Proteins Part 2

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Last updated 12:02 AM on 4/12/26
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29 Terms

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Protein digestion: Trypsinogen

Trypsinogen gets converted to trypsin in the pancreas

Trypsin activates all other enzymes (Zymogens):

  • Chymotrypsinogen → chymotrypsin

  • Protelastase → Elastase

  • Procarboxypeptidase → Carboxypeptidase

<p>Trypsinogen gets converted to trypsin in the pancreas</p><p>Trypsin activates all other enzymes (Zymogens):</p><ul><li><p>Chymotrypsinogen → chymotrypsin</p></li><li><p>Protelastase → Elastase</p></li><li><p>Procarboxypeptidase → Carboxypeptidase</p></li></ul><p></p>
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AA absorption

Facilitated diffusion

Active transport **

  • NA dependent transporter (needs ATP)

Absorbed through the PEPT1

<p>Facilitated diffusion</p><p>Active transport **</p><ul><li><p>NA dependent transporter (needs ATP)</p></li></ul><p>Absorbed through the PEPT1 </p><p></p>
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<p>Assessing Protein Quality: Protein Efficiency Ratio (PER)</p>

Assessing Protein Quality: Protein Efficiency Ratio (PER)

Values compared to 2.0 g of whole egg

<p>Values compared to 2.0 g of whole egg</p>
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<p>Assessing Protein Quality: Chemical score</p>

Assessing Protein Quality: Chemical score

Test protein is chemically digestion into free AA

<p>Test protein is chemically digestion into free AA</p><p></p>
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Nitrogen Balance

Intake of N and N loss

N should = 0

Not enough protein → NB < 0 (-ve)

  • Poor protein quality

<p>Intake of N and N loss </p><p>N should = 0</p><p>Not enough protein → NB &lt; 0 (-ve)</p><ul><li><p>Poor protein quality </p></li></ul><p></p>
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Atkins diet

High protein

Low CHO

Higher Fat intake

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South Beach diet

Protein consistent but macronutrient content varies

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Zone diet

Balanced diet

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Protein supplements

Balance of AA are best

Supplements usually high in BCAAs

Rapidly absorbed and delivered to muscle

Bypass the liver

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Marasmus

Low protein and calorie malnutrition

Body switches to starvation mode

Use energy reserves

<p>Low protein and calorie malnutrition</p><p>Body switches to starvation mode</p><p>Use energy reserves </p>
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Kwashiorkor

Protein deficiency

High CHO foods → Cassava

Weaned from breast milk to cassava

Osmotic imbalance in gut = swelling

Liver enlarged due to inability to export fat from liver (no VLDL made)

<p>Protein deficiency</p><p>High CHO foods → Cassava</p><p>Weaned from breast milk to cassava</p><p>Osmotic imbalance in gut = swelling</p><p>Liver enlarged due to inability to export fat from liver (no VLDL made)</p>
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Reactions of Protein Catabolism

Excess AA

Amino group → Ammonium

  • Gets excreted into urea cycle

  • Gets excreted into urine

Carbon skeleton → Glucose or Acetyl CoA

  • Glucogenic or ketogenic AA

<p>Excess AA</p><p>Amino group → Ammonium</p><ul><li><p>Gets excreted into urea cycle</p></li><li><p>Gets excreted into urine</p></li></ul><p>Carbon skeleton → Glucose or Acetyl CoA</p><ul><li><p>Glucogenic or ketogenic AA</p></li></ul><p></p>
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Differences in fed and fasted state

Fasted state involved formation of glutamine and alanine

Fed state mostly glutamine, involves liver and kidney

Fed state excretes NH4+ as urea

Fasted state mainly excretes as NH4+ directly

<p>Fasted state involved formation of glutamine and alanine</p><p>Fed state mostly glutamine, involves liver and kidney</p><p>Fed state excretes NH<sub>4</sub><sup>+ </sup>as urea</p><p>Fasted state mainly excretes as NH<sub>4</sub><sup>+ </sup>directly</p>
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Alkalosis

Fed state with high dietary protein intake

High AA catabolism increase Bicarbonate

Increase pH to more basic

<p>Fed state with high dietary protein intake</p><p>High AA catabolism increase Bicarbonate</p><p>Increase pH to more basic</p>
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Acidosis

