Lecture 36 Flashcards

Intro to Human Metabolic Design

1
Q

bioenergetics

A

describes the transfer and utilization of energy (energy flow) in biological systems -> think about mitochondria

pg 944

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2
Q

free energy change (Gibbs free energy, ΔG)

A

a quantitative measure of the energy transfers between chemical reactions; can predict if the reaction will take place

pg 945

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3
Q

enthalpy change (ΔH)

A

a measure of the change in heat content of the reactants and products (heat released or absorbed during a reaction)

pg 945

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4
Q

entropy change (ΔS)

A

a measure of the change in randomness or disorder of reactants and products

pg 945

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5
Q

free energy change

A
  • reactants must undergo a transition state with a higher energy level
  • exergonic reactions: products have a lower energetic state -> ΔG is negative -> favorable reaction
  • endergonic reactions: products have a higher energetic state -> ΔG is positive -> unfavorable reaction as they need added energy to take place
  • The net ΔG = 0 when the reactant and product reach equilibrium

pg 946-948

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6
Q

ΔG and reactant concentration

A
  • nonequilibrium reactions: [A]»[B], ΔG < 0, forward reaction will take place until equilibrium is reached
  • standard conditions: [A]=[B], ΔG could be positive or negative
  • equilibrium conditions: ΔG=0, concentrations likely not equal
  • ΔG of a reaction is also dependent on the concentration of the reactants

pg 949

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7
Q

energy changes of metabolic pathways

A

watch lecture

  • when the overall ΔG = ΔG1+ΔG2+ΔG3 is negative the pathway can proceed even if some ΔG of individual steps are positive
  • the actual rate of the pathway depends on the activity of the enzymes that catalyze each step

pg 950

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8
Q

coupling of reactions

A

couple reactions with overall negative ΔG allow for the unfavorable reaction to proceed (ATP->ADP often coupled with unfavorable metbolic reactions to drive them forward)

pg 951-953

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9
Q

metabolism

A

a term used to describe the interconversion of chemical compounds in the body, the pathways taken by individual molecules, their interrelationships, and the mechanisms that regulate the flow of metabolites through the pathways

pg 955

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10
Q

overview of human metabolism

A
  • energy-yielding nutrients -> catabolism -> energy-poor end products (catabolism releases chemical energy, ATP, NADH)
  • precursor molecules -> anabolism -> complex molecules (takes energy extracted from catabolism to undergo anabolism)
  • only separation of pathways is done by compartmentalization and substrate availability

pg 956

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11
Q

catabolism

A
  • releases and captures energy in the form of ATP or reduced compounds (i.e. NADH, NADPH)
  • allows nutrients to be converted into building blocks to be used for the synthesis of complex molecules of the body
  • convergent pathway
  • many precursors lead to a common intermediate

pg 957

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12
Q

catabolic pathways

A
  • energy-yielding nutrients undergo digestion and absorption to be broken down into building blocks of macromolecules
  • an activation step occurs (needed for molecules to enter a certain catabolic pathway) and then catabolism occurs
  • catabolism leads to a common intermediate -> frequently acetyl-CoA which enters citric acid cycle
  • citric acid cycle is the central metabolic pathway -> it is amphibolic (both catabolic and anabolic) and provides intermediates for anabolic pathways

pg 958

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13
Q

anabolism

A
  • combines small molecules, such as amino acids, to make complex molecules, such as proteins
  • requires energy which can be provided by: ATP or NADH or NADPH (provide electrons for chemical bonds)
  • anabolism is a divergent process in which a few common biosynthetic precursors form a wide variety of complex products

pg 959

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14
Q

metabolic maps

A

help you see all the pathways and how they interact

pg 961

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15
Q

carbohydrate metabolism

A
  • glycolysis (central pathway for all others)
  • gluconeogenesis (GNG)
  • glycogen metabolism
  • fructose and galactose

pg 962

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16
Q

carb metabolism -> TCA and ETC

A
  • Krebs cycle (TCA)
  • oxidative phosphorylation
  • electron transport chain (ETC)

pg 963

17
Q

lipid metabolism

A
  • beta-oxidation
  • FA synthesis de novo
  • TAG, PL, and SL metabolism
  • cholesterol homeostasis
  • lipoprotein metabolism

pg 964

18
Q

nitrogen metabolism: amino acids

A
  • AA metabolism
  • nitrogen disposal
  • other nitrogen-containing compounds

pg 965

19
Q

nitrogen metabolism: nucleotides

A
  • purine and pyrimidine metabolism (how they’re produced)

pg 966

20
Q

nitrogen metabolism: porphyrins

A
  • heme synthesis
  • heme degradation
  • porphyrin metabolism

pg 967

21
Q

metabolic requirements for life

A
  1. ability to synthesize everything that is not supplied by the diet but required for survival
  2. ability to protect our internal environment from: toxic xenobiotics and external environmental changes
  • To meet these we metabolize dietary components using 4 types of metabolic pathways: fuel oxidation, fuel storage, biosynthesis, detoxification (extract energy from nutrients we consume)

pg 968

22
Q

regulation of human metabolism

A
  • flux of metabolites through a pathway (relates to availability of substrates)
  • enzyme activity (determines rate of pathway)
  • interconversion of metabolic fuels (from one type to another)

pg 970

23
Q

metabolic flux

A

the rate of turnover of molecules through a metabolic reaction or pathway

  • equilibrium reactions (reversible): the forward and reverse reactions occur at equal rates and there is no net flux in either direction (lowest possible energetic state)
  • nonequilibrium reactions (nonreversible): reactants are present in concentrations that are far from equilibrium
  • “steady-state” conditions: net flux from left to right because there is a continuous supply of substrate A and continuous removal of product D

pg 971

24
Q

principles of pathway regulation

A
  • rate-limiting reaction
  • committed step in a pathway
  • feedback regulation
  • feedforward regulation
  • product inhibition

pg 972

25
Q

well-fed/absorptive state

A

Priorities

  1. maintain blood glucose levels within healthy range
  2. replenish lost glycogen and lipid stores, and proteins
  • Timing: 2-6 hours after ingestion of a normal meal
  • Plasma: increased glucose, AA, and TAGs in chylomicrons
  • Pancreas: increased insulin (signal of well-fed state), decreased glucagon release
  • Tissues: increased synthesis of glycogen, TAGs and proteins

pg 974

26
Q

fasting/post-absorptive state

A

Priorities

  1. maintain blood glucose level for tissues requiring glucose (brain, RBCs)
  2. mobilize FAs from adipose tissue and ketone bodies from liver to supply energy to all other tissues
  • Timing: > 6-12 hours after ingestion of any food
  • Plasma: decreased glucose, AA, and TAGs in chylomicrons
  • Pancreas: decreased insulin, increased glucagon (signal of lack of glucose) release
  • Tissues: increased degradation of glycogen, TAGs and proteins

pg 974

27
Q

interconversion of metabolic fuels

A
  • happens in 4 major tissues: adipose tissue, muscle, blood, and liver
  • carbs in excess of the needs of the body can readily be used for synthesis of FAs, incorporated into TAG and stored adipose tissue (and liver)
  • FAs in excess are stored predominantly in the adipose tissue as TAGs
  • Acetyl-CoA cannot be used in gluconeogeneis and synthesis of glucose; glycerol CAN
  • AAs could be used to produce glucose OR ketone bodies

pg 975