MEH diabetes

Question 1

After receiving an injection of insulin, what would you expect to happen to the plasma C-peptide concentration in a Type 1 diabetic?

Answer 1

C-peptide concentration would remain the same

not found in commercial insulin

Question 2

what is C-peptide?

Answer 2

Connecting peptide (C-peptide) is released in equimolar amounts to insulin from pancreatic β cells and is cleaved from proinsulin during the biosynthesis of insulin.

Question 3

why can’t insulin be given orally in pill form?

Answer 3

is a peptide hormone so would be broken down in the gastrointestinal tract to its consituent amino acids (rendering it inactive) if it were to be taken orally.

Question 4

mechanism of metformin?

Answer 4

decrease rate of glucneogenesis

Question 5

what is HbA1C

Answer 5

glycated form of haemoglobin measured to identify the average plasma glucose concentration over prolonged periods

Question 6

list Chronic microvascular complications of diabetes?

Answer 6

Diabetic eye disease: Changes in the lens due to osmotic effects of glucose

Retinopathy: Damage to blood vessels in retina leading to blindness.

Nephropathy: Damage to glomeruli (poor blood supply) can lead to microalbuminuria.

Neuropathy: Peripheral nerve damage producing loss of sensation.

Diabetic foot: Poor blood supply, damage to nerves, increased risk of infection. Foot ulcers.

Question 7

what are the two most significant causes of metabolic syndrome?

Answer 7

insulin resistance

high central obesity

Question 8

Which amino acid of haemoglobin does glucose react with in order to glycate it?

Answer 8

Valine

is the amino acid in haemoglobin that is reacted with glucose to create glycosylated haemoglobin.

Question 9

diabetes mellitus definition

Answer 9

chronic hyperglycaemia due to insulin deficiency

Question 10

how does type 1 and 2 compare symptoms and presentation wise?

Answer 10

type 2
- More gradual onset, often presenting with complications (visual problems, thrush, infection)
• Caused by insulin resistance and/or defective insulin secretory response.
• Normally adult onset, often obese individuals.
• Do not usually develop ketoacidosis.
• Treated, at least initially with diet, drugs and exercise. • Strong genetic component.

Question 11

why does ketoacidosis develop in untreated type 1 patients?

Answer 11

1) Increased rate of lipolysis in adipose tissue which releases large amounts of fatty acids, the substrate for ketone body formation.
2) Activation of the ketogenic enzymes in the liver.

Question 12

how to adjust diet for diabetes?

Answer 12

reduce refined sugar content. inc unrefined sugar. reduce lipid intake

Question 13

macrovascular complications?

Answer 13

• Increased risk of stroke & myocardial infarction

* Poor circulation to the periphery especially feet

Question 14

why does hyperglycaemia occur in untreated type 1?

Answer 14

• lack of insulin as B cells are destroyed,
• reduced uptake of glucose by adipose tissue and skeletal
• reduced storage of glucose by liver and skeletal muscle
• inc production of glucose by liver

↓ glycogenesis, ↑ glycogenolysis
↑ gluconeogenesis, ↓ glycolysis

Question 15

what features of a B cell make it specialised for its function?

Answer 15

• many mitochondria > active protein synthesis, storage and secretion
• extensive RER (protein synthesis)
• extensive Golgi (formation of hormone storage vesicles)
• many storage vesicles
• many microtubules or microfilaments > active secretory tissue.

Question 16

why is C peptide and insulin released in equimolar amounts?

Answer 16

insulin is synthesised as its precursor - molecular proinsulin

the conversion involves protelysis and the products are insulin, C peptide and 4 basic amino acids

> synthesised in storage vesicle together therefore secreted too via exocytosis.

Question 17

actions of insulin

Answer 17

• glucose transport into adipose and skeletal muscle
• glycogenesis inc
• glycogenolysis dec
• glucneogenesis dec
• lipolysis dec
• lipogenesis and esterification of fa in liver and adipose tissue increases (storage)
• lipoprotein lipase stimulated
• dec proteolysis

Question 18

actions of glucagon

Answer 18

Stimulates glycogenolysis, gluconeogenesis and ketogenesis in liver.
•Stimulates lipolysis in adiposetissue.

Question 19

which factors affect insulin?

Answer 19

nutrients e.g. glucose, fa, amino acids (stimulate)

catecholamines e.g. adrenaline and noradrenaline (inhibit)

gut hormones in response to ingestion and digestion (stimulate)

Question 20

What name is given to the regions of the pancreas that contain endocrine cells?

Answer 20

Islets of Langerhans

Question 21

How many disulphide bonds are present in a molecule of the hormone insulin?

Answer 21

TOTAL=3

two disulphide bonds linking the A and B chains of insulin (i.e. inter-subunit disulphide bonds)

and one intra subunit disulphide bond within the A chain making a total of 3

Question 22

which glucose transporter is the primary transporter of glucose in pancreatic β cells?

Through which channels does glucose diffuse into target tissues?

Answer 22

GLUT2

GLUT4

Question 23

With respect to the release of insulin, what effect would an increase in the intracellular concentration of ATP have on a pancreatic β cell?

Answer 23

Insulin secretion would increase
>this is the mechanism for how the β cell senses an increase in plasma glucose.

More ATP > inhibition of the ATP-sesnsitve potassium channels (KATP channels). Less potassium leaving the cell > depolarisation of the plasma membrane (i.e. makes the resting membrane potential less negative).

> voltage activated calcium channels open. Ca enter.

> influx of calcium ions into the β cell activates the insulin containing vesicles causing them to fuse with the plasma membrane and release insulin.

Question 24

What effect would a decrease in intracellular ATP concentration have on the ATP sensitive potassium channels (KATP channels) in pancreatic β cells?

Answer 24

More KATP channels would be in the open state

as KATP channels are inhibited by ATP.

will prevent insulin release.

Question 25

Which class (type) of receptor is the insulin receptor?

Answer 25

tyrosine kinase