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Diabetes Biochemistry Flashcards

1
Q

Diabetes is defined as an elevated fasting blood glucose of…

A

> 7 mmol/L

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2
Q

How was the diagnostic criteria of diabetes mellitus determined?

A

Based on risk of diabetic retinopathy (except in gestational diabetes, when it is based on risk to foetus)

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3
Q

What is the healthy range of fasting blood sugar?

A

4-6 mmol/L

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4
Q

What is the main function of insulin?

A

To lower blood glucose levels

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5
Q

Insulin has a narrow/wide therapeutic window

A

Narrow

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6
Q

Why is too much insulin a problem?

A

Can lower blood glucose too much so that hypoglycaemia occurs

There is risk of hypoglycaemic coma

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7
Q

Insulin is a poison and can cause death by…

A

Hypoglycaemic coma

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8
Q

The pancreas is predominantly exocrine/endocrine

A

Exocrine

It releases digestive juices from acinar cells

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9
Q

What are the 4 types of endocrine cells found in the pancreatic Islets of Langerhans?

A 
Alpha cells (10-20%)
Beta cells (60-80%)
Delta cells (~5%)
PP cells (<1%)
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10
Q 
What do the 4 pancreatic islet cells release?
Alpha:
Beta:
Delta:
PP:
A

Alpha: glucagon
Beta: INSULIN
Delta: somatostatin
PP: pancreatic polypeptide

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11
Q

When do beta cells produce and secrete insulin?

A

When blood glucose rises above 5 mmol/L

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12
Q

Describe the structure of insulin

A

Two peptide chains (A and B) linked by disulphide bonds

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13
Q

How is insulin formed in pancreatic beta cells?

A
  • Proinsulin is synthesised in the rough endoplasmic reticulum of pancreatic beta cells
  • Ca2+ dependent endopeptidases (PC2 and PC3) cleave proinsulin into insulin and C-peptide
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14
Q

What is the function of the C-peptide co-released with insulin?

A

It has no physiological function but can be used as a measurement of endogenous insulin (as it is released in proportion to endogenous insulin)

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15
Q

Synthetic insulin preparations are used to treat diabetes. When are short-acting vs long-acting preparations used?

A

Short-acting: given directly after eating

Long-acting: given overnight

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16
Q

Give an example of the most common ultra short-acting insulin preparation

A

Insulin Lispro

produced by swapping position of lysine and proline at the end of the B chain

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17
Q

Insulin Lispro should be injected within X minutes of beginning a meal

A

15 minutes

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18
Q

Insulin Lispro is the most rapidly acting insulin so should be used in combination with X for type I DM

A

A longer-acting preparation

unless used for continuous infusion

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19
Q

Give an example of an ultra long-acting insulin preparation

A

Insulin Glargine

produced by adding 2 arginines to the B chain and swapping asphargine to glycine at the end of the A chain

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20
Q

Insulin Glargine has prolonged action as it…
A - is peakless
B - has multiple peaks

A

A - is peakless

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21
Q

Insulin Glargine is administered as a single morning dose. T/F

A

False

It is administered as a single bedtime dose

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22
Q

Why is it clinically helpful to have different forms of insulin?

A

So they can be given at different times depending on their rate of action in the body

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23
Q

Summarise pancreatic beta cell release of insulin in response to increased glucose

A
  • Glucose enters through GLUT2
  • Glucose is used to generate ATP through glycolysis
  • ATP binds to and closes ATP sensitive K+ channels
  • K+ builds up in the cell, causing the membrane to depolarise
  • Voltage gated Ca2+ channels open
  • Ca2+ induced insulin release occurs
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24
Q

