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zESA2 > MEH session 10 > Flashcards

MEH session 10 Flashcards

1
Q

Is the pancreas mainly composed of endocrine or exocrine tissue?

A

Exocrine tissue - approximately 99% of the weight of the organ

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2
Q

Blood from the pancreas drains into…

A

Hepatic portal vein via superior mesenteric vein

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3
Q

Blood supply to the pancreas is via…

A

Coeliac artery

Superior mesenteric artery

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4
Q

Describe the location of the pancreas.

A

The pancreas is an oblong-shaped and flattened organ, about the size of a hand. Aside from the tail, it is a retroperitoneal structure (lies behind the peritoneal cavity), located deep within the upper abdomen.

Stomach – lies anteriorly and superiorly.
Duodenum – situated anteriorly and medially, curving around the head of the pancreas.
Spleen – located posteriorly and laterally. It is connected by ligaments to the tail of the pancreas.
Vasculature – the aorta and inferior vena cava pass posteriorly to the head of the pancreas.

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5
Q

From which embryonic tissue does the pancreas develop?

A

Outgrowth of the foregut

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6
Q

What is the exocrine function of the pancreas?

A

◦ Produces digestive enzymes secreted directly into duodenum

◦ Alkaline secretions through pancreatic duct to duodenum

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7
Q

How does the ultrastructure of the beta-cell relate to the synthesis and storage if insulin?

A

They have characteristics of tissues that synthesise proteins for export:
• Extensive RER
• Abundant golgi
• Abundant mitochondria
• Well-defined system of microtubules and microfilaments

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8
Q

Which hormones are released by the endocrine pancreas and from which cells?
Where are these cells found?

A

Endocrine cells are in the Islets of Langerhans

  • Insulin - beta cells
  • Glucagon - alpha cells
  • Somatostatin - delta cells
  • Pancreatic polypeptide - PP cells
  • Ghrelin - e cels
  • Gastrin - G cells
  • Vasoactive intestinal peptide
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9
Q

Which hormones released by the pancreas are particularly important in the control of plasma glucose?

A

Insulin - lowers blood glucose levels

Glucagon - raises blood glucose levels

These hormones regulate the metabolism of carbohydrates, proteins and fats.

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10
Q

Which hormone is secreted by the stomach to control acid secretion and is also secreted by the pancreas?

A

Gastrin - secreted by G cells

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11
Q

What are the effects of insulin on appetite?

A

Decreases appetite by stimulating the primary inhibitory neurone in the arcuate nucleus

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12
Q

Why is it important that plasma glucose concentration is tightly controlled?

A
  • Some cells have an absolute requirement for glucose
  • Brain uses glucose at fastest rate in the body so is sensitive to fluctuations in plasma glucose concentrations
  • Plasma glucose concentrations affects plasma osmolality
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13
Q

What is normal plasma glucose concentration?

A

3.3-6mmol/L

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14
Q

What can plasma glucose concentration rise to immediately after a meal?

A

7-8mmol/L

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15
Q

What is the renal threshold for glucose and what is the significance of this?

A

10mmol/L - above this concentration, kidney cannot reabsorb glucose so it is lost in the urine (glucosuria)

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16
Q

When does renal threshold for glucose change?

A

Pregnancy - decreases

Elderly - increases

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17
Q

Describe the structure of insulin.

A
  • Polypeptide hormone with alpha helix structure
  • 51 amino acids
  • Two polypeptide chains (A and B) linked covalently by two disulphide bonds
  • Intra-chain disulphide bond within the A chain
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18
Q

How is insulin synthesised?

A

Preproinsulin - Signal leader sequence on N-terminal directs it to be co-translationally inserted into the ER membrane. Signal sequence is cleaved by signal peptidase

Proinsulin- disulphide bonds between cysteine residues in ER, endopeptidase cleaves part of the polypeptide in golgi to form insulin and C-peptide, and O-linked glycosylation occurs

Insulin- Packaged in a vesicle where it is stored as a crystalline zinc-insulin complex and released from beta cells by exocytosis. When released, it dissolves in the plasma and circulates as a free hormone.

