Session 2

Question 0

Describe how dietary carbohydrates are digested and absorbed

Answer 0

Digestion:
Starch + glycogen –> glucose, maltose, dextrins (hydrolysed by glycosidase enzymes) salivary amylase in mouth, pancreatic amylase in duodenum
Maltose, dextrins, lactose, sucrose –> glucose, fructose, galactose
Lactase, glycoamylase, sucrase in duodenum and jejunum
Absorption:
Glucose, fructose, galactose actively transported into absorptive cells lining gut (absorptive cells - blood - tissues) by facilitated diffusion
Glucose transport proteins (GLUT1-GLUT5)
GLUT4 - skeletal muscle, adipose is hormonally controlled (more insulin = more glucose uptake)

Question 1

Describe the general structures and functions of carbohydrates

Answer 1

Structures:
General formula - (CH2O)n
Aldehyde (aldose) or keto (ketose) group
Mono, di or poly-saccharides
Multiple OH groups
Hydrophilic - can’t pass through cell membrane without help
Functions:
Used as fuel by tissues (oxidised to CO2 and H2O)
Stored as glycogen
Component of cellular polymers (e.g. Nuclei acids, glycolipids, glycoproteins)
Stored as TAGs in adipose tissue

Question 2

Explain why cellulose is not digested in the human GI tract

Answer 2

No significant hydrolysis

No enzymes to attack B1-4 linkages

Question 3

Describe the glucose dependency of some tissues

Answer 3

RBCs, WBCs, kidney medulla, lens of eye - glucose is an absolute requirement
CNS prefers glucose
Liver and adipose need glucose for specialised functions (synthesis of TAGs)

Question 4

Describe the key features of glycolysis

Answer 4

2 ATP in
Glucose --> glucose-6-phosphate --> fructose-6-phosphate
2 NADH
4 ATP out
Net of 2 ATP 
2x pyruvate

Question 5

Explain why lactic acid (lactate) production is important in anaerobic glycolysis

Answer 5

Enables ATP to continue to be produced

Question 6

Explain how the blood concentration of lactate is controlled

Answer 6

Lactate is converted into pyruvate which can then go into the Kreb’s cycle as acetyl CoA or be released as CO2 or be converted into glucose in the liver
Elevations of lactate (>5 mmol/L) - exceeds renal threshold for lactate - affects buffering capacity - lactic acidosis
Lactic acidosis is brought on by strenuous exercise, hearty eating, shock and congestive heart disease

Question 7

Explain the biochemical basis of the clinical conditions of lactose intolerance and galactosaemia

Answer 7

Lactose intolerance:
Lack of lactase enzyme so lactose can’t be broken down - persists in colon - increases osmotic pressure - water drawn in - diarrhoea - colonic bacteria produce H2, CO2, methane - bloated feeling and discomfort
Galactosaemia:
Unable to utilise galactose
Lack of kinase - accumulation of galactose in tissues - reduction to galactitol by aldose reductase - depletes NADH - cataracts/glaucoma - blindness
Lack of transferase - accumulation if galactose + galactose-1-phosphate - damage to liver, kidney, brain - phosphate unavailable for ATP synthesis

Question 8

Explain why the pentose phosphate pathway is an important metabolic pathway in some tissues

Answer 8

Important in liver, RBC, adipose tissue
Produce NADPH:
Reducing power (e.g. For lipid synthesis)
Maintaining free -SH gps on cysteine
Detoxification
Produce C5 riboses:
Synthesis of nucleotides
High activity in dividing tissues e.g. bone marrow
Glucose-6-phosphate dehydrogenase is the main enzyme

Question 9

Describe the clinical condition of glucose-6-phosphate dehydrogenase deficiency and explain the biochemical basis of the signs and symptoms

Answer 9

X-linked recessive - point mutation for G6PD gene - reduced activity of enzyme in RBCs - low levels of NADPH - disulphide bridges form - Hb becomes cross-linked - Heinz bodies - haemolysis of RBCs - anaemia
Episodes triggered by antimalarials, sulphonamides, broad beans (reduced NADPH levels)

Question 10

Explain the key role of pyruvate dehydrogenase in glucose metabolism

Answer 10

Pyruvate dehydrogenase (PDH) converts pyruvate into acetyl CoA so it can progress into the Kreb’s cycle.
Loss of CO2 is irreversible
Acetyl CoA can’t be converted back into pyruvate therefore can’t be converted into glucose by gluconeogenesis
Acetyl CoA inhibits PDH allosterically
ATP + NADH inhibits, ATP activates PDH allosterically (energy status)
Insulin activates the enzyme by promoting dephosphorylation