Fasting/starvation

AA broken down and release glucogenic AA

pH drops

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Glutamate

Important in AA catabolism

End product of transamination rxns

α-ketoacid → α-ketoglutarate

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Aspartate

Donates Amino group in urea cycle (turns into asparagine)

α-ketoacid → oxaloacetate

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Alanine

Inter-organ N carrier

Muscle to liver

α-ketoacid → pyruvate

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Glutamine

Most abundant

Inter-organ carrier

Donate amino group to other rxn (turns into glutamate)

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4 rnx more N → organs → excretion: Transamination

amino acid α-keto acid → Aminotransferases

  • Aminotransferases → GPT and GOT

Glutamate almost always present in transamination reactions

α-ketoglutarate is almost always one of the reactants

  • α-ketoglutarate = amino group acceptor

Glutamate is almost always one of the products

<p>amino acid <span data-name="left_right_arrow" data-type="emoji">↔</span> α-keto acid → Aminotransferases</p><ul><li><p>Aminotransferases → GPT and GOT</p></li></ul><p>Glutamate almost always present in transamination reactions</p><p>α-ketoglutarate is almost always one of the reactants</p><ul><li><p>α-ketoglutarate = amino group acceptor</p></li></ul><p>Glutamate is almost always one of the products</p>
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4 rnx more N → organs → excretion: Oxidative deamination

Glutamate main AA that undergoes oxidative deamination

  • Because its main product of transamination

Amino group released from glutamate backbone

Glutamate → α-ketoglutarate + NH4+

  • Done by Glutamate dehydrogenase

<p>Glutamate main AA that undergoes oxidative deamination</p><ul><li><p>Because its main product of transamination</p></li></ul><p>Amino group released from glutamate backbone </p><p>Glutamate → α-ketoglutarate + NH<sub>4</sub><sup>+ </sup></p><ul><li><p>Done by Glutamate dehydrogenase</p></li></ul><p></p>
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4 rnx more N → organs → excretion: Glutamine production

Glutamate → Glutamine

  • Done by Glutamine synthetase

Fed: NH4+ travels to liver in

Fasted: NH4+ travels to kidney

<p>Glutamate → Glutamine </p><ul><li><p>Done by <em>Glutamine synthetase </em></p></li></ul><p>Fed: NH<sub>4</sub><sup>+ </sup>travels to liver in </p><p>Fasted: NH<sub>4</sub><sup>+ </sup> travels to kidney</p>
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4 rnx more N → organs → excretion: Glutamate regeneration

Opposite to glutamine production

Release Amino group from glutamine side chain

Fed: active in liver → amino group for urea synthesis

Fasted: active in kidney

<p>Opposite to glutamine production</p><p>Release Amino group from glutamine side chain</p><p>Fed: active in liver → amino group for urea synthesis</p><p>Fasted: active in kidney </p>
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4 rnx more N → organs → excretion: Urea Cycle

Toxic NH4+ converted to urea in liver

Urea transported to kidney

Aspartate donates Amino group (to form urea)

Uses Bicarbonate nearby (prevent alkalosis)

Requires ATP

<p>Toxic NH<sub>4</sub><sup>+ </sup>converted to urea in liver</p><p>Urea transported to kidney</p><p>Aspartate donates Amino group (to form urea)</p><p>Uses Bicarbonate nearby (prevent alkalosis)</p><p>Requires ATP</p>
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Cahill cycle (Glucose Alanine Cycle)

Pyruvate transaminated to Alanine

α-ketoglutarate + alanine → glutamate + pyruvate

Glutamate → Urea

Pyruvate → Glucose

<p>Pyruvate transaminated to Alanine</p><p>α-ketoglutarate + alanine → glutamate + pyruvate</p><p>Glutamate → Urea</p><p>Pyruvate → Glucose</p>
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Fed state N metabolsim

AA catabolism → Glutamine formation (from glutamate)

Glutamine transported to liver

Deliver Amino group for urea production

Urea transported to kidney

Excreted in urin

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Fasted state of N metabolsim

AA catabolism → Glutamine formation (from glutamate) + Alanine (from pyruvate)

Glutamine transported to kidney

  • Converted to glutamate and remove amino group

  • Amino group excreted as urine

Alanine sent to liver

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Ketogenic

Degraded AA can be converted into Acetyl CoA

Leucine and Lysine

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Glucogenic

Degraded AA can be converted into Glucose

Alanine, Glutamate, Aspartate