Protein Metabolism

1. Protein Metabolism

2.

Protein Molecules - organic substances consisting of amino
acids connected in a chain by peptide bonds.

3. Protein Classification

I. Simple:
a) Globular: albumins, globulins, protamines, histones,
prolamins, glutelins
b) Fibrous: collagen, elastin, keratin
II. Complex: glycoproteins, lipoproteins, chromoproteins,
phosphoproteins, metalloproteins, nucleoproteins

4. Functions of Proteins

• Catalytic (enzymatic)
• Transport
• Protective
• Contractile
• Structural
• Hormonal
• Energetic
• Colloid-osmotic (oncotic)

5. Protein Metabolism

A source
Gastric
juice
The enzyme
Pepsin
Formed from pepsinogen under the action hydrochloric acid. Optimum pH for
action pepsin - 1,0 – 2,0
Gastrixin
Formed from pepsinogen. Optimum pH for actions gastrixin – 3,0
Rinnin
It is found in the gastric juice of infants children's. Causes milk to clot. Optimum pH for
action rinnina – 4,0 - 5,5
Trypsin
Chymotrypsin
Pancreatic juice
Carboxypeptidases A, B
Intestinal juice
Note
It is formed from trypsinogen under the action of enterokinases in the
intestinal cavity
Formed by from chymotrypsinogen under action of trypsin in the
intestinal cavity
Metalloproteins, which formed by from
procarboxypeptidase under the action of trypsin
in the intestines
Elastase
Formed by from proelastases and destroys connective tissue elastin
Aminopeptidases
Carry out stepwise cleavage amino acids from the polypeptide chain
Dipeptidases
They destroy it dipeptides up to free
amino acids

6.

Pathways of Amino Acid Utilization in the Body:
• Synthesis of proteins
• Formation of hormones, mediators
• Breakdown with the formation of carbohydrates, lipids,
ketone bodies, etc.

7. Detoxification Of Ammonia In The Body

Detoxification Pathways:
• Synthesis of urea. Detoxification and removal of ammonia are
carried out in the liver.
• Formation of ammonium salts. Occurs in the kidneys, where
ammonia is delivered in the form of amides of aspartic and
glutamic acids. Ammonium salts are excreted in the urine.
• Formation of amides of aspartic and glutamic
acids. Synthesized asparagine and glutamine are excreted in
the urine. The process occurs predominantly in nervous tissue,
rarely - in muscle tissue and kidneys.
• Reductive amination. Occurs to a small extent and is
insignificant in ammonia detoxification.

8. Urea

• Synthesized in the liver in the ornithine cycle (urea cycle).
• Excreted from the body through the kidneys and
extrarenally: through sweat and feces.
• A condition where the concentration of urea in the blood
is several times higher than normal is called uremia.

9.

Causes of Increased Blood Urea Levels:
• I. Prerenal
• Protein-rich diet
• High protein catabolism during fevers, heavy muscular work
• Diet poor in chloride ions (a compensatory adaptive reaction aimed at maintaining
blood osmotic pressure)
• Heart failure
• Blood loss
• Acute dehydration
• Leukemias
• Severe infectious diseases
• Burns
• Shock
• II. Renal (kidney diseases accompanied by decreased glomerular filtration and loss
of nephrons)
• III. Postrenal
• Obstruction of the urinary tract
• Prostate adenoma
• Tumors of the urinary system

10.

Causes of Decreased Blood Urea Levels:
1) Congenital deficiency of urea synthesis
2) Severe liver failure

11. Uric Acid

• The final product of purine nucleotide (adenine, guanine)
metabolism.
• Poorly soluble in water, and its salt crystals – urates –
deposit in joints and urinary tracts (gout and formation of
uric acid stones in the kidneys).
• The main part of uric acid is produced by the liver.
• Uric acid is excreted by the kidneys and extrarenally (with
sweat and feces).

12. Primary Uricemia

1) Defect of the enzyme hypoxanthine-guanine
phosphoribosyltransferase (Lesch-Nyhan syndrome: selfinjury, aggressiveness, cognitive impairment,
choreoathetosis, renal failure).
2) Increased activity of the enzyme phosphoribosyl
pyrophosphate synthetase, which stimulates the breakdown
of purine metabolism products into uric acid.
3) Decreased tissue sensitivity to elevated uric acid
concentration (loss of feedback).
4) Deficiency of the plasma protein that transports uric acid.
5) Congenital functional features of the kidneys.