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19
Q

What is the clinical significance of C-peptide formed after cleavage of proinsulin?

A
  • As C-peptide is released with insulin in equimolar amounts, its level in plasma is a useful marker of endogenous insulin release. Therefore, measurement of plasma C-peptide levels in patients receiving insulin can be used to monitor endogenous insulin secretion as it has a longer half life and is more stable than insulin in plasma
  • Research suggests it protects against vascular damage in diabetics.
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20
Q

How is insulin secreted and from which cells?

A

Beta-cells of islet of Langerhans

  1. When glucose concentrations reach 10mM, glucose is transported into the beta cells through a glucose transporter.
  2. B cell metabolises the glucose to form ATP increasing the ATP/ADP ratio
  3. ATP binds to ATP-sensitive K+ channel causing a conformational change which closes its aqueous ion pore.
  4. K+ does not pass out from the membrane. The membrane of the B cell depolarises.
  5. The increase in membrane potential opens VOCC’s in the membrane of the B cell.
  6. Ca2+ enters the cell. Ca2+ causes insulin vesicles to fuse with the membrane and insulin is secreted by exocytosis.
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21
Q

Why does insulin secretion need to be tightly controlled?

A

Insulin is the major hormone that acts to lower the blood glucose concentration and its secretion must be controlled to ensure that the glucose concentration stays within the normal physiological range under a variety of situations.

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22
Q

How is insulin secretion controlled?

A 
• Metabolites - stimulate secretion 
	◦ Glucose
	◦ Amino acids 
	◦ Fatty acids 
• GI hormones - stimulate secretion 
	◦ Gastrin 
	◦ Secretin 
	◦ Cholecystokinin 
• Neurotransmitters 
	◦ Adrenaline - inhibit secretion 
	◦ Noradrenaline - inhibit secretion 
	◦ Acetyl choline - stimulate secretion
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23
Q

Describe the structure of glucagon.

A
  • Single polypeptide
  • 29 amino acids
  • No disulphide bonds
  • Flexible 3-D structure
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24
Q

Describe glucagon synthesis and where does this occur?

A
  • Synthesised by pancreatic alpha cells in RER
  • Pre-proglucagon undergoes post-translational processing in golgi to produce the biologically active molecule
  • Secreted due to low glucose levels in alpha cells
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25
Q

How is glucagon secretion controlled?

A
  • Decrease in blood concentration - stimulates release

* Increase in blood concentration and insulin concentration - inhibits release

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26
Q

What are the common hormonal properties of insulin and glucagon?

A
  • Water soluble - carried dissolved in plasma (no transport proteins)
  • Short half life - so we can constantly adjust plasma glucose levels depending on demand
  • Interact with cell surface receptors on target cells
  • Receptor with hormone bound can be internalised - inactivation
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27
Q

In which tissues do insulin and glucagon mainly exert their effects?

A 
Insulin:
Liver
Skeletal muscle
Adipose tissue 
(insulin is required for the normal growth and development of most tissues in the body)

Glucagon:
Liver
Adipose tissue

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28
Q

How does insulin exert its actions?

A

Insulin receptor - tyrosine kinase receptor
◦ Activation of insulin receptor causes translocation of GLUT4 receptor onto cell surface membrane (Skeletal muscle and adipose tissue)

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29
Q

Describe the structure of the insulin receptor.

A

Receptor is a dimer

2 identical subunits spanning the cell membrane

Each subunits are made of one alpha chain and one beta chain, connected by a single disulphide bond

Alpha chain on exterior of cell surface membrane
Beta chain spans the cell surface membrane

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30
Q

How does glucagon exert its actions?

A

Insulin receptor - tyrosine kinase receptor
◦ Activation of insulin receptor causes translocation of GLUT4 receptor onto cell surface membrane (Skeletal muscle and adipose tissue)

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31
Q

The actions of insulin are

Anabolic/catabolic?

A

Anabolic

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32
Q

The actions of glucagon are

Anabolic/catabolic?

A

Catabolic

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33
Q

Explain the roles of insulin in the liver.

