FSHN 3600 - Exam 2

Proteins, Metabolic Integration, & Exercise

Primary protein structure

AAs linked together in a specific sequence based on genetic code.

____ protein structure forms a peptide backbone.

Primary

Secondary protein structure

H bonding occurring in peptide backbone of AAs in a protein.

Hydrogen bond

electrostatic attraction between polar groups.

Hydrogen bonding can occur between ___ & ___ groups of peptide backbone forming alpha-helix and beta-pleated sheets. 

amine, carboxyl

Secondary protein structures are ___ & ___. 

protective, rigid

Tertiary protein structure

3D confirmation, contains disulfide bridges.

Disulfide bridges must be broken by ___. ___ is responsible for breaking these bridges.

reduction, HCl

___ transporters have primary, secondary, & tertiary protein structures working in unison in the ___ regions. 

GLUT, transmembrane

_____ structures can occur between an acidic AA & a basic AA.

Tertiary

Tertiary Protein Structure

____ (nonpolar) AA in protein core to avoid an ___ environment.

Hydrophobic, aqueous

Tertiary Protein Structure

___ (polar) AA on surface.

Hydrophilic

How are AAs linked together?

dehydration synthesis (condensation)

Peptide bond

Between 1 AA and 1 hydroxyl group of a carboxyl end of another AA.

How is protein broken down?

Using HCl and proteases.

Free AAs use ___ transport and are ___ dependent

active, Na

The liver makes __ -- ____ AAs.

non-essential

Essential/indispensable AA

The body cannot make it. 

Non-essential/dispensable AA

The body can make it.

Conditionally essential AA

AAs that are normally non-essential, but must be consumed at specific times.

(e.g. illness or stress)

Carnitine is involved with __ transport into the mitochondria membrane for __-oxidation

FA, beta

Transamination

transferring an AA group

NEAA synthesis used ___ in the ___ state.

transamination, fed

Gluconeogenesis uses ___ in the ___ state and is ___.

transamination, fasted, hepatic

Deamination

Losing a N group

An example of deamination:

hepatic urea-genesis

Free ___ is toxic.

nitrogen

N-containing Compounds:

• Carnitine

• Creatine phosphate

• Glutathione (GSH)

• Purines/Pyrimidines

• Niacin

N-containing non-proteins

Carnitine is made from ___.

lysine

N-containing non-proteins

Carnitine attaches to ___ at the cytosol to carry into the ___ for ___-oxidation.

FAs, mitochondria, beta

N-containing non-proteins

Creatine phosphate is a quick ___ source to form ___.

energy, ATP

Creatine is made exclusively in the ___. 

liver

Purines and pyrimidines make up ___ and ___ bases.

DNA, RNA

Glutathione (GSH) is an ____.

antioxidant

Purines/pyrimidines are involved in ___.

DNA

Neurotransmitter Synthesis

Dopamine is made from ____.

tyrosine

Neurotransmitter Synthesis

Serotonin is made from ___.

tryptophan

Neurotransmitter Synthesis

Vitamins can make ___ from tryptophan.

niacin

Branched Chain AAs (BCAA) that flow through the liver

• Valine

• Leucine

• Isoleucine

Branched Chain Keto Acid (BCKA) in the muscle

___ triggers ___ growth.

Leucine, muscle

Increased AA in the blood = an uptake in:

• ___ ___

• ___- ___ ___

• ___ (primarily in the liver)

• protein synthesis

• N-containing compounds

• NEAAs

___ stimulates and/or induces enzymes involved in ___ degradation and ___. 

Glucagon, protein, urea-genesis

____ is a transporter of N to the liver.

Glutamine

T/F

Essential AAs must become non-essential AAs before it can enter the TCA cycle.

True

How is one supposed to get all AAs needed from the diet?

Eating foods composed of complimentary proteins. 

e.g., Beans — limiting AA is methionine, but have plenty of lysine.

What is the purpose of the alanine-glucose cycle?

To shuttle pyruvate to the liver in order for gluconeogenesis to occur in fasting conditions. 

