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RDA > Lecture 25 - 2018/2017 > Flashcards

Lecture 25 - 2018/2017 Flashcards

1
Q

What is gluconeogenesis?

A

Glucose is being made.

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2
Q

What is glycolysis?

A

Glucose is being broken down.

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3
Q

What is glycogenolysis?

A

Glycogen is converted to glucose (occurs in the muscle and the liver).

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4
Q

How much glucose does the brain consume?

A

80% of whole body glucose.

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5
Q

How is glucose taken up by the brain?

A

NIMGU - non-insulin mediated glucose uptake.

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6
Q

How many islets of langerhans are there in the pancreas?

A

Approximately 1 million - they account for 1-2% of mass of the pancreas but 20% of blood flow.

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7
Q

What are the cells in the pancreas? And what do they produce?

A

Alpha cells = glucagon.
Beta cells = insulin.
D cells = somatostatin.
F cells = pancreatic polypeptide for bicarbonate regulation.

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8
Q

What happens when a person gets pancreatitis?

A

Digestive enzymes are released into pancreatic tissue and can damage the pancreas i.e. damage to langerhans, which can lead to subsequent development of diabetes.

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9
Q

Where does the pancreas drain into?

A

The liver.

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10
Q

What are the transporters involved in glucose uptake?

A

GLUT1 - found in erythrocytes and brain (NIMGU).
GLUT2 - found in pancreas (beta-cells) and liver.
GLUT3 - found in neurons (placenta).
GLUT4 - found in fat and muscle (insulin-mediated glucose uptake; also exercise induced).

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11
Q

How is insulin released from the beta cells?

A
  1. Glucose enters the pancreas via GLUT2 transporter in the beta cells.
  2. Once in the beta-cell glucose undergoes glycolysis to make ATP.
  3. The ATP will turn off the potassium sensitive channel which will result in depolarisation of the calcium channels.
  4. The calcium channels are now open which will result in an influx of calcium into the cell.
  5. There is a rise in intracellular calcium which which will trigger insulin translocation and exocytosis - release of insulin.
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12
Q

What does GLP-1 do in terms of the pancreas?

A

The glucagon-like peptide receptor in beta cells will respond to GLP-1 incretin hormone produced by the gut) which will cause a decrease in blood glucose.

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13
Q

What is the C peptide? and what clinical relevance does it have?

A

C peptide has no biological function but it is what is released when insulin is produced. It is measured when patients present with spontaneous hypoglycaemia, such as distinguishing factitious hypoglycaemia and insulin producing tumour.

  1. Factitious hypoglycaemia (caused by unneeded injections of insulin), then low C peptide level.
  2. If it is the tumour, then high C peptide level.
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14
Q

What is insulin regulation?

A

It is pulsatile (9-14 minutes) - turns on and off quite quickly.

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15
Q

What is the major regulator of insulin?

A

Glucose - fast acute phase release and then a slower second phase. Other regulators are amino acids such as arginine, glucagon, incretins and somatostatin.

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16
Q

What causes insulin to rise?

A
  1. Increasing glucose.
  2. Increasing glucagon.
  3. Vagus nerve stimulation.
  4. Release of arginine, incretin hormones (GLP1).
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17
Q

What inhibits insulin release?

A
  1. Falling glucose.
  2. Sympathetic nerve stimulation.
  3. Somatostatin.
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18
Q

What protects us from hypoglycaemia?

A
  1. Glucagon.
  2. Adrenaline.
  3. GH.
  4. Cortisol.

They act on gluconeogenesis and glycogenolysis.

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19
Q

What do patients with T2DM blood glucose look like in the morning?

A

Higher blood glucose levels in the morning, even though they haven’t eaten. That is because when we are waking up, GH and cortisol are released - makes you insulin resistant.

20
Q

What does the release of incretin (GLP1) result in?

A
  1. Reduced glucagon release from alpha cells.
  2. Increase in insulin release from beta cells.
    This response to GLP1 is glucose dependent, this means the higher the glucose the more GLP1 released. When glucose levels go back down GLP1 levels go back down.
21
Q

How does insulin allow for glucose uptake?

A

Take in case glucose being taken up by fat and muscle (GLUT4):

  1. Insulin binds to the insulin receptors in fat and muscle.
  2. Insulin bound to the insulin receptor will cause a phosphorylation cascade, which will cause GLUT4 to be transported to the cells surface.
  3. GLUT4 now allows for the uptake of glucose into the cell.
22
Q

How does insulin work in the liver?

A
  1. Inhibits glycogenolysis (stops breakdown of glycogen to glucose) and gluconeogenesis.
  2. Increases glycolysis and glycogen synthesis.
  3. Increase in lipid and protein synthesis.
  4. Decrease in ketogenesis.
23
Q

How does insulin work in muscle?

