Which of the following hormones increase blood glucose by inhibiting insulin? Check all that apply.
Adrenaline
Cortisol
Growth hormone
Glucagon
Secretin
Which hormone increases blood glucose by inhibiting insulin over a long period of time?
Which hormone counteracts insulin by stimulating glucose and lipid metabolism but shares insulin's anabolic properties with respect to protein?
Which hormone stimulates insulin secretion after food intake before blood glucose increases?
Cholecystokinin
Gastrin
Pancreatic peptide
Which type of glucose transporters are present on the B cells of the islets of Langerhans?
GLUT1
GLUT2
GLUT3
GLUT4
Which glucose kinase is present in the B cells of the islets of Langerhans?
Glucokinase
Hexokinase
Fill in the blanks to describe the stimulation of insulin secretion from the pancreatic B cells. 1. The B cells have glucose transporters - these have affinity so glucose only enters these cells at concentration. 2. kinase is present in the B cells which has Km so glucose with affinity. This initiates . 3. from inhibits -sensitive channels on the membrane. 4. The prevention of leakage causes the membrane to become . 5. -gated channel proteins open. 6. enters the cell stimulating and release of insulin.
What is proinsulin?
Commercially synthesised insulin for use in diabetes management
Inactive prehormone form of insulin
The inactive form of insulin secreted by the pancreas of those with type 2 diabetes
Insulin when bound in a vesicle in the pancreatic B cells
How do we activate proinsulin?
Cleave off the C-peptide
Cleave off the B-peptide
Hydrolyse the disulfide bridges
Substitution of histidine for proline on the a-chain
What type of receptor is the insulin receptor?
Tyrosine kinase
GPCR
Free cytosolic
Transmembrane channel
Which domain are the 2 a-subunits of the insulin receptor found?
Extracellular
Intracellular
Which domain are the 2 b-subunits of the insulin receptor found?
The insulin receptor is described as being catalytic.
What happens when insulin binds to the insulin receptor?
Autophosphorylation of tyrosine residues
Autophosphorylation of lysine residues
Activation of a G protein
Opening of transmembrane channel
Fill in the blanks below to describe the activation of protein kinase B by insulin. 1. Insulin binds to its receptor. 2. This binding stimulates of residues. 3. This allows of (IRS 1/2). 4. activates . 5. phosphorylates to in the cell membrane. 6. activated . 7. activates .
Fill in the blanks below to describe how insulin activates glycogen synthesis. 1. When insulin binds to its tyrosine kinase receptor, is activated by a series of . 2. causes channels to be translocated to the membrane via to encourage glucose uptake. 3. phosphorylates . This glycogen synthase kinase. 4. remains unphosphorylated so remains in its form. 5. Glycogen syntheiss can take place.
The active form of glycogen synthase kinase is...
Phosphorylated
Not phosphorylated
The active form of glycogen synthase is...
Fill in the blanks below to describe how insulin inhibits lipolysis. 1. When insulin binds to its receptor, is activated by a series of . 2. phosphorylates to activate it. 3. converts to AMP. 4. is therefore inhibited and thus is not activated. 5. Triacylglycerols are not hydrolyses and the triacylglycerol store in adipose tissue is preserved.
What hormone activates hormone sensitive lipase to cause TAG hydrolysis?
Insulin
Ghrelin
Fill in the blanks below to describe how insulin affects gene expression. 1. Insulin binds to its receptor stimulating of residues. 2. This phosphorylation leads to activation of . 3. activates the protein kinase cascade to phosphorylate first , then , then . 4. or MAPK activates or inhibits leading to gene activation or suppression.
The brain and erythrocytes will always take up glucose and metabolise it. Why?
GLUT3 transporters have high affinity
Glucokinase present which has high Km
Membranes freely permeable to glucose
Insulin directs glucose towards these tissues
In excess, how will pyruvate from glycolysis leave the liver?
As VLDL
As HDL
As LDL
As chylomicrons
Why does muscle and adipose tissue only uptake glucose at very high concentrations?
GLUT4 transporters present
Hexokinase present
Glucokinase present
Glycogen synthase present
Which biomolecules deposit fatty acids into adipose tissue in the fed state? Select all that apply.
Chylomicrons
VLDL
HDL
LDL
What are the actions of cortisol?
Long term blood glucose regulation
Stimulation of amino acid mobilisation from muscle
Stimulation of gluconeogenesis
Stimulation of TAG release from adipose tissue
Activation of glycogen synthase
Inhibition of lipoprotein lipase
Recruitment of GLUT4 transporters to cell membranes
The liver is engaged in gluconeogenesis at all times except during...
The fed state
The fasting state
Prolonged starvation
Satiety signalling
Why is the glucose kinase in the liver glucokinase, which has low affinity?
No competition for glucose with the brain when concentration is low
Concentration of glucose in the liver is always high
To compete for glucose against the brain when concentration is low
Concentration of glucose in the liver is always low
During the fed state, acetyl CoA carboxylase is activated to form malonyl CoA. What does malonyl CoA do?