A

CARBOHYDRATES

  • stimulates glycogenesis
  • inhibits glycogenolysis
  • inhibits gluconeogenesis

AMINO ACIDS

  • stimulates amino acid uptake and protein synthesis
  • inhibits breakdown of amino acids in liver

FAT
-inhibits fatty acid metabolism

-decreases ketogenesis

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34
Q

Explain the role of insulin in adipose tissue.

A

CARBOHYDRATES
-stimulates glucose uptake via insertion of GLUT4 into cell membrane

FAT

  • stimulates lipogenesis and esterification of fatty acids
  • stimulates lipoprotein lipase activity in the capillary bed
  • inhibits lipolysis
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35
Q

Explain the role of insulin in skeletal muscle.

A

AMINO ACIDS

  • stimulates amino acid uptake and protein synthesis
  • inhibits proteolysis

CARBOHYDRATES

  • stimulates glucose transport via insertion of GLUT4 into surface membrane
  • stimulates glycogenesis
  • inhibits glycogenolysis
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36
Q 
What are the effects of insulin on:
Glycogenesis 
Gluconeogenesis
Lipolysis
Ketogenesis
A

Increases glycogenesis

Decreases gluconeogenesis

Decreases lipolysis

Decreases ketogenesis

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37
Q 
What are the effects of glucagon on:
Glycogenesis 
Gluconeogenesis
Lipolysis
Ketogenesis
A

Decreases glycogenesis
Increases gluconeogenesis
Increases lipolysis
Increases ketogenesis

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38
Q

When glucose concentrations are above 5mM, what would the insulin:glucagon ratio be?

A

High

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39
Q

When glucose concentrations are below 5mM, what would the insulin: glucagon ratio be?

A

High

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40
Q

After a meal high in protein and low in carbohydrates, what would plasma concentration of insulin and glucagon be?

A

Both are high

Insulin - convert amino acids to stores

Glucagon - convert amino acids to glucose (gluconeogenesis)

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41
Q

After a meal rich in carbohydrates and proteins, would plasma concentration of insulin and glucagon be high or low?

A

Insulin - high
Convert amino acids to stores

Glucagon - low

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42
Q

What are the effects of insulin and glucagon on glycolysis?

A

Insulin - stimulates glycolysis

Glucagon - inhibits glycolysis

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43
Q

What are the effects of insulin and glucose on ketogenesis?

A

Insulin - inhibits ketogenesis

Glucagon - increases ketogenesis

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44
Q

Insulin and glucagon have delayed effects on which metabolic processes?

A

Lipogenesis

Lipolysis

Ketogenesis

45
Q

Insulin and glucagon have rapid effects on which metabolic processes?

A

Glucose uptake

Amino acids uptake

46
Q

What is Diabetes Mellitus?

A

Diabetes mellitus is a group of metabolic disorders characterised by chronic hyperglycaemia (elevated blood glucose concentration), due to insulin deficiency, insulin resistance, or both. There are two major types of the disease, clearly distinguished by their epidemiology and probable causation: Type 1 and Type 2.

47
Q

What tests and test results are used to confirm a diagnosis of Diabetes Mellitus?

A

Random venous plasma glucose OR
Oral glucose tolerance test (2 hours after 75g anhydrous glucose)
> or equal to 11.1 mmol/L

Fasting plasma glucose concentration
> or equal to 7.0mmol/L

HbA1c > 10%

48
Q

What investigations are often requested in patients suspected to have Diabetes Mellitus?

A

Urine - glucose and ketones

Finger prick - glucose and ketones

Smell of acetone on breath

Blood sample for measurement of:
Glucose, urea and electrolytes, HbA1c

49
Q

What would you look for on examination of a patient suspected to have Diabetes Mellitus?

A

Signs of dehydration

Blood pressure

Chest sounds

Respiration rate

Smell of acetone on breath (nail varnish)

50
Q

Can diabetes be diagnosed based on a single glucose determination?

A

If symptomatic, 1 abnormal test required

If asymptomatic, 2 abnormal tests required. Repeat test on another day.

