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Endocrinology > Introduction to diabtes mellitus > Flashcards

Introduction to diabtes mellitus Flashcards

1
Q

Describe the basic effects of insulin on glucose

A

decrease HGO

increase muscle uptake

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2
Q

Describe the basic effects of insulin on protein

A

decrease proteolysis

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3
Q

Describe the basic effects of insulin on lipids

A

Decrease lipolysis

Decrease ketogenesis

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4
Q

Describe the mitogenic actions of insulin

A 
Lipoproteins
Smooth muscle hypertrophy- Important in high blood pressure 
Ovarian function
Clotting
Energy expenditure
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5
Q

Describe the structure of the GLUT 4 receptor

A

Outer core is hydrophobic- to keep it embedded in the hydrophobic core of the phospholipid bilayer
Inner region is hydrophilic- to allow glucose, which is also hydrophilic, to move through the transporter by facilitated diffusion

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6
Q

What is the action of insulin on the expression of GLUT 4 channels and what is the consequence of this

A

Vesicles containing GLUT 4 are insulin responsive. Insulin acts on these pre-made GLUT 4 receptors and recruits them into the plasma membrane of muscle cells and adipose tissue, driving glucose into these cells. This results in a 7-fold increased glucose uptake into the cell.

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7
Q

What is the main glucose sink in the body

A

Muscle

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8
Q

What happens to protein synthesis inside a muscle cell when insulin is released

A

When insulin is present, as well as IGF1, protein synthesis is driven.
Amino acids — Protein

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9
Q

What happens to proteins in muscle cells in the absence of insulin

A

Proteolysis is stimulated- cortisol stimulates this too.
Protein — Amino Acids
These amino acids can be respired in the Krebs cycle.
If they are gluconeogenic amino acids (alanine) they can enter the bloodstream and be taken to the Liver, where they can be used to make glucose

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10
Q

Describe the presence of glucose in the blood

A

Glucose present in blood all time, not only after meals

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11
Q

What is glycogen

A

Glycogen in liver is stored glucose

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12
Q

Describe the effect of insulin on protein synthesis in the Liver

A

In the presence of insulin, protein synthesis is stimulated.

Amino acids — Protein

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13
Q

Describe the effects of an absence of insulin on proteolysis in the liver.

A

A lack of insulin, protein deficiency and glucagon stimulates the proteolysis of protein into amino acids in the liver.
Protein — amino acid

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14
Q

What is the potential fate of these amino acids in the liver

A

In the absence of insulin, but in the presence of glucagon, cortisol, and catecholamines, these amino acids may be converted into glucose via gluconeogenesis.
This glucose is then released into the blood stream (increased hepatic glucose output).

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15
Q

What else can be used in gluconeogenesis

A

Pyruvate and lactate

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16
Q

Describe the characteristics of fat fuel stores in the body

A

Weight (9-10kg)
Energy (37kJ/G)
Time (30-40 days)

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17
Q

Describe the characteristics of protein fuel stores in the body

A

Weight (8-9kg)
Energy (17KJ/G)
Time (15 days)

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18
Q

Describe the characteristics of carbohydrate fuel stores in the body

A

Weight ( 0.5kg)
Energy (16KJ/g)
Time ( 16 hours)

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19
Q

What takes longer to breakdown, fat or protein

A

Fat

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20
Q

Describe the events that take place in lipoproteins in response to insulin

A

Lipoprotein lipase in lipoproteins is sensitive to insulin. Catalyses the breakdown of triglycerides into NEFA and Glycerol, NEFA enters

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21
Q

Why is it important that we breakdown Triglycerides

A

Triglycerides are too big to pass through plasma membranes on their own, hence they need to be broken down

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22
Q

What happens in adipocytes in response to insulin

A

Increased expression of GLUT 4 channel proteins on surface.
Glucose enters the adipocyte
Glucose – acetyl co-A — NEFA
Some glucose is also converted into glycerol-3-phosphate
Glycerol-3-phosphate + NEFA — Triglyceride.

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23
Q

What happens to the triglycerides in adipocytes in the absence of insulin

A

In the absence of insulin, but in the presence of catecholamines, cortisol, and growth hormone, triglycerides will be broken down into glycerol and NEFAs

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24
Q

Why is it important that we have separate circulation for the gut and liver

A

So that food can be processed before it enters the circulation

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25
Q

What is a consequence of this different circulation for the gut

A

Adipocytes in omental circulation are different to that of the systemic circulation, such as in the arms and legs. As a result of their different anatomical location, they are more metabolically active, and have a faster turnover rate. Omental adipocytes predict ischaemic heart disease

26
Q

Can NEFAs be used in gluconeogenesis

A

No, they are used in the TCA cycle instead

27
Q

Describe gluconeogenesis in the liver

A

In absence of insulin, presence of glucagon.
Glycerol enters the liver- converted into glycerol-3-phosphate.
Some triglycerides in the liver are also broken down into glycerol-3-phosphate.
This glycerol-3-phosphate is converted into glucose in gluconeogenesis.

28
Q

What percentage of the HGO does gluconeogenesis account for after a 10 hour fast

A

25%

29
Q

Describe the different fuels for the brain

A 
Can use
Glucose
Ketone bodies
Can not use 
Fatty acids
30
Q

What does insulin prevent the formation of

A

Ketone bodies

31
Q

What allows the brain to survive during a fast

A

Ketone bodies

32
Q

What is a key sign of insulin deficiency

A

The presence of ketones in the blood when blood glucose levels are also high

33
Q

Describe glycogen stores in the muscle

A

The glucose released can only be used by the muscle cells themselves.

