CATEDRA BIOCHIMIE I BIOCHIMIE CLINIC INDICA II METODICE FACULTATEA MEDICIN II, ANUL II Analizat i aprobat la edin a catedrei din 17.01.2014, proces verbal nr. 11 eful Catedrei Biochimie i Biochimie Clinic , conf. universitar, dr. hab. în medicin Olga Tagadiuc____________________ Methodical indication 17. Lipids - classification, structure, physico-chemical properties, biological role. Biological membranes 1: Total lipid's assay in blood serum with phosphovanillinic reagent Method's principle: Serum. Lipids are hydrolized with concentrated H2SO4. The final products react with phosphovanilinic reagent to form a red complex compound Procedure:
Mix the solutions and incubate 40-50 min at room-temperature
Measure the extinction of the experimental and standard solutions using control
solutions for comparison, 3 mm cuvettes and green filter
Calculation:C(g/l) = (A/B) · 8, where A - extinction of the experimental solution B – extinction of the standard solution 8 – lipid’s content in standard solution (g/l) Normal values are 4-8 g / l Clinical importance. Content of lipids in serum is increased (hyperlipidemia) in diabetes mellitus, nephrosis, biliary cirrhosis, obesity, atherosclerosis, etc. Physiological hyperlipidemia is found above 1 - 4 hours after eating (postprandial hyperlipemia). Rezult: ________________________________________________________________________ ________________________________________________________________________ Conclusion: _________________________________________________________________ _________________________________________________________________ Initial level of knowledge
1. Classification of lipids (structural, functional, according physical and chemical properties). 2. Saturated and unsaturated fatty acids. Structure, physico-chemical properties, representatives.
www.biochimia.usmf.md CATEDRA BIOCHIMIE I BIOCHIMIE CLINIC INDICA II METODICE FACULTATEA MEDICIN II, ANUL II Self-preparing questions:
1. Biological functions of lipids. 2. Storage lipids: triacylglycerols - structure, physico-chemical properties, representatives.
3. Protoplasmatic and membrane lipids. Structure, physico-chemical properties, biomedical role.
- Glycerophospholipids - phosphatidylserines, phosphatidylethanolamines (cephalins), phosphatidylcholines (lecithins), phosphatidylinositols, phosphatidylglycerols (cardiolypins) plasmalogens - Sphingophospholipids- sphingomyelins
b) Glycolipids - galacto-and glucocerebrosides, sulphatides, gangliosides c) Cholesterol and Cholesterides. Structure, physico-chemical properties, biomedical role.
• The biological and medical role • Chemical composition - lipids, proteins, carbohydrates. Their functional role. • Structural and functional organization - fluid-mosaic model of Singer-Nicolson • The properties of membranes: fluidity, motility, selective permeability, asymmetry, self-assembling and self-repairer. • Structural and functional diversity and specificity. • Membrane transport:
• simple diffusion; • facilitated diffusion - glucose transporters (GLUT), anion exchangers; • channel type alpha and beta (structural features).
• primary (Na+, K+-ATPase, Ca2+-ATPase, ABC-transporters); • secondary (amino acid transporters, glucose).
c) diseases caused by deficiency of membrane channels and transporters.
Situation problems
1. Vegetable oils are liquid triglycerides and animal fats - solid triglycerides. Write a
triacylglycerol structure present in oil and a triacylglycerol present in animal fat.
2. What fatty acids are essential for the human body? Write their structure. What are the main
food sources of the essential fatty acids?
3. What are the differences between the cytoplasmic membranes of a normal cell and a cancer 4. What cell organelles have membranes formed from a single layer of lipids? How does this
structural feature reflect on their properties?