51
Q

List the main differences between Type 1 and Type 2 diabetes.
(Onset, symptoms, weight loss, weight, ketogenesis, C-peptide, auto-immunity)

A

Onset:
Type 1 - childhood, sudden
Type 2 - middle age, gradual

Symptoms:
Type 1 - severe acute symptoms
Type 2 - may be few acute symptoms but long term chronic effects may be severe

Recent weight loss:
Type 1 - YES
Type 2 - generally NO (sometimes there is)

Weight:
Type 1 - usually lean
Type 2 - usually obese

Ketogenesis:
Type 1 - YES, risk of ketoacidosis
Type 2 - NO

C-peptide:
Type 1 - NONE
Type 2 - detectable

Auto-immunity
Type 1 - markers present
Type 2 - no markers present

52
Q

How would C-peptide detection vary in people with Type 1 and Type 2 diabetes?

A

Type 1: no C-peptide (no insulin production/secretion)

Type 2: C-peptide detectable (there is insulin production and secretion but insulin sensitivity is decreased)

53
Q

In Type _____ Diabetes Mellitus, patients may not initially need treatment with insulin but sufferers usually progress to a state where they eventually do.

A

2

54
Q

Why does Type 1 Diabetes Mellitus commonly present in teenage years or later rather than at birth?

A
  • Genetic predisposition to the disease. Associated with the genetic markers HLA-DR3 and HLA-DR4
  • Interacts with an environmental trigger to produce immune activation
  • There is a strong seasonal variation, suggesting a link with a viral infection acting as a trigger to a rapid deterioration
55
Q

What is the difference between absolute and relative Type 1 Diabetes Mellitus?

A

Reduced production/secretion of insulin by pancreatic beta cells due to:

  1. Absolute - destruction of pancreatic beta cells.
    90% - autoimmune response
    10% - idiopathic
  2. Relative - secretory response of pancreatic beta cells is abnormally slow or small
    This is due to a mutation in Kir6.2 which results in a defect in the K-ATP channels which become less sensitive to ATP. The severity of insensitivity depends on the mutation.
56
Q

What is insulitis?

A

Inflammation of the islets

Chronic inflammatory mononuclear cell infiltrate consisting of T-lymphocytes and macrophages is found associated with the islets of newly diagnosed Type1 diabetics

57
Q

Which auto-antibodies are involved in autoimmune destruction of pancreatic beta cells in the Islet of Langerhans?

When can these be detected relative to onset of symptoms?

A

ICAs - Islet Cell Auto-antibodies

IAAs - Insulin Auto-antibodies

IA2 - an islet secretory protein

GAD - Glutamic Acid Decarboxylase

Detected before onset of diabetes (months- years)

58
Q

What are the risk factors for Type 2 diabetes?

A 
Obesity - accounts for 85%
Muscle and liver fat deposition 
Elevated circulating free fatty acids 
Physical inactivity 
Genetic influences
59
Q

What happens in Type 2 diabetes?

A

Insufficient insulin production from beta cells in the setting of insulin resistance due to:

  1. Defective insulin receptor mechanism -
    Change in receptor number
    Change in affinity
  2. Defective post-receptor events
  3. Excessive or inappropriate glucagon secretion
60
Q

What varies among individuals with Diabetes mellitus?

A

Proportion of insulin resistance vs Beta cell dysfunction

Some primarily have insulin resistance with a minor defect in insulin secretion.
Others have a slight insulin resistance with a primary lack of insulin secretion

61
Q

Rate of fatality is slower in type _____Diabetes Mellitus

A

2

62
Q

Insulin resistance is present before the onset of hyperglycaemia and development of type 2 diabetes.

Describe the sequence of events that begins due to resistance to insulin, eventually resulting in type 2 diabetes.

A

Initially,
Beta cells compensate for insensitivity to insulin by increasing insulin production - maintains normal blood glucose

Eventually,
Beta cells are unable to maintain increased insulin production - impaired glucose tolerance

Finally,
Beta cell dysfunction leads to relative insulin deficiency - overt Type 2 diabetes

63
Q

What are the common presenting features of Type 1 and Type 2 diabetes?

