein kinase AMPK
AMPK
mediator of overall energy state
AMPK is activated by AMP, the lowest E form of the Phosphate bond carrier ATP
-ampK can be activated via kinase as well
AMPK operates via covalent mod of target proteins-phosphorylation
-activated, activates catabolic to produce energy and inhibit anabolic pathways consuming E
Energy source (where is it from)
Energy extracted from the following via oxidation, waste is CO2 and H2O
source- dietary source - body reserve source
carbs - monosacc - glycogen (glucose)
proteins - AA and Lipids - muscle/cellular protein (AA)
lipids - dietary lipids in micelles - triacylglycerol in adipose tissue
each oxidized by providing energy to the enery carrier molecules in a final common pathway through TCA and ETC paths
Energy from Metabolic Fuels
- micromolecules to monomeric building blocks
- building blocks toa common intermediate (acetyl CoA (and pyruvate))
- TCA cycle oxidizes acetyl CoA to CO2 and E is released as NADH and FADH2
- evenry of NADH and FADH2 is released via electron transport chain (ETC) to produce ATP. Requires O2
energy carrier molecules must be stored and or transferred to other pathways
Ways to store energy
Chemical bond energy regulation and biosynthetic reactions
- GTP ATP (lower energy ADP AMP GDP)
- diffuse throughout cell carrying bond energy from generation to use, ATP hydrolysis, used to drive endergonic reaction
Electron Energy: transferring e from one reaction to power another reaction
- NADH, NADPH NAD+ NADP+
- precursors NAD NADH Niacin vit B3
- FAD FADH Riboflavin vit B2
why have to sources of water soluble energy carriers
regulation-need independent control of e transfer reactions
NAD+/NADH 700/1 Catabolic (accepts E in cat rx)
- oxidized form by ETC mainly, lactate dehydrogenase in anaerobic glycolysis
- reduced form generated by glycolysis, TCA cycle, B oxid
NADP+/NADPH 1/10 Anabolic (donate E in ana rx)
- oxidized form generated in multiple rxns
- red form generated bu HMP shunt, malic enzyme (cells with mito)
WHAT IS THE SIGNIFICANCE OF THE RATIOS
Role of Liver in E and Glucose Homeostasis
liver can remove glucose and export it back
-liver sees large variation from 60mg/dL to 300mg/dL after meal
- glucokinase (hepatocyte sugar trap) ahs Km of 180mg/dL so glucose will decrease rapidly paring blood glucose for peripheral tissues
- normal fasting glucose (90-100mg/dL) a level where liver will utilize little. Instead the liver ahs the unique role of maintaining that blood glucose level in fasting.
Liver in Glusose
two blood sources
-hepatic portal vein (nutrient rich from int, O2 poor)
-hepatic artery
mix as they enter
leaves via hepatic vein
-deoxygenated, detoxified, normal nutrient levels , 170-180mg/dL glucose for toher tissue
overview of liver met
- assume eating a mixed meal
- Fed state: postprandial: absorptive phase: 0-4 hours
- Fasting State: Post absorptive phase: 5-24 hours after eating
long term fasting: greater than 24
know conditions under which pathoways are more or less active
know how they communicate with eachother
SEE LAST THREE SLIDES FOR COMMUNICATION, DRAW THESE FUNCTIONS OUT