Tests for self-evaluation 1. For the human body the following fatty acids are essential:
a) ligno eric b) oleic c) palmitoleic d) linolenic e) linoleic
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2. Acylglycerols :
a) are constituents of biological membranes b) are esters of glycerol and fatty acids c) represent a form of energy storage d) are soluble in water e) are derivatives of phosphatidic acid
2. Phosphatidylcholine and phosphatidylethanolamine:
a) are representatives of waxes b) are the main components of cell membranes c) represent a form of energy storage d) are derivatives of phosphatidic acid e) have different electric charge
3. Sphingosine:
a) is a saturated dihydroxy aminoalcool b) is a component of sphingomyeline c) is a component of glycolipids d) is a constituent of glycerophospholipids e) doesn’t enter in the composition of the ceramide
4. Cerebrosides:
b) contain a beta-galactose or a beta-glucose bound to ceramide c) contain oligosaccharides d) sulfatides are a class of sulfated cerebrosides e) the white matter of the brain contains cerebrosides in large amounts
5. Gangliosides:
a) contain several residues of glycerol b) contain N-acetylneuraminic acid (NANA) c) contain only glucose in the oligosaccharide d) contain sulfate residues linked to galactose e) are situated on the inner surface of membranes
6. Glycolipids:
a) contain mono-or oligosaccharides that are bound to ceramide b) gangliosides contain one or more residues of sialic acid c) gangliosides represent glycerophospholipids d) gangliosides contain phosphatidic acid e) gangliosides contain N-acetylneuraminic acid
7. Cholesterol:
a) is the precursor of steroid hormones b) is hydrophobic c) is a storage lipid d) enter into the composition of biological membranes e) is the precursor of all fat-soluble vitamins
8. Main properties of the membranes:
a) symmetry b) fluidity c) asymmetry d) immobility of components e) lipid monolayer
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9. Biological membranes are stabilized by:
a) hydrophobic interactions b) Van-der-Waals forces c) hydrogen bonds d) peptide bonds e) disulfide bonds
Methodical indication 18. Digestion and absorption of lipids. Plasma lipoproteins. Tissue catabolism of lipids. 1:Identification of bile acids. Method's principle: When sucrose is treated with concentrated H2SO4 oxymethylfurfurol is formed. It reacts with bile acid to generate a red-violet complex compound. Procedure: Put into a test-tube:
Rezult: ________________________________________________________________________ Conclusions: _________________________________________________________________ _________________________________________________________________
Initial level of knowledge
1. The oxidative decarboxylation of pyruvate, Krebs cycle, respiratory chain, oxidative
Self-preparing questions:
1. The importance of lipids in the diet. Indispensable fatty acids.
2. Digestion and absorption of dietary fat:
• The structure and role of bile acids. • Digestion of triacylglycerols, phospholipids, cholesterides: enzymes, hydrolysis products. • Absorption of lipid hydrolysis products. • Hormonal regulation (action of cholecystokinin, secretin). • Disorders of digestion and absorption of lipids. Pancreatic, liver and intestinal steatorrhea.
3. Lipid resynthesis in enterocytes. Formation of chylomicrons.
4. Blood transport of lipids. Plasma lipoproteins: structure, methods of separation, fractions
(chilomicronii, VLDL, LDL and HDL), chemical composition (lipids and apoproteins), metabolism, functions.
5. Triacylglycerol catabolism - reactions, enzymes, hormonal regulation (action of catecholamines,
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• Pathways for using. • Oxidation: reactions, enzymes, energy efficiency.
• saturated with even number of carbon atoms (location, steps, reactions, enzymes, coenzymes, energy efficiency, regulation); • unsaturated with odd number of carbon atoms (features); • in peroxisomes (features), the biological role.
8. Tissue catabolism of glycerophospholipids, sphingomyelins and glycolipids (location, enzymes,
9. Hereditary tissue lipidoses (Neimann-Pick, Tay-Sachs) – causes, biochemical changes, clinical
Situation problems
1. Write the reaction catalyzed by pancreatic phospholipase A2. Indicate the names of the
substrate and reaction products. Cobra and bees venom contains phospholipase A2. How does the enzyme affect the bitten persons?
2. What are the causes of steatorrhea? What metabolic disorders may develop persistent
steatorrhea? What clinical manifestations and biochemical changes may be present depending on the cause of steatorrhea?
