Biochemistry Flashcards

1
Q

What is the normal level of blood glucose?

A

5mM

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2
Q

Which pancreatic cells are the main insulin producers?

A

Beta-cells

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3
Q

What is cleaved off proinsulin to yield insulin?

A

C (connecting) peptide

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4
Q

Insulin lispro has a lysine and a proline residues reversed. It is fast/slow and short/long acting

A

fast and short acting

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5
Q

Insulin glargine precipitates in the subcutaneous tissue. It is ______ acting. How many doses are required?

A

ultra-long acting

1 dose /day

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6
Q

What enzyme acts as a glucose sensor? How?

A

Glucokinase

  1. A small change in glucose concentration triggers a large increase in glucokinase activity
  2. Increased glucose metabolism increases ATP levels
  3. ATP inhibits ATP-sensitive K+ channels (Katp), causing cell membrane depolarisation
  4. Ca2+ channels open in response to depolarisation
  5. Ca2+ influx leads to fusion of secretory vesicles and insulin exocytosis
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7
Q

In T2DM the beta cells lose the ability to secrete insulin (T/F)

A

False

  • insulin is produced
  • hyperglycaemia means that glucokinase loses ability to respond to fluctuations in glucose concentrations
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8
Q

Release of insulin is biphasic. Why are there 2 phases of insulin release?

A

There are two insulin pools:

  • Readily releasable pool (5%)
  • Reserve pool - preparatory reactions are required for its release
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9
Q

Beta cells (in pancreas) only secrete insulin when they detect a fall in glucose below 5mM (T/F)

A

False

Beta cells produce insulin in response to high glucose levels, >5mM

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10
Q

T1DM results in the loss of beta cells (T/F)

A

True

-autoimmune destruction of beta cells

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11
Q

Sulphonylurea drugs (e.g. Tolbutamide) are used in T2DM treatment. What is their mode of action?

A

Katp channel inhibitors

  • mimic action of ATP to depolarise beta cells
  • depolarisation triggers insulin secretion
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12
Q

MODY (maturity-onset diabetes of the young) is a form of early onset _______ diabetes, characterised by defects in ______ ______ function and/or loss of _____ _____

A

Type II diabetes

defects in Beta cell function
and / or
loss of insulin secretion

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13
Q

What is impaired in MODY2? What are the implications?

A

Glucokinase mutations cause diminished sensitivity to rising glucose levels

-insulin is secreted at higher glucose levels

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14
Q

What are the glucose uptake channels in Beta cells?

A

GLUT2 channels

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15
Q

HNF Transcirption factors mutations are present in MODY 1 and 3. These TFs regulate differentiation and function of…

A

Beta cells

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16
Q

What is the purpose of genetic screening in diabetes?

A

Differentiate between MODY and Type 1 diabetes

17
Q

1st line treatment for MODY is insulin injections (T/F)

A

False

-Sulfonylurea (induces secretion of insulin)

18
Q

Insulin is ______ hormone. It therefore elicits what metabolic effects?

A

an Anabolic hormone

Induces:

  • protein and DNA synthesis
  • glucose and amino acid uptake in muscle
  • lipogenesis in adipose and liver
  • glycogen synthesis in liver and muscle

Inhibits:

  • lipolysis
  • gluconeogenesis
19
Q

What type of receptor does insulin bind to?

What does insulin binding induce in the receptor?

A

Receptor tyrosine kinase

  1. Dimerisation of Beta subunits, which autophosphorylate themselves
  2. Activation of relay proteins (via phosphorylation)
20
Q

Donohue syndrome (Leprechaunism) is associated with severe insulin resistance. It arises due to defects in _____ _____ or_____ ______ signalling

A

insulin binding or

insulin receptor signalling

21
Q

List the symptoms of diabetic ketoacidosis.

A

Vomiting
Dehydration (thirst)
Increased HR
Ketone smell on breath

22
Q

How are ketone bodies formed?

A

In liver mitochondria from acetyl-CoA - from Beta oxidation of fats

23
Q

What effects does insulin have on ketone body production?

A

Decreases it by promoting glucose uptake by cells and inhibiting lypolysis

24
Q

In what type of diabetes is Diabetic Ketoacidosis a possible complication?

A

T1DM

-insulin is low, thus there is a drive for lipolysis

25
Q

Diabetic ketoacidosis can arise in T2DM (T/f)

A

True

-a lot more common in T1DM

26
Q

AcetylCoA is a product of ____ _____ _____.

If ________ is present, AcetylCoA enters the TCA cycle. If not, it is converted to Ketone bodies.

A

fatty acid oxidation

oxaloacetate (from glycolysis)

27
Q

How does acidosis arise in diabetic patients ?

A
  1. Insulin shortage limits the uptake of glucose by tissue
  2. Energy has to be obtained from fatty acid oxidation - excess ketone bodies are formed
  3. Oxaloacetate is normally derived from glycolysis - low glucose in tissues means low oxaloacetate (also used for gluconeogenesis)
  4. AcetylCoA cannot enter TCA cycle in the absence of Oxaloacetate - it is converted to ketones.
  5. Glucose excretioncauses dehydration, driving acidosis further