A 
-typical symptoms of hyperglycaemia:
Polyuria
Polydipsia
Blurring of vision
Urogenital infections - thrush

-symptoms of inadequate energy utilisation
Tiredness
Weakness
Lethargy

Severity of these symptoms depends on the rate of rise of blood glucose as well as the absolute levels of glucose achieved.

64
Q

How does type 1 diabetes typically present?

A

Rapid onset (usually weeks) of a triad of symptoms:

  • polyuria
  • polydipsia
  • weight loss

If presentation is late there may be symptoms of ketoacidosis:

  • vomiting
  • nausea
  • hyperventilation
  • abdominal pain

The patient is usually young.

65
Q

Explain why polyuria and glucosuria a symptom of Diabetes Mellitus.

A
  1. In the nephron of a healthy individual, all of the glucose filtered from the blood is reabsorbed at the end of the proximal tubule
  2. Reabsorption in this part of the kidney is isoosmotic.
  3. In Diabetes Mellitus, hyperglycaemia means large quantities of glucose are filtered by the kidney. Not all of this glucose is reabsorbed. (Renal threshold for glucose in 10mmol/L).
  4. The extra glucose remains in the nephron tubule.
  5. This places an extra osmotic load on the nephron so less water is reabsorbed to maintain the isosmotic character of this section of the nephron.
  6. The extra water then remains with the glucose in the nephron tubule and is excreted in the urine.
66
Q

What is polydipsia and why is it a symptom of Diabetes Mellitus?

A

Excessive thirst

Excess water loss.
Osmotic effects of glucose on the thirst centres

67
Q

Why is weight loss a symptom of Type 1 diabetes?

A

Low insulin to glucagon ratio stimulates lipolysis and gluconeogenesis.

68
Q

Why can people who present late with Type 1 diabetes get ketoacidosis?

A

Low insulin to glucagon ratio stimulates:

-lipolysis and fatty acid degradation
Fatty acids are produced for beta-oxidation in the liver following excessive lipolysis in adipose tissue.
This supplies the substrate acetyl coA.
High NADH from lipolysis inhibits TCA cycle so acetyl coA is fed into pathway for ketone production

-ketogenesis
Lyase is activated
HMG coA reductase is inhibited

69
Q

What are the effects of a lack of insulin and a corresponding elevation in glucagon in Type 1 Diabetes Mellitus?

A

FATS

  • rapid lipolysis in adipose tissue
  • fatty acid oxidation in liver

CARBOHYDRATES

  • glycogenolysis
  • peripheral glucose uptake reduced

PROTEINS
-gluconeogenesis

70
Q

What are the features of ketoacidosis?

A
  • Prostration
  • Hyperventilation
  • Nausea
  • Vomiting
  • Dehydration
  • Abdominal pain
71
Q

Describe the typical presentation of Type 2 Diabetes Mellitus.

A

Gradual worsening onset of symptoms due to hyperglycaemia:

  • polyuria
  • polydipsia
  • lethargy

Symptoms may include complications of Diabetes including:

  • persistent infections (thrush of genitalia, infections of feet)
  • visual problems

NO URINARY KETONES/SIGNS OF KETOACIDOSIS
USUALLY NO WEIGHT LOSS

Patient is usually obese and middle aged > 40 yrs old

72
Q

What are the consequences of hyperglycaemia?

A
  1. Abnormal metabolism of glucose to products that may be harmful to cells because the uptake of glucose into certain cells (peripheral nerves, eye, kidney) does not require insulin. It is metabolised by the enzyme aldose reductase:
    Glucose + NADPH + H —> sorbitol + NADP+
    This reaction depletes cellular NADPH and leads to increased disulphide bond formation in cellular proteins, altering their structure and function.
    In addition, accumulation of sorbitol causes osmotic damage to cells.
  2. Increased glycation of plasma proteins which leads to disturbances in their function.
73
Q

What is the difference between glycosylation and glycation?

A

Glycosylation is post-translational modification mediated by enzymes.
Glycation is a non-enzymatic reaction.

Glycosylation is when a defined carbohydrate molecule is added to a pre-determined region of the protein. Glycation is when a sugar is covalently attached to a protein creating an unnatural glycated product.