3. Write the reaction catalyzed by lecithin—cholesterol acyltransferase (LCAT). Indicate the
names of substrates and reaction products. What lipoprotein fractions this enzyme is associated with? What is the fate of the reaction products? What are the metabolic consequences of the enzyme LCAT deficiency?
4. What is the substrate and the products of the reaction of hydrolysis catalyzed by the enzyme
lipoprotein lipase (LPL)? Which tissues is the enzyme located in? What is the fate of the hydrolysis products? What biochemical and metabolic disorders are characteristic for enzyme LPL deficiency?
5. Under stress and starvation an intense mobilization of triacylglycerols from adipose tissue
occurs. What hormone stimulates lipolysis? Indicate schematic ways to use the products of hydrolysis of triglycerides?
6. What will be the effects on the fatty acids oxidation of a diet rich in fats and without
carbohydrates? Use of which fatty acids - with an even or odd number of carbon atoms - is more suitable in the absence of carbohydrates in the diet? Please explain your answer.
7. Write a triacylglycerol structure consisting of a saturated fatty acid, an unsaturated fatty acid
and one with odd number of carbon atoms. Calculate the energy efficiency of complete oxidation of this triglyceride.
Tests for self-evaluation
1. Bile acids:
a) are derivatives of cholic acid b) consist of 28 carbon atoms c) are conjugated in the liver with bilirubin d) are polar compounds e) participate in the emulsification of fats
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2. Lipolytic enzyme action in the gastrointestinal tract:
a) phospholipases (A1, A2, C, D) break down phosphoglycerides b) cholesterol-esterase cleaves free cholesterol c) ceramidase cleaves sphingosine d) gastric lipase is active in adults e) pancreatic lipase cleaves the acyl-residue in the beta-position of triglycerides.
3. The fate of lipid digestion products absorbed in the intestine:
a) are eliminated in the blood via the portal vein b) are eliminated in the blood via the hemorrhoidal veins c) are included in the resynthesis of complex lipids in the enterocytes d) are included in the resynthesis of complex lipids in the intestine e) resynthesized lipids interact with apo-proteins and form chylomicrons
4. Where is the location of the following lipoprotein synthesis?
a) LDL enterocytes b) VLDL blood circulation c) liver chylomicrons d) HDL liver, enterocytes
5. What apolipoproteins are present in the following lipoproteins?
a) LDL B100, C, E b) VLDL A, C, D, E c) chylomicrons B100 d) HDL B48, C, E
6. What is the main function of the following lipoproteins?
a) LDL transport endogenous triglycerides to adipose tissue, muscle, myocardium b) V transport cholesterol to extrahepatic tissues c) Chylomicrons carry cholesterol from extrahepatic tissues to the liver d) HDL transport exogenous triglycerides to muscle, myocardium, adipose tissue
7. In the result of one turn of beta-oxidation the fatty acid undergoes the following changes:
a) is oxidized b) is reduced c) becomes shorter by 4 carbon atoms d) becomes shorter by 2 carbon atoms e) one molecule of acetyl-CoA is formed
8. Oxidation of polyunsaturated fatty acid requires:
a) the presence of cis- 3-trans- 2-enoyl-CoA isomerase b) an additional molecule of HSCoA c) the presence of trans- 2-cis- 4-dienoyl-CoA-reductase d) an additional molecule of NAD + e) energy efficiency is the same as in the saturated fatty acid oxidation
9. Oxidation of fatty acids with odd number of carbon atoms:
a) in the last cycle of beta-oxidation a molecule of propionyl-CoA and one of acetyl-CoA are obtained b) propionyl-CoA complete oxidation requires vitamins H and B12 c) propionyl-CoA is included directly in the Krebs cycle d) propionyl-CoA complete oxidation requires CO2, ATP, Mg2 + e) propionyl-CoA is included in the Krebs cycle in the form of succinyl-CoA
www.biochimia.usmf.md CATEDRA BIOCHIMIE I BIOCHIMIE CLINIC INDICA II METODICE FACULTATEA MEDICIN II, ANUL II Methodical indication 19: Biosynthesis of lipids 1: Identification of ketone bodies in urine Method's principle: Ketone bodies (acetone, acetoacetic acid and -hydroxybutyric acid) interact in basic medium with sodium nitroprusside and concentrated acetic acid forming a cherry-red compound. Procedure: Use only dry test-tubes! Put in 2 test-tubes: Reagents I test-tube II test-tube Shake the test-tubes. Content of the test-tubes turn into red-orange.
