The following exercises are available in this section
Fats and oils - are all fats the same?
By the end of this exercise you should be able to:
- Explain why there is a need for fat in the diet, and how a high fat diet contributes to the development of obesity
- Describe the different classes of physiologically important lipids
- Explain what is meant by saturated, mono-unsaturated and polyunsaturated fatty acids, state the relative amounts of each that are considered desirable in the diet, and describe the effects of saturated and unsaturated fatty acids on serum cholesterol
- Explain the importance of polyunsaturated fatty acids in cell membrane phospholipids
- Explain what is meant by cis-trans isomerism and the problems associated with an excessive intake of trans-fatty acids
- Explain the shorthand notation for naming fatty acids and the importance of n-3 and n-6 polyunsaturated fatty acids
Children with fatty diarrhoea
By the end of this exercise you should be able to:
- Describe the processes involved in the digestion and absorption of dietary triacylglycerol
- Explain the importance of lipase
- Explain how non-esterified fatty acids, monoacylglycerol, bile salts and unesterified cholesterol emulsify triacylglycerol into micelles
- Describe in outline the formation of chylomicrons
- Explain the difference between the absorption of water-soluble products of digestion (monosaccharides and amino acids) and lipid-soluble compounds
- Describe the different routes of absorption of long-chain and medium-chain fatty acids
- Describe the clearance of chylomicrons from the circulation and the control of lipoprotein lipase
Gripping abdominal pain and jaundice
By the end of this exercise you should be able to:
- Explain how liver disease and obstruction of the bile duct can lead to jaundice, and how these two causes of jaundice can be differentiated by a simple blood test
- Describe the composition of bile and explain how gall stones are formed
- Describe in outline the biosynthesis of the primary and secondary bile salts, and the entero-hepatic circulation of bile salts
- Describe the role of bile salts in lipid digestion and absorption
- Explain how inhibition of bile salt reabsorption can reduce serum cholesterol
Muscle weakness, heart failure and profound hypoglycaemia in a young girl
By the end of this exercise you should be able to:
- Explain how carnitine deficiency affects fatty acid metabolism, and how impaired fatty acid metabolism leads to non-ketotic fasting hypoglycaemia
- Explain how impaired fatty acid metabolism leads to ready fatigue and muscle weakness, and cardiomyopathy, leading to heart failure
- Explain how measurement of plasma enzymes can be useful in the diagnosis of liver and muscle disease
- Describe the role of carnitine in the uptake of fatty acids into mitochondria for oxidation, and the roles of carnitine acyltransferase and the carnitine / acyl carnitine transport protein
Muscle weakness and hypoketotic coma on fasting
By the end of this exercise you should be able to:
- Explain why the pathway of oxidation of fatty acids to acetyl CoA is called beta-oxidation.
- Describe the pathway of beta-oxidation:
- dehydrogenation to form a carbon-carbon double bond
- addition of water across the carbon-carbon double bond forming a hydroxyl group at the beta-carbon
- oxidation of the hydroxyl group to an oxo group
- cleavage of the oxo-fatty acyl CoA to yield acetyl CoA and a fatty acyl CoA 2 carbons shorter
- Calculate the ATP yield from the oxidation of palmitate (C16:0)
- Explain why none of the intermediates of fatty acid oxidation is normally found in tissues
- Explain why children with genetic defects of the long-chain fatty acid trifunctional protein develop hypoketotic coma on fasting and outline an appropriate way of treating them.
Do we need to synthesise fatty acids?
By the end of this exercise you should be able to:
- Explain the importance of biotin in the carboxylation of acetyl CoA to malonyl CoA as the first step in fatty acid biosynthesis
- Explain the importance of the acyl carrier protein and describe its prosthetic group
- Describe the reactions involved in fatty acid biosynthesis
- Explain why none of the intermediates in the pathway is found when studying the mammalian fatty acid synthase
- Explain why, although there is an unsaturated intermediate in the reaction sequence, the only product of cytosolic fatty acid synthase is the saturated fatty acid derivative, palmitoyl CoA
- Describe the processes of fatty acid chain elongation and desaturation that occur in the endoplasmic reticulum
Is fructose fattening?
By the end of this exercise you should be able to:
- Describe how phosphofructokinase acts as the main regulator of glycolysis.
- Describe how phosphofructokinase is about 90% inhibited by normal intracellular concentrations of ATP, and how this inhibition is relieved by 5'AMP; describe how 5'AMP is formed as ADP begins to accumulate in the cell.
- Explain the metabolic importance of the inhibition of phosphofructokinase by phosphoenolpyruvate.
- Explain the metabolic importance of the inhibition of phosphofructokinase by citrate.
- Describe the role of citrate in providing a source of acetyl CoA in the cytosol for fatty acid synthesis and explain how it is that citrate does not leave the mitochondrion unless there is enough to maintain full activity of the citric acid cycle. Explain how citrate, which is a symmetrical molecule, behave asymmetrically.
- Explain the metabolic importance of the sequence of reactions between oxaloacetate and pyruvate in the cytosol.
- Explain how it is that fructose metabolism is not controlled by the need for ATP synthesis or cytosolic citrate, and how it is that a high fructose intake will lead to increased fatty acid synthesis.
Not an ounce of fat on her - and extreme emaciation in patient with advanced cancer
By the end of this exercise you should be able to:
- Explain the origin of the glycerol moiety of triacylglycerols.
- Explain why fatty acids are bound to serum albumin in the bloodstream and esterified with either carnitine or CoA inside cells, and describe how fatty acids are activated for triacylglycerol synthesis.
- Describe the pathway of triacylglycerol from glycerol 3-phosphate and fatty acyl CoA.
- Explain why the fatty acid at carbon-2 of a triacylglycerol is commonly a polyunsaturated fatty acid.
- Explain why a patient with congenital generalised lipodystrophy has fasting hypertriglyceridaemia, an enlarged liver and a muscular appearance.
- Explain how activation of hormone sensitive lipase in adipose tissue leads to hypermetabolism, emaciation and wasting in patients with advanced cancer.
Two boys with profound fasting hypoglycaemia and no ketone bodies
By the end of this exercise you should be able to:
- Describe the pathway of ketone body synthesis.
- Explain why it is beneficial to reduce acetoacetate to beta-hydroxybutyrate before export from the liver.
- Explain why a child who lacks one or other of the enzymes of ketone body synthesis becomes profoundly hypoglycaemia after a relatively prolonged fast, or when s/he has an infection.
- Explain why infusion of beta-hydroxybutyrate will maintain the plasma concentration of glucose after an overnight fast in a child who lacks one or other of the enzymes of ketone body synthesis.