In glycosylation, carbohydrates play a natural role in protein function. Glycation impairs protein function and stability.

Glycosylation is not associated with a disease process. Glycation is associated with disease processes.

74
Q

Chronic hyperglycaeamia results in

Glycation or glycosylation

Of proteins?

A

Glycation

75
Q

Explain the principle and practice of measuring glycosylation of haemoglobin as an index of blood glucose control in a diabetic.

A

The terminal valine of haemoglobin molecules is glycated in hyperglycaemia to form glycated haemoglobin (HbA1c).

The percentage of HbA1c is related is a good indicator of average blood glucose concentration over the preceding 2-3 months since red blood cells usually spend 120 days in the circulation.

In healthy individuals, 4-6% of haemoglobin is glycated
In poorly controlled diabetics, >10% of haemoglobin can be glycated

76
Q

How is Type 1 Diabetes managed?

A

A. Diet and exercise

B. Insulin therapy

(Oral glucose-lowering drugs generally avoided in Type 1 diabetes due to risk of hypoglycaemia)

77
Q

When might a Type 1 Diabetic have to adjust their insulin dose?

A
  • patient has an infection
  • suffered from some trauma
  • risk of diabetic ketoacidosis
78
Q

Once injected, effects of insulin are largely irreversible. What advice might you give to a patient to avoid hypos?

A
  • regular food and meal times
  • unrefined carbohydrates in preference to refined
  • carry sugar or sweets
  • regular self-monitoring of blood glucose and feet
79
Q

How is Type 2 Diabetes managed?

A

A. Diet and exercise

B. Oral hypoglycaemic therapy eg. Sulphonylurea, metformin

C. Insulin therapy

80
Q

How does sulphonylurea work?

What is it used in the treatment of?

A

Sulphonylurea binds to sulphonylurea receptor on the membrane of beta cells. This closes the ATP-sensitive K+ channel regardless of whether ATP has bound and independently of glucose concentration. Therefore, more insulin is secreted

Type 2 Diabetes

81
Q

How does metformin work?

What is it used in the treatment of?

A

Reduces plasma glucose and hence hepatic glucose output by inhibiting gluconeogenesis

Type 2 diabetes

82
Q

What are the acute complications of Type 1 Diabetes?

A
  • acute complications of hyperglycaemia (polyuria, polydipsia, weight loss)
  • diabetic ketoacidosis
83
Q

What are the acute complications of type 2 diabetes?

A
  • acute complications of hyperglycaemia (polyuria, polydipsia, maybe weight loss)
  • hyperosmolar non-ketotic syndrome
84
Q

What are the acute complications of hypoglycaemia and why are diabetics at risk of this?

A

Coma - brain needs glucose

Caused by hypoglycaemic therapy

85
Q

What are the chronic implications of diabetes?

A

Macrovacular:

  • stroke
  • MI
  • poor circulation to periphery - particularly feet

Microvascular:

  • diabetic eye disease
  • diabetic kidney disease (nephropathy)
  • diabetic neuropathy
  • diabetic feet
86
Q

Describe what happens in diabetic eye disease.

A
  • Visual problems from changes in lens due to osmotic effects of sorbitol —> glaucoma and possibly cataracts

-diabetic retinopathy - damage to blood vessels in retina can lead to blindness. Damaged blood vessels leak and form protein exudates on the retina/rupture and cause bleeding into eye.
Additionally, new blood vessels may form (proliferative retinopathy)- these vessels are very weak and can easily bleed.

87
Q

Explain diabetic kidney disease (nephropathy).

A

Damage to the glomeruli
Poor blood supply due to changes in kidney blood vessels
Damage from infections of UTIs (more common in diabetes)

88
Q

What is a sign of nephropathy?

A

Microalbuminuria (increased amount of protein in urine)

89
Q

What is diabetic neuropathy?

A

Damage to:

Peripheral nerves - loss of sensation and other effects

Autonomic nerves

90
Q

Explain diabetic feet.

A

Poor blood supply
Damage to nerves
Increased risk of infection
Care is needed to keep feet in good condition and prevent foot loss through gangrene

91
Q

What is metabolic syndrome?