The urine containing ketones bodies becomes red-purple. The color intensity varies in direct proportion to the concentration of ketone bodies in urine
Result: ___________________________________________________________________
____________________________________________________________________ Conclusions: ________________________________________________________________ ________________________________________________________________ Self-preparing questions:
1. Biosynthesis of fatty acids - location, steps, reactions, enzymes, coenzymes, regulation: • saturated with even number of carbon atoms;
• unsaturated with even number of carbon atoms; • arachidonic acid biosynthesis (general concepts).
2. Biosynthesis of triacylglycerol: location, reactions, enzymes and coenzymes, regulation. 3. Biosynthesis of glycerophospholipids: location, reactions (synthesis de novo and salvage
pathway), enzymes and coenzymes. Lipotropic substances, their role.
4. Biosynthesis of sphingophospholipids and glycolipids: precursors, the main reactions,
5. Cholesterol biosynthesis - stages, the first stage reactions (up to mevalonate acid), enzymes,
coenzymes, regulation. Catabolism and excretion of cholesterol (general concepts).
• representatives, chemical structure; • biosynthesis (location, substrate side); • using (tissue reactions, the final products, energy efficiency); • ketonemia and cetonuria (causes, mechanism).
Situation problems
1. After ingesting a high-fat ration the storage of lipids in adipose tissue takes place. Indicate
how occur: the food triglycerides digestion, the hydrolysis products absorption, lipids resynthesis in enterocytes, the transport of triglycerides to adipose tissue and their synthesis in adipocytes.
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2. After ingestion of sucrose, the excess of glucose and fructose is converted to fatty acids in
liver. Synthesis of fatty acids requires acetyl-CoA, ATP and NADPH. Indicate the ways of these compounds obtaining from carbohydrates. What is the subsequent fate of the fatty acids?
3. Why the linoleic and linolenic acids can not be synthesized in the human body, but
arachidonic acid is synthesized. Write reactions for the synthesis of arachidonic acid. What is the role of arachidonic acid?
4. Clinical and diagnostic value of determination of serum cholesterol. Causes and mechanisms
of hypercholesterolemia. What lipoprotein fractions is cholesterol transported by and which is the diagnostic value of there determination?
5. Explain the mechanism of lipotropic factors action. Name the lipotropic factors, reactions
and processes in which they participate.
Tests for self-evaluation
1. Differences between oxidation and fatty acid biosynthesis:
a) fatty acid synthesis occurs in mitochondria, but the oxidation – in the cytosol b) in fatty acid synthesis intermediates are bound to ACP, but in oxidation – to the HSCoA c) in oxidation NAD+ and FAD are used, in the synthesis - NADPH d) in beta-oxidation the enzymes are associated in a polyenzymatic complex, but in synthesis – are not e) malonyl is used in synthesis, but in beta-oxidation – is not.
