Diabetes Flashcards

1
Q

Is insulin and anabolic or catabolic hormone? Describe what this means.

A

Anabolic This means it is an “add up” hormone - i.e. stimulates growth or development within a tissue

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2
Q

Which cells secrete insulin?

A

beta cells of Islet cells (islets of Langerhans) of the pancreas

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3
Q

What is the major action of insulin?

A

Insulin causes the up-regulation of GLUT-4 transport protein

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4
Q

Define: mitotic pathway

A

Mitotic pathways = encourage cell differentiation and growth. Insulin does this

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5
Q

At what stages of glycolysis does insulin work?

A

Reaction 1 (glucose –> glucose-6-phosphate)

Reaction 3 (fructose-6-phosphate –> fructose-1,6-bisphosphate)

Reaction 10 (phosphoinolpyruvate –> pyruvate)

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6
Q

What is the main function of insulin?

A

To drive glucose into cells and drives glycolysis

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7
Q

List the minor/alternative functions of insulin

A
  • Inhibits nutrient breakdown (i.e. catabolism)
  • Stimulates FA synthesis and esterification
  • “store cupboard hormone” – storage of energy, repair and growth
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8
Q

Physiological effects of insulin - list the major stimulatory and inhibitory effects of the hormones

A
  • Stimulatory*
  • Glucose uptake into skeletal muscle and adipose tissue (GLUT-4 mediated)
  • Amino acid uptake and protein synthesis (in muscle)
  • Lipogenesis
  • Glycogen synthesis
  • Activity of Na/K ATPase pump
  • NO synthesis & Renal Na reabsorption
  • Inhibitory*
  • Gluconeogenesis
  • Proteolysis
  • Lipolysis and ketogenesis
  • Glycogenolysis
  • Glucagon secretion
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9
Q

When are levels of insulin at their highest?

A

Post-prandially (i.e. after a meal)

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10
Q

Define hyperglycaemia

A

High blood glucose levels

  • Normal ranges = 4-6 mmol/L during fasting*
  • Diabetic ranges = >7 mmol/L during fasting *
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11
Q

What is a common cause of hyperglycaemia

A

Insulin deficiency (this is Type I diabetes)

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12
Q

List the osmotic symptoms of hyperglycaemia

A
  • Polyuria – excessive urine
  • Nocturia – urination at night
  • Polydypsia – increased thirst
  • Dehydration
  • Pre-renal failure – acute kidney injury
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13
Q

How does the endothelium get damaged as a result of hyperglycaemia?

A

Oxidative stress occurs due to increases in glucose resulting in ROS.

ROS build up causes endothelial damage (most problematic in the glomerulus, eye and nerves)

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14
Q

How does hyperglycaemia affect ATP levels?

A

There is extracellular hyperglycaemia, but intracellular hypoglycaemia resulting in low ATP - consequence is that the cell must find alternative energy sources (eg: fats and ketones)

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15
Q

What are the consequences of mobilising fat stores and ketones?

A
  • Mobilisation of adipose tissue to use fats (first triglycerides then free fatty acids)
  • Eventually, amino acids will be used (substrate of gluconeogenesis – however, there is an insulin deficiency therefore it cannot be absorbed)
  • Ketoacids are eventually used
    • Utilised by CNS, synthesised in the liver (ketoacids –> actyl coA –> mitochondrial ATP)
    • However in excess causes acidosis (specifically ketoacidosis) due to the production and build up of acetone and b-hydoxybutyrate
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16
Q

How does diabetes cause hyperkalaemia? What are the consequences?

A

Potassium enters the cell 1:1 with glucose

A lack of insulin = extracellular hyperkalaemia –> cardiac instability (action potentials) & muscle weakness

17
Q

What is the link between insulin & cholesterol?

A

Insulin stimulates HMG CoA reductase activity –> increase de novo synthesis

18
Q

How does having Type I diabetes affect cholesterol levels and overal CV health?

A
  • Important in managing macrovascular risks
  • Insulin deficiency leads to fall in cholesterol synthesis & LDL levels
  • Treatment of Type I often leads to increase in HDL
  • Mobilise cholesterol from peripheral cell membranes
  • This appears healthy however, type I diabetics have increased CV risk
19
Q

What is Type I diabetes

A

T cell mediated autoimmune destruction of beta cells resulting in absolute insulin deficiency

20
Q

List the major epidemiological factors of Type I diabetes

A
  • More likely to have it, if you have a pre-existing autoimmune condition (the converse is also true)
  • Occurs mostly in younger people
  • Degree of family history
21
Q

List the short term effects of Type I diabetes

A
  • Weight loss
  • Osmotic symptoms
  • Dehydration
22
Q

List the long term effects of Type I Diabetes

A
  • Blindness
  • Renal failure
  • Neuropathy (autonomic & peripheral)
23
Q

What are the potential complications associated with type I diabetes?

A
  • Untreated metabolic effects = hyperglycaemia, elevated free fatty acids, ketosis, hyperkalaemia, acidosis
  • Elevated total cholesterol
  • Retinopathy leading to blindness if left untreated
  • Nephropathy (requiring dialysis)
  • Neruopathy causing foot ulceration
  • Disordered blood supply to lower limbs
  • Large vessel disease (eg: atherosclerosis)