BC 23 Metabolism Concepts Flashcards Preview

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Flashcards in BC 23 Metabolism Concepts Deck (17):
1

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

2

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

3

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

4

insulin

Liver/adipose/muscle

RTK receptor

RTK phosphorylation, signal cascade, dephosphorylated state of covalently regyulated met enz. altered Gene expression

5

Glucagon

liver only

Gs coupled receptor, Galpha s

cAMP increased activity PKA

overall phosphorylated state of cov met enz
altered GE

6

Epinephrine

Liver, adipose muscle

Gs coupled receptor Galpha s

cAMP increased activity of PKA
overall phosphorylated state of cov reg met enz
altered GE

7

Two regulatory considerations

1. feul source(fed/fast)
2. energy level: need or surplus , doe we have enough ATP
-allosteric modifiers,
-AMP activated protein kinase AMPK

8

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

9

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

10

Energy from Metabolic Fuels

1. micromolecules to monomeric building blocks
2. building blocks toa common intermediate (acetyl CoA (and pyruvate))
3. TCA cycle oxidizes acetyl CoA to CO2 and E is released as NADH and FADH2
4. 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

11

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

12

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

13

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.

14

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

15

overview of liver met

1. assume eating a mixed meal
2. Fed state: postprandial: absorptive phase: 0-4 hours
3. 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

16

0-4 hours after eating

HIGH insulin/glucagon ratio

-glucose to glycogen (glycogenesis)
-glucose to Glycolysis
-glycolysis to TCA
-TCA to FA synth TAG syunth

17

5-24 hours after eating

-glycogen to glucose (glycogenolysis
-Fatty acid oxidation to Ketogenesis
-fatty acid oxidation to TCA cycle
-TCA cycle to Gluconeogenesis-make glucose

know how the NAD and such are with each

greater than 24 non goes to glycogen, and glycogen not broken down