2. Activator (1) and inhibitor (2) of the acetyl-CoA carboxylase (the regulating enzyme in the synthesis of fatty acids): a) ATP ADP b) AMP ATP c) malonic AMP d) acetoacetate citrate e) citrate palmitoyl-CoA
3. NADPH serves as a donor of reducing equivalent in fatty acid synthesis. It is generated in the following process: a) tricarboxylic acid cycle b) glycolysis c) reaction catalyzed by malic enzyme d) beta-oxidation of fatty acids e) pentose-phosphate pathway of glucose oxidation
4. Biosynthesis of triacylglycerols:
a) takes place exclusively in adipose tissue b) increases in starvation c) is amplified in diabetes mellitus type I d) is activated by insulin e) storage of triglycerides in adipose tissue is unlimited
5. Phosphatidylinositols:
a) are precursors of fat soluble vitamins b) are precursors of second messengers: inositolphosphates and diacylglycerols
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c) are stored in adipose tissue d) enter into the composition of biological membranes e) have the energy function
6. Rate-limiting reaction in cholesterol synthesis is:
a) acetoacetyl-CoA formation b) beta-hydroxy-beta-methylglutaryl-CoA (HMG-CoA) synthesis c) squalene cyclization d) 5-pirophosphomevalonate formation e) synthesis of mevalonic acid from HMG-CoA
7. Ketonemia:
a) can occur in starvation b) can be generated by a diet low in fat c) is determined by a ration rich in carbohydrates d) is caused by increased synthesis of ketone bodies in liver e) is determined by the intensive use of ketone bodies in tissues
8. Use of ketone bodies in tissues
a) are used only in liver b) are used efficiently in the myocardium, skeletal muscles as an source of energy c) require the presence of oxaloacetate d) can be converted into pyruvate and then into glucose e) their accumulation leads to ketoacidosis
Methodical indication 20 Metabolism of eicosanoids and fat soluble vitamins. Regulation and pathochemistry of lipid metabolism. 1: -lipoproteins assay in blood serum Method's principle: -lipoproteins react with heparin to form a complex compound, that is precipitated with CaCl2. The intensity of turbidity is proportional to -lipoproteins content. Procedure: put in a test-tube:
Shake the solution and measure the extinction of the solution (E1) using CaCl2 as
comparison solution (5 mm cuvettes, red filter). Pour the solution back into the test-
Shake the solution and exactly 4 min later measure again the extinction (E2).
Calculation: C (Units) = (E2-E1) · 100 Normal values: 35-55 Units Clinical-diagnostic significance: -lipoprotein content increases in atherosclerosis, jaundice, diabetes mellitus, obesity etc. -lipoprotein content decreases very rarely, for example in plasmocytoma. Result: _____________________________________________________________________ Conclusion: ____________________________________________________________________ __________________________________________________________________ www.biochimia.usmf.md CATEDRA BIOCHIMIE I BIOCHIMIE CLINIC INDICA II METODICE FACULTATEA MEDICIN II, ANUL II Initial level of knowledge
1. Fat-soluble vitamins A, D, E, K: chemical structure, food sources, the diurnal demand. 2. Glycolysis, gluconeogenesis, pentose phosphate pathway of glucose oxidation.
Self-preparing questions:
1. Eicosanoids - prostaglandins, leukotrienes, thromboxanes- precursor, chemical structure,
synthesis pathways, enzymes, biomedical role.
2. Metabolic role of fat-soluble vitamins A, D, E, K. hypo-and hypervitaminosis (causes and
3. Neurohormonal regulation of lipid metabolism. Action of catecholamines, glucagon, insulin,
glucocorticoids, lipotropinelor, thyroid hormone.
4. Interrelations between energy, carbohydrate and lipid metabolism. 5. Normal values of serum lipids. Diagnostic importance of determination of serum
triglycerides, total cholesterol, HDL-and LDL-cholesterol level.
6. Dyslipidemia - causes, biochemical, clinical manifestations:
a) primary hypolipoproteinemia - (general concepts). Tangier disease - cause biochemical changes.; b) primary hyperlipoproteinemia (familial hypercholesterolemia, family hiperchilomicronemia) c) secondary (acquired) hyperlipoproteinemia - in diabetes mellitus, alcoholism.
