4 Energy Storage Carbs,lipids, Proteins Flashcards
Describe the reactions involved in glycogen synthesis and breakdown
Synthesis(requires ATP):
Glucose -(hexokinase/ glucokinase)- glucose 6 phosphate -phosphoglucomutase)- glucose 1 phosphate - UDP glucose-(glycogen synthase/ branching enzyme)- glycogen
Breakdown:
Glycogen -(glycogen phosphorylase)- glucose 1 phosphate -(phosphoglucomutase)- glucose 6 phosphate (enter glycolysis in skeletal) -(glucose6phosphatase)- glucose (enter blood in liver)
Describe the major energy stores in a 70 kg man
Glycogen - store of glucose, used to prodide glucose between meals and during exercise.
TAG - used to produce fatty acids which are metabolised during starvation and prolonged exercise and glycerol which can enter glycolysis once turned into DHAP
Protein/glucogenic amino acids - can be converted to acetyl CoA. Used in times of extreme starvation.
Compare the functions of liver and muscle glycogen
Muscle glycogen - produce glucose during exercise for the muscle.
Liver - produce glucose for the blood and other tissues when the concentration lowers (starvation) supplying glucose to tissues dependent on it e.g. Rbc and CNS.
Explain the clinical consequences of glycogen storage disease
Genetics affect enzymes in disease.
Excess storage affects liver and muscles and causes tissue damage. Diminished storage (hypoglycaemia) leads to poor exercise tolerance.
E.g. Von gierke’s disease - deficiency of G6phosphatase.
Explain why and how glucose is produced from non carbohydrate sources
This allows glucose to be produced and used when glycogen stores have been depleted. Some tissues have absolute requirement e.g. Rbc, CNS & kidneys.
Lactate and gluconeogenic amino acids can be converted to pyruvate which undergoes several reactions to form glucose (PEPCK and 1,6 bisphosphatase needed). Galactose, fructose and glycerol also can create glucose however they do not need PEPCK.
Explain why triacylglycerols can be used as efficient energy storage molecules in adipose tissue
These molecules are highly reduced and so have the potential to produce large amounts of useable energy. Hydrophobic so group together in anhydrous form which is under hormone control.
Describe how dietary triacylglycerols are processed for storage
Broken down by pancreatic lipases and absorbed through the gut wall as fatty acids and glycerol. They then recombine and are transported to tissues via chylomicros and stored in adipose tissue.
Describe how fatty acid degradation differs from fatty acid synthesis
Fatty acid synthesis. Acetyl CoA - malonyl CoA. Cycle occurs and each time c2 is added to a chain using fatty acid synthase per cycle until a fatty acid is formed. Requires ATP and NADH. Occurs in cytoplasm
Fatty acid degredation -FA activated - reacts with acetylCoA. Is transferred into mitochondria using carnitine and carnitine shuttle transporter. Enters cycle which creates many acetyl CoA molecules (C2) also produces reducing power fad2h and NADH.
Describe how amino acids are catabolised in the body
Amino acids are either glucogenic or ketogenic.
Glucogenic amino acids can be broken down into pyruvate or oxaloacetate which can then enter glycolysis.
Ketoacids can be synthesised.
Amino acid + a-ketoglutarate –> glutamate + keto acid.
Amino + oxaloacetate –> aspartate + keto acid.
Alanine aminotransferase converts alanine to glutamate.
Aspartate aminotransferase converts glutamate to aspartate.
Aspartate can then enter the urea cycle and be broken down to produce urea.
NH2 amino group is toxic once removed as ammonia NH3 so the body converts it to urea or glutamine. Urea is non toxic and has a useful osmotic effect in the kidneys. The urea cycle also removes NH3 from the liver. Glutamine can be converted to urea. Kidneys can excrete NH3 directly.
Important gas signalling molecules can also be generated.
Arginine –> NO, a vasodilator, neurotransmitter and inflammatory mediator
Cysteine –> H2S, vasodilator, neuromodulator
Explain the clinical consequences of a defect in phenylalanine metabolism.
Defect is often an absence of phenylalanine hydroxylase leading to PKU (phenylketonuria). This means that phenylalanine cannot be converted to tyrosine which is important to create neurotransmitters such as dopamine and other chemicals such as adrenaline and noradrenaline. Tyrosine supplements are therefore needed. Phenylpyruvate (phenylketone) is produced from phenylalanine which can be detected in the urine.
It can lead to intellectual disability and seizures.
Treatment involves PHE restricted diet
Explain the clinical relevance of measuring creatinine in blood and urine
Creatinine levels are proportional the muscle mass. Creatinine levels will be higher in muscle wasting or kidney dysfunction. Can be used as a marker for urine dilation.
Describe how ammonia is metabolised in the body.
NH2 amino group is toxic once removed as ammonia NH3 so the body converts it to urea or glutamine. Urea is non toxic and has a useful osmotic effect in the kidneys. The urea cycle also removes NH3 from the liver. Glutamine can be converted to urea. Glutamine is used to create purines and pyridamines. Kidneys can excrete NH3 directly.