Glucose enters beta cells through the GLUT2 transporter by active transport. T/F

A

False

Glucose passes through GLUT2 via facilitated diffusion

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25
In the beta cell, glucose is phosphorylated by X to be made into Y which is used in glycolysis
X - glucokinase | Y - glucose-6-phosphate
26
In a healthy person, why does increase in glucose conc. lead to a dramatic increase in glucokinase activity?
Glucokinase's Km for glucose lies within the normal range of glucose conc. (4-6 mmol/L)
27
Why is glucokinase almost maximally active all the time in diabetes?
Fasting glucose is >7 mmol/L which is outwith glucokinases Km for glucose
28
How many ATP molecules does each glucose molecule produce?
36 | 2 from glycolysis, 34 from TCA + oxidative phosphorylation
29
In beta cells, how does an increase in internal Ca2+ lead to insulin secretion?
Increased Ca2+ causes secretory vesicles to fuse with the cell membrane and release insulin + C-peptide
30
In type I DM, beta cells are mostly lost. T/F
True
31
In type II DM, beta cells are mostly lost. T/F
False Beta cells are still present and insulin is still being produced but the cells are insulin resistant
32
Why is insulin release glucose independent in type II DM?
Hyperglycaemia takes the glucose conc. outwith the Km of glucokinase The cell loses its ability to respond to changes in glucose
33
Describe the 2 phases of insulin release
Phase 1: initial spike of hyperglycaemia soon after eating Phase 2: gradual increase and decrease in blood glucose related to the amount and duration of glucose intake
34
Why is insulin release biphasic?
There are 2 pools of insulin granules in the beta cells: - Readily releasable pools (RRP) - Reserve pools
35
Describe the readily releasable and reserve pools of insulin
- RRP - 5% of insulin granules are available for immediate release which leads to the initial spike of insulin release - Reserve pools must undergo preparatory reactions to become mobilised for release. This leads to the 2nd, slower release phase
36
How is the biphasic nature of insulin release affected by type II DM?
Insulin release is weakened and flattened (i.e., not biphasic) due to reduced insulin sensitivity
37
Give 5 examples of conditions arising from defective insulin secretion and sensitivity
- Type I DM - Type II DM - Gestational diabetes - Maturity onset diabetes of the young (MODY) - Neonatal diabetes
38
What is the cause of type I diabetes?
Autoimmune destruction of pancreatic beta cells, resulting in no insulin or C-peptide production
39
What is the cause of type II diabetes?
Insulin resistance and subsequent hyperglycaemia and hyperinsulinaemia
40
What is the cause of gestational diabetes?
Pregnancy (usually in pre-diabetic women i.e., blood glucose 6-7 mmol/L with high risk of future T2DM)
41
What is maturity onset diabetes of the young (MODY)?
Monogenic disease with characteristics of type I and II DM Beta cell dysfunction is seen but it is not autoimmune
42
What is the cause of maturity onset diabetes of the young (MODY)?
Mutations in at least 6 different genes, most of which are in glucokinase or transcription factors which are involved in pancreatic development
43
Describe the result of the glucokinase gene mutation in MODY2
The glucose sensing ability of glucokinase is impaired, so more glucose is required to activate it
44
Describe the result of the transcription factor mutations in MODY1 and MODY3
Foetal pancreatic development is affected
45
Why is it important to differentiate between MODY from type I DM?
Type I DM is treated with insulin MODY can be treated with sulphonylureas as they usually have some beta cell function available
46
What is neonatal diabetes?
Monogenic diabetes caused by mutations in the glucose sensing mechanism
47
What is the cause of neonatal diabetes?
Mutations in ATP sensitive K+ channel subunits (Kir6.2 and SUR1) which leads to increased activation or numbers of KATP channels
48
How is neonatal diabetes treated?
Sulfonylureas (these inhibit ATP sensitive K+ channels)
49
How does insulin control nutrient storage?
Liver: turns on lipogenesis and glycogen synthesis, turns off lipolysis and gluconeogenesis Muscle: increases amino acid and glucose uptake, turns on glycogen synthesis Adipose tissue: increases glucose uptake and turns on lipogenesis
50
Near complete absence of adipose can result in insulin resistance. T/F
True Normal adipose functionality is a key mediator in insulin sensitivity as both obesity and severe lack of adipose tissue can cause insulin resistance
51
List 2 syndromes where insulin resistance is a key feature
Donohue syndrome aka Leprechaunism Rabson Mendenhall syndrome
52
What is Donohue syndrome (Leprechaunism)?
A genetic syndrome caused by mutations in the insulin receptor gene Severe insulin resistance and developmental abnormalities (elfish appearance, absence of subcutaneous fat) are seen
53
What is Rabson Mendenhall syndrome?
A genetic syndrome characterised by insulin resistance, hyperglycaemia, hyperinsulinaemia, developmental abnormalities and hyperpigmentation Patients are very prone to diabetic ketoacidosis
54
What is diabetic ketoacidosis?
A life-threatening complication of diabetes (mainly type I) caused by accumulation of ketone bodies in the blood turning the blood acidic
55
How are ketone bodies formed?
Fatty acid oxidation produces acetyl CoA and if this is not used for the TCA cycle, it is used to generate ketone bodies
56
How does diabetes cause diabetic ketoacidosis? (2)
1) When glucose is not available, fatty acids are oxidised to provide energy Excess acetyl-CoA is converted to ketone bodies 2) Insulin normally inhibits lipolysis which reduces the risk of ketone body over load Reduced insulin production (e.g., type I DM) means that more lipolysis can occur and so more ketone bodies are produced
57
What are the symptoms of diabetic ketoacidosis? (4)
Vomiting Dehydration Increased heart rate Distinctive acetone smell on breath
58
Why do ketone bodies increase in starvation?
Oxaloacetate is consumed for gluconeogenesis so excess acetyl-CoA is converted to ketone bodies
59
What biochemical test results confirm diabetic ketoacidosis?
- High ketone - Very high glucose - Low or absent insulin - Low blood pH
60
How is diabetic ketoacidosis treated?
- IV fluids (rehydration, electrolyte balance) | - Insulin

LR Endocrine (12 decks)

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