7. Acquired tissue lipidoses: obesity, atherosclerosis and alcoholism. Causes, metabolic
Situation problems
1. What indicators will change in plasma lipids in diabetes mellitus? Causes and mechanisms
2. Is it possible the synthesis of glucose from triglyceride? If it is possible, please write the
3. Is it possible the synthesis of triglyceride from glucose? If it is possible, please write the
4. The use of aspirin in some patients induces bronchospasm and bronchial asthma. What
causes these effects? What enzyme is inhibited by aspirin and other non-steroidal anti-inflammatory preparations?
5. Why ethanol can turn into lipids, but not in carbohydratest? What type lipids synthesis is
stimulated by excessive alcohol consumption? Indicate the pathway of ethanol conversion into fatty acids.
Tests for self-evaluation
1. Atherosclerosis:
a) is caused by increased level of HDL-cholesterol in plasma b) there is an accumulation of cholesterol in macrophages c) chylomicron are proatherogenic lipoproteins d) LDL is antiatherogenic lipoprotein e) oxidized LDL promotes atherosclerosis
2. Obesity:
a) is characterized by excessive accumulation of phospholipids in the adipose tissue b) is caused by hyperinsulinemia c) predisposes to cardiovascular disease, diabetes type II d) is the result of sedentary lifestyle and high calorie food e) does not depend on diet and physical activity
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3. According the eicosanoids the following statements are correct:
a) are synthesized from arachidonic acid b) act as second messengers c) the prostaglandins, prostacyclins and tromboxans are obtained in cyclooxygenase pathway d) the leukotrienes are obtained the lipoxygenase pathway e) all eicosanoids act through cAMP
4. Inhibitors of the eicosanoids synthesis:
a) aspirin inhibits the lipoxygenase b) aspirin inhibits the cyclooxygenase c) steroidal antiinflammatory preparations inhibits phospholipase A2 d) steroidal antiinflammatory preparations lead to a decrease of prostaglandins synthesis only e) steroidal antiinflammatory preparations leads to adecrease of leukotriene synthesis only
5. Liposoluble vitamins:
a) include ascorbic acid, biotin, folic acid, pantothenic acid b) include vitamins A, E, K and D c) are not stored in the body d) can be accumulated in muscle tissue e) require the presence of lipids to be absorbed from the intestine
6. Vitamin A:
a) includes -, -, -and -tocopherols b) includes retinol, retinoic acid and retinal c) enters in the rhodopsin structure d) has an antioxidant action e) is synthesized in the human body
Vitamin K:
a) vicasol is a vegetal form of vitamin K b) treatment with antibiotics cause hypovitaminosis K c) has anti hemorrhagic action d) has anticoagulant action e) is the coenzyme of enzyme carboxylase that participates in carboxylation of glutamic acid in the composition of coagulation factors II, VII, IX and X
8. Metabolism of vitamin D:
a) is synthesized in the skin under the action of ultraviolet light b) the active form of vitamin D is colecalciferol c) the active form is calcitriol d) calcitriol is synthesized in the skin by hydroxylation of cholesterol e) calcitriol formation is activated by parathyroid hormone
9. Calcitriol:
a) is the vegetal vitamin D b) is synthesized by two consecutive hydroxylation in the liver and kidney from cholecalciferol c) regulates calcium and phosphate level in the blood d) inhibit biosynthesis of Ca-binding protein that provides Ca2+ absorption from the intestine e) the mechanism of action includes intracellular cAMP formation
www.biochimia.usmf.md CATEDRA BIOCHIMIE I BIOCHIMIE CLINIC INDICA II METODICE FACULTATEA MEDICIN II, ANUL II Methodical indication Test on the chapter “Metabolism of lipids”
1. Biological functions of lipids. 2. Classification of lipids (structural, functional, according physical and chemical properties). 3. Saturated and unsaturated fatty acids. Structure, physico-chemical properties,
4. Storage lipids: triacylglycerols - structure, physico-chemical properties, representatives.
5. Protoplasmatic and membrane lipids. Structure, physico-chemical properties, biomedical
role. Glycerophospholipids, Sphingophospholipids (sphingomyelins), Glycolipids, Cholesterol and Cholesterides. Structure, physico-chemical properties, biomedical role.