A

The metabolic syndrome is defined as a group of dangerous risk factors associated with cardiovascular disease:
• Insulin resistance
• Dyslipidaemia (high VLDL and LDL, low HDL)
• Glucose intolerance
• Hypertension associated with central adiposity

92
Q

What are the criteria for metabolic syndrome?

A 
• Waist: hip ratio 
	◦ > 0.9 for men 
	◦ >0.85 women 
• BMI 
	◦ >30kg/metres squared 
• Blood pressure 
	◦ > 140/90mmHg
• Triglycerides 
	◦ >1.7mmol/L
• HDL cholesterol 
	◦ <0.9 mmol/L in men
	◦ <1mmol/L in women 
• glucose fasting or 2 hr after glucose load 
	◦ >7.8mmol/L
93
Q

Which type of diabetes is metabolic syndrome strongly associated with?

A

Type 2

Present in approx 80% of type 2 diabetics

94
Q

What are the major factors that cause metabolic syndrome?

A
  • Insulin resistance
  • Central obesity
  • Genetics
  • Physical inactivity
  • Ageing
95
Q

Which term is used to describe the excretion of glucose in urine?

A

Glucosuria

96
Q

The half-life of insulin and glucagon in plasma is approximately…

A

5 mins

Insulin needs to respond very quickly to glucose concentrations on a minute to minute basis. In order to allow the body to rapidly respond to changes in glucose concentration (eg. After a meal), both glucagon and insulin have relatively short half lives.

97
Q

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

A

3

2 link A and B chains

1 intra-subunit disulphide bond in A chain

98
Q

Which glucose transporter is the primary transporter of glucose in pancreatic beta cells?

Where else is this transporter found?

A

GLUT2

Liver

It is a bidirectional transporter, allowing glucose to flow in both directions. It therefore allows hepatocytes to export glucose made by gluconeogenesis into the blood.

99
Q

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

A

Insulin secretion would increase - this is how beta cells detect an increase in plasma glucose.

100
Q

What effect would a decrease in intracellular ATP conc have on ATP sensitive potassium channels in pancreatic beta cells?

A

More K-ATP channels would be in the open state.

101
Q

What is the medical term used to describe excessive thirst?

A

Polydipsia

102
Q

Which type of diabetes is more likely to show sudden onset in childhood?

A

Type 1

103
Q

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

A

C-peptide conc would remain the same

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. However, commercial insulin preparations for injection just contain insulin (no C-peptide is added to the preparation). For this reason measuring C-peptide can give an indictaion of any residual endogenous insulin secreting capacity of a diabetic receiving insulin injections since any C-peptide must have come from endogenous insulin synthesis rather than injected insulin. Since C-peptide is thought to be a hormone in its own right, many would argue that commercial insulin preparations should also contain this peptide, especially as it has been shown to help alleviate some of the long term microvascular complications associated with diabetes (e.g. nephropathy, retinopathy

104
Q

Briefly explain why insulin has to be injected and cannot be taken orally in pill form?

A

It is a peptide hormone so would be denatured in the GI tract to its constituent amino acids if taken orally

105
Q

Name the glycated form of haemoglobin that is measured as an indicator of average plasma glucose concentration over a prolonged time.

A

HbA1c

106
Q

Is the glycation of haemoglobin to form HbA1c catalysed by an enzyme?

A

No

107
Q

How would you expect the levels of the following to be in a patient diagnosed with metabolic syndrome?
HDL
LDL
VLDL

A

Reduced HDL
High LDL
High VLDL

108
Q

Name the two most significant factors underlying the aetiology of metabolic syndrome?

A

Central obesity

Insulin resistance

109
Q

Epidemiological studies have shown that the children of women who were exposed to famine during early pregnancy are more susceptible to diabetes, obesity and cardiovascular disease in adult life.
Which change DNA is the most likely cause of this increased suceptibility to dssease?

A

DNA methylation

Epigenetic changes such as DNA methylation and histone modifications are thought to underlie this type of suceptibility to disease

zESA2 (21 decks)

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