13. Secondary Uricemia

1)
Consumption of food containing large amounts of purines: offal (liver, kidneys, tongue),
veal, meat extracts, smoked meats, caviar, coffee, and strong tea.
2) Starvation (tissue breakdown)
3) Hematological diseases (breakdown of nuclear cells, lysis of erythrocytes, which contain
large amounts of uric acid).
4) Leukocytoses, erythrocytoses.
5) Renal failure.
6) Epilepsy, intense muscle load.
7) Glycogen storage disease type I.
8) Hyperlactatemia, ketonemia (competition for the uric acid secretion mechanism in the
kidneys).
9) Dehydrations.
10) Diabetes mellitus.
11) Hypertension.
12) Malignant neoplasms.
13) Psoriasis.

14.

Causes of Decreased Blood Uric Acid Levels:
1) Defect of the enzyme xanthine oxidase, resulting in
xanthine, not uric acid, being the final product of purine
metabolism.
2) Decreased tubular reabsorption.
3) Pulmonary tuberculosis, especially in the acute stage
(impaired ability of tissues to retain uric acid).

15. Creatine and Creatinine

• Creatinine is formed in the body from creatine.
• The synthesis of creatine occurs in two stages.
• The first stage takes place in the kidneys, where a precursor of
creatine is formed from arginine and glycine.
• The final formation of creatine is completed in the liver.
• Creatine travels via the blood to the muscles, which
produce creatine phosphate.
• During muscle contraction, creatine phosphate breaks down
with the formation of ATP and creatinine.
• Then creatinine is excreted by the kidneys.

16.

Causes of Increased Creatine in the Blood:
1) In children, adolescents, during pregnancy.
2) Consumption of large amounts of proteins.
3) Necrosis or atrophy of skeletal muscles.
4) Dermatomyositis, myasthenia gravis, myositis, myotonia (increase in
creatine is associated with impaired utilization by diseased muscles).
5) Convulsive states.
6) Endocrine diseases (diabetes mellitus, hyperthyroidism, acromegaly,
eunuchoidism).
7) Leukemias.
8) Liver diseases.
9) Rheumatoid arthritis.
10) Burns.
11) Bone fractures.

17.

Causes of Increased Creatinine in the Blood:
1) Acromegaly, diabetes mellitus.
2) Impaired kidney filtration of any origin.
3) Physical load.
4) Crush syndrome (long-term compression syndrome).
5) Radiation sickness.
6) Dehydration.
7) Excessive consumption of meat products.

18. Indican

• Indican is formed in the liver from indole, which, in turn, is
formed during bacterial putrefaction of proteins in
the intestines.
• The decomposition of the amino acid tryptophan in the
intestine leads to the formation of the toxic
substance indole, which enters the liver via the portal
system and is inactivated by binding with sulfuric or
glucuronic acid in the liver.
• The resulting indican is non-toxic and is excreted by
the kidneys via filtration.

19.

Causes of Increased Blood Indican Concentration:
1) Functional renal failure (decreased urine output).
2) Extraintestinal formation of indole during autolysis of
tissue protein and its bacterial decay (purulent
appendicitis, lung abscess, purulent osteomyelitis).
3) Enhanced putrefactive processes in the intestine,
stagnation of intestinal contents (prolonged constipation
and intestinal obstruction).

20. Blood Plasma Proteins

• IN CLINICAL DIAGNOSTIC LABORATORIES, THE FOLLOWING
ARE MEASURED:
1. TOTAL PROTEIN
2. PROTEIN FRACTIONS
3. INDIVIDUAL PROTEINS

21. Total Protein

Normal blood protein level:
Newborns – 47 – 65 g/L;
Age 1 month – 41 – 55 g/L;
1 year – 57 – 78 g/L;
1-4 years – 59 – 79 g/L;
5-14 years – 62 – 82 g/L;
Adults – 60 – 85 g/L.

22.

Causes of Increased Total Blood Protein:
1) Acute and chronic infections
2) Autoimmune diseases
3) Paraproteinemic hemoblastoses (e.g., multiple
myeloma)
4) Lymphogranulomatosis (Hodgkin's disease)
5) Sarcoidosis
6) Dehydrations (relative hyperproteinemia)

23.