34
Q

Describe the formation of ketone bodies in the liver

A

NEFA taken into the liver
NEFA is converted into fatty acyl coA (shuttle on mitochondrial membrane)
In the presence of glucagon, absence of insulin:
Fatty acyl coA – Acetyl coA
Acetyl coA- – Acetoacetate
Acetoacetate — Acetone + 3-hydroxybutyrate

35
Q

Describe the process of glycogenesis in the presence of insulin

A

Glucose is taken into the liver.
Glucose — Glucose-6-phosphate
G6P — Glycogen

36
Q

Describe the process of glycogenolysis

A

In the absence of insulin, presence of glucagon
Glycogen— G6P
G6P — Glucose
This glucose is then released into the bloodstream to increase HGO

37
Q

Describe the characteristics of the fasted state

A 
low insulin to glucagon ratio
[glucose] 3.0-5.5mmol/l
 [NEFA]
low  [amino acid] when prolonged
Increased  Proteolysis
Increased  Lipolysis
Increased  HGO from glycogen and gluconeogensis
Muscle to use lipid
Brain to use glucose, later ketones
 Ketogenesis when prolonged
38
Q

Describe the characteristics of the fed state

A 
Stored insulin released then 2nd phase
High [insulin] to [glucagon] ratio 
Stop HGO, 
 Glycogen                          gluconeogenesis
 protein synthesis
 proteolysis 
 Lipogenesis
39
Q

What do patients with ischaemic heart disease and obesity normally have

A

Insulin resistance- regardless of whether they are diabetic or not.

40
Q

What is T1DM defined as

A

Absolute insulin deficiency (although not always the case)

41
Q

Describe the presentation of T1DM

A 
Absolute insulin deficiency
Proteolysis with weight loss
Hyperglycaemia- Increased HGO
Glycosuria with osmotic symptoms
Ketonuria
Increased lipolysis
42
Q

Explain why glycosuria occurs

A

As GLUT 4 is not activated, glucose is not transported into the relevant cells, so although there is a lot of glucose in the circulation, it is not available for cellular metabolism. The increase in plasma glucose overcomes the renal threshold for glucose reabsorption, and glycosuria results. The glucose draws water with it by osmosis, so the patients claim of passing large amount of urine night and day, making them very thirsty, so they complain of polydipsia and polyuria

43
Q

What is a more serious aspect of type 1 diabetes

A

The enormous increase in ketogenesis. Although ketones are a useful fuel when needed, if produced in excess they cause a fall in pH, as they are weak ketoacids. The danger is that the pH can fall dangerously low, which in turn can have a negative impact on the activity of a number of brain and other enzymes. This is known as diabetic ketoacidosis.

44
Q

What is cachexia

A

The extreme loss of weight

45
Q

Describe insulin induced hypoglycaemia

A 
Increased:  insulin
 Glucagon 
 Catecholamines
 Cortisol
 Growth hormone
Glucose enters muscles
Increased  HGO later with glycogenolysis and gluconeogenesis (glucagon triumphs)
Lipolysis increased
Patients cannot switch off the insulin injected, prolonged effect. However, it will get better, glucagon produced
46
Q

What is the role of subcutaneous insulin

A

To switch HGO off

47
Q

What is the role of intramuscular glucagon

A

Administered when the patient is unconscious.
Reverse insulin induced hypoglycaemia.
Restores HGO.

48
Q

Where does insulin resistance reside

A

All metabolic sites and all arms of intermediary metabolism

49
Q

In T2DM, what is there enough insulin to suppress

A

Enough insulin to suppress
Ketogenesis
proteolysis

50
Q

Describe the two different reaction pathways of insulin

A

Binding of insulin to the insulin receptor may cause tyrosine kinase to phosphorylate IRS (insulin receptor substrate). This passes down the PI3K-Akt pathway
and is responsible for the metabolic effects of insulin.
However, it may also phosphorylate different substrates in the MAPK pathway to simulate mitogenesis- also important in blood pressure and dyslipidaemia.

51
Q

Which pathway is resistant to insulin

A

PI3K-Akt pathway

52
Q

Describe what happens in insulin resistance when the patient can still make insulin

A

Beta cells try to overcome the resistance by making more insulin, so the patient becomes hyperinsulinemic and euglycemic. Increased mitogenic reactions.

53
Q

Describe the metabolic actions of insulin in insulin resistance

A

GLUCOSE
PROTEIN
LIPID
All normal

54
Q

Describe the mitogenic reactions of insulin in insulin resistance

A

Lipoproteins- low HDL
Smooth muscle hypertrophy- high blood pressure
Ovarian function- polycystic ovarian syndrome
Clotting- abnormal effects
Energy expenditure- abnormal effects

55
Q

What can patients with DM have

A

Urinary tract infections- due to high presence of glucose.

56
Q

Describe the presentation of T2DM

A 
Insulin resistance
60-80% obese 
Dyslipidaemia
Later insulin deficiency
Hyperglycaemia
Less osmotic symptoms
With complications
Adipocytokines
Inflammatory state
Energy expenditure
High [TG]
Low [HDL
Hypertension
BP>135/80
Waist circumference
Men>102   
Women>88
Fasting glucose
>6.0mmol/l
57
Q

What is meant by dyslipidaemia

A

Abnormal carriage of lipoproteins in the blood

58
Q

Is insulin resistance a disease

A

No, it is a pathophysiological state

59
Q

What does T2DM usually present with

A

Myocardial infarction

60
Q

Describe a diet for T2DM

A 
Total calories control
reduce calories as fat 
reduce calories as refined carbohydrate
increase calories as complex carbohydrate
increase soluble fibre
Decrease sodium
61
Q

What is key for the diet in patients with T2DM

A

Control portion sizes

Endocrinology (11 decks)

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