Inhibits acyl carnitine transferase to prevent entry of fatty acids into mitochondrion for oxidation
Activations acyl carnitine transferase to encourage entry of fatty acids into mitochondrion for oxidation
Activates lipoprotein lipase to encourage TAG storage in adipose tissue
Activates LCAT to increase cholesterol uptake from peripheral tissues
Why does the brain rely on glucose as fuel?
Fatty acids cannot cross the blood-brain barrier
Fatty acids are broken down in the cerebrospinal fluid
Fatty acids are toxic to neurons
The neurons have no mitochondria
Glucose transport into the brain and erythrocytes is independent of insulin.
The erythrocytes have no mitochondria.
When do blood glucose concentrations peak?
1 hour after eating
2 hours after eating
4 hours after eating
30 mins after eating
Following a meal, when have blood glucose levels normally returned to normal by?
2 hours
1 hour
4 hours
6 hours
Why can't fatty acids be used in gluconeogenesis?
Acetyl CoA cannot be converted back to pyruvate - acetyl CoA is an end product of B-oxidation
Fatty acids cannot cross the hepatocyte cell membranes
It is more efficient to store fatty acids as TAGs in adipose tissue
Fatty acids cannot be converted to citrate
Which of the following molecules are gluconeogenic substrates?
Lactate
Glycerol
Glucogenic amino acids
Ketogenic amino acids
Fatty acids
Malonyl CoA
Ketone bodies consist of two molecules of what bonded together?
Acetyl CoA
Carbon dioxide
What is the purpose of the ketone bodies?
Provide a source of acetyl CoA to the muscles
Provide a source of acetyl CoA to the brain
Buffer system in the blood
Activate glycogen phosphorylase
In the fasting state, glucagon activates . Thus, is phosphorylated and put into its state. This means is phosphorylated and can enter the blood.
Where is lactate sourced from for gluconeogenesis?
Erythrocytes
Brain
Adipose tissue
Kidney
Why do the erythrocytes produce lactate?
Can only perform anaerobic respiration
Can only perform aerobic respiration
Haem breakdown
Byproduct of oxyhaemoglobin formation
When does acetyl CoA form ketone bodies?
When it exceeds the capacity of the TCA cycle
When insulin activates hepatocytes
When ATP concentration is high in the hepatocytes
During the fed state
Why do ketone bodies stimulate insulin secretion?
To prevent muscle breakdown
To prevent fatty acid oxidation
To prevent urea toxicity
To prevent hepatocyte death
The brain can use ketone bodies in metabolism.
When does urea excretion and thus protein breakdown peak during starvation?
After 12 hours
1 week
2 weeks
After 48 hours
Why does urea excretion and thus protein breakdown decrease over time?
Ketone bodies stimulate insulin secretion
Ketone bodies stimulate glucagon secretion
After a certain period there is no mobilisable protein left
After a certain period urea transporters in the nephron are saturated
Why do the muscle begin to utilise fatty acids for energy as starvation progresses?
To increase availability of ketone bodies to brain
To reduce urea toxicity
To increase availability of amino acids to brain
To prevent kidney damage
For how long can a human survive without food?
40 days
20 days
80 days
7 days
Fill in the blanks below to describe type 1 diabetes. Type 1 diabetes is caused by the destruction of cells in the . It often has an onset. Symptoms include polyuria, polydipsea, (excessive appetite), fatigue and weakness as well as weight loss and muscle wasting. It requires treatment with exogenous whereby the dosage is matched with .
Which of these indicate type 1 diabetes?
Hyperglycaemia and ketoacidosis
Hyperglycaemia only
Ketoacidosis only
Hypoglycaemia and ketoacidosis
Fill in the blanks below to describe Type 2 diabetes. Type 2 diabetes is caused by insulin . Is is usually onset than type 1. Type 2 diabetes can be treated with dietary changes and oral agents.
What do biguanides do in the treatment of Type II diabetes?
Increase recruitment of GLUT4 to increase glucose uptake
Reduce recruitment of GLUT4 to reduce glucose uptake
Act on B cells to improve insulin secretion
Destroy ketone bodies in the blood
What do sulphonylureas do in the treatment of Type 2 diabetes?
Destroy ketone bodies
Increase recruitment of GLUT4 to encourage glucose uptake
Which hormone acts unopposed in diabetes mellitus?
In a healthy individual, stimulate release to limit muscle protein breakdown. In diabetics, this cannot occur. Thus, protein is broken down in an uncontrolled matter, is not controlled, fat breakdown is not controlled and production is not controlled. Glucose and may be present in the urine.
Drag and drop the correct pathologies to name some of the complications of diabetes mellitus. ❌ - disease of the capillaries causing thickening of the wlals ❌ - damage to the retina affecting vision ❌ - damage to the kidneys ❌ - results in impotence, foot ulcers etc
To be diagnosed with metabolic syndrome, patients must have any 1 of: fasting glucose, resistance or diabetes. Patients must also have any 2 of tension, (abnormal lipid content in blood), obesity (fat buildup around the abdomen) or microalbuminuria