A
  1. Increases glucose transport into muscles and glycolysis.
  2. Increase glycogen synthesis.
  3. Increase in amino acid uptake and protein synthesis.
  4. Increase ketone uptake.
24
Q

How does insulin work in adipose tissue?

A
  1. Increases glucose transport into muscle and glycolysis.
  2. Increase in lipogenesis.
  3. Decrease in lipolysis.
25
Q

How does insulin work with fat?

A
  1. Increases triglyceride storage.
  2. Inhibits lipolysis (decrease hormone sensitive lipase).
  3. Inhibits FFA production.
26
Q

How does insulin work with protein?

A

Insulin is anabolic so it increases transport of amino acid into liver and muscle.

27
Q

How much carbohydrate is stored as energy?

A

1-2%.

28
Q

What is carbohydrate stored as?

A

Glycogen.

29
Q

What does glycogenolysis result in?

A

Rapid release of glucose.

30
Q

How much fat is stored as energy?

A

70-80%.

31
Q

How much protein is stored as energy?

A

20%.

32
Q

What happens in gluconeogenesis?

A

Formation of new molecules of glucose.

33
Q

What happens in glycolysis?

A

Breakdown of glucose to pyruvate, which enters the krebs cycle to produce ATP.

34
Q

What happens in glycogenolysis?

A

Breakdown of glycogen to G6P which can then:
-be used for energy (muscle, cannot convert glycogen straight to glucose) -> glycogen in muscle to break down to lactate and lactate goes into the krebs cycle and can convert to ATP or used to form glucose.

35
Q

What happens in protein hydrolysis?

A

Breakdown of proteins to amino acids (alanine in muscle) which enters the krebs cycle for gluconeogenesis or are oxidised directly to ATP.

36
Q

What is lipolysis?

A

Breakdown of fat to glycerol (glycerol us used for gluconeogenesis via Krebs cycle) and FFA (these cannot enter the krebs cycle so the make ketone bodies).

37
Q

What is ketogenesis?

A

When ketones are produced via oxidation of FFA.

38
Q

What ketones are made via oxidation of FFA?

A
  1. Aceto acetate.
  2. Acetone.
  3. Beta hydroxybutyrate.
39
Q

What are ketones used for?

A

Fuel for muscle and liver but not for brain or RBC.

40
Q

What can occur with T1DM?

A

Prolonged and profound insulin deficiency:

  1. GLUT4 is inactive (as there is no insulin to bring it to the surface) so there is no glucose uptake - hyperglycaemia.
  2. Because insulin is not there, there is uncontrolled hormone sensitive lipase, this means there will be fat lipolysis and the formation of ketones which are acidic.
  3. Protein hydrolysis is unchecked and amino acids enter the uncontrolled krebs cycle which results in uncontrolled gluconeogenesis.
  4. Glycogenolysis is uncontrolled which results in an increasing glucose production and hepatic glucose output.
  5. Overall it results in DKA.
41
Q

What is the normal fasting glucose range?

A

3.5-5.5mmol/l.

42
Q

What does insulin primarily do?

A

Stop hyperglycaemia.

43
Q

What happens if glucose falls in a fasting state (in a normal person)?

A

Insulin is switched off and counter-regulatory hormones (glucagon) are released to prevent hypoglycaemia. The ANS will activate the hypothalamus to release adrenaline and noradrenaline. The pituitary gland is also activated to release GH and ACTH. ACTH will stimulate the adrenal glands to release cortisol. The person becomes aware of the hypoglycaemic attack and starts toe at.

44
Q

What happens if glucose falls in a fasting state (in a T1DM person)?

A

People with T1DM can get hypoglycaemic attacks regularly, as it is difficult to match insulin injections to normal physiology. A recurrent hypoglycaemia will lead to the person to stop producing an ANS response. The hypothalamus thinks it’s normal for the blood glucose to be low, because it is so often that low during the week. The person will start to develop an unawareness of having a hypoglycaemic attack - now their first response to a hypoglycaemic attack will be cognitive dysfunction i.e. confusion. Untreated hypoglycaemia will lead to more serious effects such as convulsions and coma/death.

45
Q

What happens to hypoglycaemic attacks in a person (4-5 years of having diabetes)?

A

The patient may stop producing glucagon in response to hypoglycaemia. This is because the glucose levels are not going down due to too much circulating insulin - alpha cells see al the circulating insulin and will not produce glucagon. These patients are very vulnerable as they have a problem with their hypothalamus not responding to glucose and they have a problem with the pancreas not producing glucagon. They are more vulnerable to severe hypoglycaemic episodes.

46
Q

What are the causes of hypoglycaemia?

A
  1. Too much insulin in patients with diabetes.
  2. Sulphonylurea therapy.
  3. Insulinoma (rare tumour in pancreas that overproduces insulin).
  4. Severe hormone deficiency such as Addison’s disease (rare cortisol deficiency).

RDA (19 decks)

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