MEH diabetes Flashcards
After receiving an injection of insulin, what would you expect to happen to the plasma C-peptide concentration in a Type 1 diabetic?
C-peptide concentration would remain the same
not found in commercial insulin
what is C-peptide?
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.
why can’t insulin be given orally in pill form?
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.
mechanism of metformin?
decrease rate of glucneogenesis
what is HbA1C
glycated form of haemoglobin measured to identify the average plasma glucose concentration over prolonged periods
list Chronic microvascular complications of diabetes?
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.
what are the two most significant causes of metabolic syndrome?
insulin resistance
high central obesity
Which amino acid of haemoglobin does glucose react with in order to glycate it?
Valine
is the amino acid in haemoglobin that is reacted with glucose to create glycosylated haemoglobin.
diabetes mellitus definition
chronic hyperglycaemia due to insulin deficiency
how does type 1 and 2 compare symptoms and presentation wise?
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.
why does ketoacidosis develop in untreated type 1 patients?
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.
how to adjust diet for diabetes?
reduce refined sugar content. inc unrefined sugar. reduce lipid intake
macrovascular complications?
- Increased risk of stroke & myocardial infarction
* Poor circulation to the periphery especially feet
why does hyperglycaemia occur in untreated type 1?
- 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
what features of a B cell make it specialised for its function?
- 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.
why is C peptide and insulin released in equimolar amounts?
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.
actions of insulin
- 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
actions of glucagon
Stimulates glycogenolysis, gluconeogenesis and ketogenesis in liver.
•Stimulates lipolysis in adiposetissue.
which factors affect insulin?
nutrients e.g. glucose, fa, amino acids (stimulate)
catecholamines e.g. adrenaline and noradrenaline (inhibit)
gut hormones in response to ingestion and digestion (stimulate)
What name is given to the regions of the pancreas that contain endocrine cells?
Islets of Langerhans
How many disulphide bonds are present in a molecule of the hormone insulin?
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
which glucose transporter is the primary transporter of glucose in pancreatic β cells?
Through which channels does glucose diffuse into target tissues?
GLUT2
GLUT4
With respect to the release of insulin, what effect would an increase in the intracellular concentration of ATP have on a pancreatic β cell?
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.
What effect would a decrease in intracellular ATP concentration have on the ATP sensitive potassium channels (KATP channels) in pancreatic β cells?
More KATP channels would be in the open state
as KATP channels are inhibited by ATP.
will prevent insulin release.