Protein Regulation & Turnover

Insulin is an ____ hormone, it promotes ____ ____.

anabolic, protein synthesis

Protein Regulation & Turnover

Glucagon is a ____ hormone, it promotes ____ ____.

catabolic, protein degradation

Neurotransmitter Synthesis

AAs are precursors for the formation of neurotransmitters. Which neurotransmitters correspond to the AA below…

Tyrosine

 (listed AA) —→ 5OH-tyrosine —→ DOPA —→ Dopamine —→ norepinephrine —→ epinephrine 

Neurotransmitter Synthesis

AAs are precursors for the formation of neurotransmitters. Which neurotransmitters correspond to the AA below…

Tryptophan

(listed AA) —→ serotonin —→ melatonin

Neurotransmitter Synthesis

AAs are precursors for the formation of neurotransmitters. Which neurotransmitters correspond to the AA below…

Glutamate

(listed AA) —→ gamma-aminobutyric acid (GABA)

Inborn Errors of Metabolism

What are two examples of inborn errors of metabolism related to AA metabolism?

Homocysteinemia & phenylketonuria (PKU)

Inborn Errors of Metabolism

The problem with homocysteinemia:

The enzyme responsible for converting homocysteine (from methionine) to cystathionine and then to cysteine, further into glutothionine is not present because of a genetic defect. 

Inborn Errors of Metabolism

Due to the problem of homocysteinemia, toxic levels of homocysteine build up in the blood leading to _____. This is a risk factor for ___ ___ and other issues. 

hyperhomocysteinemia, cardiovascular disease

Inborn Errors of Metabolism

What is the dietary recommendation for homocysteinemia?

Limit intake of methionine in the diet.

Inborn Errors of Metabolism

What is the problem with phenylketonuria (PKU)?

The conversion of phenylalanine to tyrosine. The enzyme that carries out this reaction is phenylalanine hydroxylase. Patients with PKU lack this enzyme. 

Inborn Errors of Metabolism

Due to the problem with PKU, high concentrations of _____ build up in the blood. If high concentrations persist, they can be converted into phenylpyruvic acid which in high concentrations, lead to ___ ___ and other issues. 

phenylalanine, mental retardation

Inborn Errors of Metabolism

What is the dietary recommendation for PKU?

Severely limit the intake of phenylalanine AA in the diet.

(T/F) 1% of the population has polymorphisms.

T

____ occurs in the liver.

Ketogenesis

What processes take place in the fasted state?

• Protein degradation

• Gluconeogenesis

• Urea genesis

What is the Cori cycle?

Converts lactate produced during anaerobic exercise in muscles into glucose in the liver.

When there is an increase in AA in the blood there is an uptake in:

• Protein synthesis

• N-containing compounds

• NEAAs

___ is needed for the TCA cycle to function.

Pyruvate

Type 1 muscle fiber

Slow twitch, increased mito density

Type __ muscle fibers are utilized in long term exercise.

1

Type 2 muscle fibers

fast twitch

Type 2a muscle fiber

intermediate mito density, aerobic & anaerobic

Type 2b muscle fibers

low mito density, aerobic

Creatine phosphate is a substrate for a ___ ___ source.

burst energy

____ stimulates and/or induces enzymes involved in ____ degradation and ____ ____. 

Glucagon, protein, urea genesis

(REVIEW)

Induction

turns on gene for increased abasolute abundance of a protein

(REVIEW)

PTM

Activation or inactivation of protein function or tagging for degradation.

(REVIEW)

Allosteric Regulation

Ability to stimulate or inhibit enzymes.

(REVIEW)

Feedback Inhibition

Reduces enzyme activity when enough product is made.

Label 1-3

1-3: Lactate

The Cori cycle occurs during ___ conditions (induced by ___) in order to mobilize lactate from muscle into the liver, and make ___ to raise blood glucose levels and use them for ___ in other tissues.

fasting, glucagon, glucose, energy

We have an AA pool which comes from the ___ and ___ ___.

diet, protein breakdown

If the AA pool is low one ___ will predominate to promote ___ ___.

enzyme, protein degradation

If the AA pool is full another ___ will predominate to promote ___ ___.

enzyme, protein synthesis