6. Biological membranes. The biological and medical role. Chemical composition - lipids,
proteins, carbohydrates. Their functional role. Structural and functional diversity and specificity.
7. Structural and functional organization of biological membranes - fluid-mosaic model of
8. The properties of membranes: fluidity, motility, selective permeability, asymmetry, self-
9. Membrane transport: simple and facilitated diffusion; active primary and secondary
transport. Diseases caused by deficiency of membrane channels and transporters.
10. The importance of lipids in the diet. Indispensable fatty acids. 11. Digestion and absorption of dietary fat: the structure and role of bile acids, digestion of
triacylglycerols, phospholipids, cholesterides: enzymes, hydrolysis products, absorption of lipid hydrolysis products, hormonal regulation (action of cholecystokinin, secretin), disorders of digestion and absorption of lipids. Pancreatic, liver and intestinal steatorrhea.
12. Lipid resynthesis in enterocytes. Formation of chylomicrons. 13. Blood transport of lipids. Plasma lipoproteins: structure, methods of separation, fractions
(chilomicronii, VLDL, LDL and HDL), chemical composition (lipids and apoproteins), metabolism, functions.
14. Triacylglycerol catabolism - reactions, enzymes, hormonal regulation (action of
catecholamines, glucagon, insulin, glucocorticoids).
15. Glycerol metabolism: Pathways for using. Oxidation: reactions, enzymes, energy
16. Beta-oxidation of fatty acids: saturated with even number of carbon atoms (location, steps,
reactions, enzymes, coenzymes, energy efficiency, regulation); unsaturated with odd number of carbon atoms (features); in peroxisomes (features), the biological role.
17. Energy efficiency of the complete oxidation of triacylglycerols. 18. Tissue catabolism of glycerophospholipids, sphingomyelins and glycolipids (location,
19. Hereditary tissue lipidoses (Neimann-Pick, Tay-Sachs) – causes, biochemical changes,
20. Biosynthesis of fatty acids - location, steps, reactions, enzymes, coenzymes, regulation:
saturated with even number of carbon atoms; unsaturated with even number of carbon atoms.
21. Arachidonic acid biosynthesis (general concepts). 22. Biosynthesis of triacylglycerol: location, reactions, enzymes and coenzymes, regulation. 23. Biosynthesis of glycerophospholipids: location, reactions (synthesis de novo and salvage
pathway), enzymes and coenzymes. Lipotropic substances, their role.
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24. Biosynthesis of sphingophospholipids and glycolipids: precursors, the main reactions,
25. Cholesterol biosynthesis - stages, the first stage reactions (up to mevalonate acid), enzymes,
coenzymes, regulation. Catabolism and excretion of cholesterol (general concepts).
26. Ketone bodies: representatives, chemical structure; biosynthesis (location, substrate side);
using (tissue reactions, the final products, energy efficiency); ketonemia and cetonuria (causes, mechanism).
27. Eicosanoids - prostaglandins, leukotrienes, thromboxanes- precursor, chemical structure,
synthesis pathways, enzymes, biomedical role.
28. Metabolic role of fat-soluble vitamins A, D, E, K. hypo-and hypervitaminosis (causes and
29. Neurohormonal regulation of lipid metabolism. Action of catecholamines, glucagon, insulin,
glucocorticoids, lipotropinelor, thyroid hormone.
30. Interrelations between energy, carbohydrate and lipid metabolism. 31. Normal values of serum lipids. Diagnostic importance of determination of serum
triglycerides, total cholesterol, HDL-and LDL-cholesterol level.
32. Dyslipidemia - causes, biochemical, clinical manifestations. 33. Primary hypolipoproteinemia - (general concepts). Tangier disease - cause biochemical
34. Primary hyperlipoproteinemia (familial hypercholesterolemia, family
35. Secondary (acquired) hyperlipoproteinemia - in diabetes mellitus, alcoholism. 36. Acquired tissue lipidoses: obesity, atherosclerosis and alcoholism. Causes, metabolic
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