Causes of Decreased Total Blood Protein:
• I. Decreased Protein Synthesis:
1) Poor nutrition
2) Malabsorption (celiac disease, exudative enteropathy, enteritis, cystic fibrosis,
pancreatitis)
3) Liver diseases
4) Long-term treatment with glucocorticoids
• II. Increased Protein Loss by the Body:
1) Nephrotic syndrome
2) Ascites, exudates, transudates
3) Burns
4) Bleeding
• III. Increased Protein Breakdown in the Body:
1) Thyrotoxicosis
2) Fever
3) Trauma
4) Tumors
• IV. Hyperhydration (relative hypoproteinemia)

24. Protein Fractions

1) ALBUMINS - 55-65%
2) α1-GLOBULINS - 2-5%
3) α2-GLOBULINS - 7-13%
4) β-GLOBULINS - 8-15%
5) γ-GLOBULINS - 12-22%

25. α1-Globulins

Causes of Increased α1Globulin Fraction:
1) Acute inflammatory
processes in the body
2) Exacerbations of chronic
diseases
3) Allergic diseases
4) Burns
5) Trauma
6) Autoimmune diseases
7) Malignant neoplasms
α1-globulins include the following
individual proteins:
a) α1-fetoprotein
b) α1-antitrypsin
c) Prothrombin
d) Transcortin
e) Thyroxine-binding globulin
f) Retinol-binding globulin
g) Transcobalamin

26. α2-Globulins

Causes of Increased α2Globulins:
1) Acute inflammation
2) Exacerbations of chronic
diseases
3) Allergic diseases
4) Burns
5) Trauma
6) Autoimmune diseases
7) Malignant neoplasms
Individual proteins belonging to
α2-globulins:
Ceruloplasmin
Haptoglobin
Antithrombin III
Antithrombin IV
C1 and C9 components of
complement
α2-globulin that binds uric acid
Plasminogen
Erythropoietin

27. β-Globulins (β1- and β2-globulins)

Causes of Increased βGlobulin Fraction:
1) Chronic inflammation
2) Cholestasis
3) Hyperlipoproteinemias
4) Nephrotic syndrome
5) Diabetes mellitus
6) Hypothyroidism
Individual proteins
belonging to β-globulins:
β-lipoproteins (LDL - LowDensity Lipoproteins)
Transferrin
Hemopexin
C2-C8 components of
complement
Fibrinogen
CRP (C-reactive protein)

28. γ-Globulins

Hyperimmunoglobulinemia
occurs in:
1) Chronic inflammatory
processes in the body;
2) Autoimmune diseases;
3) Allergic diseases;
4) Parasitic diseases;
5) Paraproteinemic
hemoblastoses.
Individual proteins
belonging to γ-globulins:
• Ig G
• Ig M
• Ig E
• Ig A
• Ig D

29.

1. Acute Inflammatory Type Proteinogram:
Total Protein – Normal (N)
Albumins – Decreased (↓)
α1-globulins – Increased (↑)
α2-globulins – Sharply Increased (↑↑)
β-globulins – Normal (N)
γ-globulins – Normal (N) (slight increase possible)
CRP – Strongly Positive (++++)
Albumin/Globulin Ratio – Decreased (↓) (normal 1.3 – 2.3)

30.

2. Chronic Inflammatory Type Proteinogram:
Total Protein – Normal (N)
Albumins – Decreased (↓)
α1-globulins – Normal (N)
α2-globulins – Normal/Increased (N/↑)
β-globulins – Increased/Normal (↑/N)
γ-globulins – Sharply Increased (↑↑)
CRP – Negative
Albumin/Globulin Ratio – Decreased (↓)

31.

3. Nephrotic Type Proteinogram:
Total Protein – Decreased (↓)
Albumins – Sharply Decreased (↓↓)
α1-globulins – Normal/Increased (N/↑)
α2-globulins – Normal/Increased (N/↑)
β-globulins – Increased (↑)
γ-globulins – Sharply Decreased (↓↓)
CRP – Negative/Positive
Albumin/Globulin Ratio – Sharply Decreased (↓↓)

32.

4. Hepatic Type Proteinogram (Hepatitis):
Total Protein – Normal/Decreased (N/↓)
Albumins – Decreased (↓)
α1-globulins – Normal (N)
α2-globulins – Normal/Decreased (N/↓)
β-globulins – Increased/Sharply Increased (↑/↑↑)
γ-globulins – Sharply Increased (↑↑)
CRP – Negative
Albumin/Globulin Ratio – Decreased (↓)