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(LUSUMA) Metabolism, Endocrinology & Haematology > S10) The Endocrine Pancreas > Flashcards

S10) The Endocrine Pancreas Flashcards

1
Q

Describe the two functions of the pancreas

A
  • Produces digestive enzymes (exocrine action ~99%)
  • Hormone production (endocrine action ~1%)
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2
Q

Important polypeptide hormones are secreted by the pancreas.

Identify them

A
  • Insulin
  • Glucagon
  • Somatostatin
  • Pancreatic polypeptide
  • Ghrelin
  • Gastrin
  • Vasoactive intestinal peptide
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3
Q

Identify the seven main cell types in pancreatic islets

A
  • β cells – Insulin
  • α cells – Glucagon
  • d cells – Somatostatin
  • PP cells – Pancreatic polypeptide
  • e cells – Ghrelin
  • G cells – Gastrin
  • VIP
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4
Q

Describe the role of insulin and glucagon

A

Insulin & Glucagon – regulation of metabolism of carbohydrates, proteins, and fats

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5
Q

Both insulin and glucagon are controllers of plasma glucose.

Describe their respective functions

A
  • Insulin – lowers blood glucose levels
  • Glucagon – raises blood glucose levels
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6
Q

Compare and contrast the metabolic actions of insulin and glucagon in terms of the following:

  • Onset
  • Target tissues
  • Affected metabolism
  • Actions
A
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7
Q

Describe how the measured plasma glucose concentration may vary

A
  • Normally: 3.3-6 mmol/L
  • After a meal: 7-8 mmol/L
  • Renal threshold: 10 mmol/L (≥ glycosuria)
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8
Q

Describe the shared properties of insulin and glucagon in terms of the following:

  • Solubility
  • Transport
  • Half life
  • Receptors
  • Inactivation
A
  • Solubility – water soluble hormones
  • Transport – transported dissolved in plasma
  • T½ – 5 mins (short)
  • Receptors – cell surface receptors on target cells
  • Inactivation – receptor-hormone complex can be internalised
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9
Q

Insulin is the hormone of energy storage.

In light of this, state four of its unique properties

A

Insulin favours energy storage:

  • Anabolic
  • Anti-gluconeogenic
  • Anti-lipolytic
  • Anti-ketogenic
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10
Q

Describe the structure of insulin

A
  • Insulin is a large polypeptide with an alpha helix structure
  • It is composed of 2 un-branched peptide chains, connected by 2 disulphide bridges for stability
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11
Q

Outline the synthesis and secretory pathway of insulin

A
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12
Q

Explain the metabolic regulation of KATP channels and insulin secretion

A
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13
Q

Insulin binds to the insulin receptor on cell surfaces.

Describe the properties of the insulin receptor

A

Insulin receptor is a dimer, connected together by a single di-sulphide bond:

  • α-chain on exterior of the cell membrane
  • β-chain spans the cell membrane in a single segment
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14
Q

How does insulin increase glucose uptake into target cells and glycogen synthesis?

A

Insertion of Glut 4 channel

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15
Q

Describe the effects of insulin-uptake on metabolism in the following tissue locations:

  • Liver
  • Muscles
  • Adipose tissue
A
  • Liver – increases glycogen synthesis and inhibits breakdown of amino acids
  • Muscles – increase uptake of amino acids promoting protein synthesis
  • Adipose tissue – increases the storage of triglycerides and inhibits breakdown of fatty acids
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16
Q

Glucagon is the hormone of energy mobilisation.

In light of this, state four of its unique properties

A

Glucagon favours energy mobilisation:

  • Catabolic
  • Gluconeogenic
  • Lipolytic
  • Ketogenic
17
Q

Describe the structure of glucagon

A
  • 29 amino acids in 1 polypeptide chain
  • No disulphide bridges i.e. flexible structure
18
Q

Glucagon is secreted due to low glucose levels in α-cells.

In 5 steps, outline in synthesis and secretory pathway

A

⇒ Synthesised in rER

⇒ Transported to Golgi

⇒ Packaged in granules

⇒ Storage granules move to cell surface (margination)

⇒ Exocytosis – fusion of vesicle membrane with plasma membrane with the release of the vesicle contents

19
Q

Describe the effects of glucagon-uptake on metabolism in the following tissue locations:

  • Liver
  • Adipose tissue
A
  • Liver – increases the rate of glycogenolysis and stimulates pathway for gluconeogenesis from amino acids
  • Adipose tissue – stimulates lipolysis to increase plasma fatty acid
20
Q

Describe the net effects of glucagon and insulin on carbohydrate metabolism as well as their relative speed

A
21
Q

Describe the net effects of glucagon and insulin on lipid metabolism as well as their relative speed

A
22
Q

Describe the net effects of glucagon and insulin on amino acid metabolism as well as their relative speed

A
23
Q

What happens when insulin and glucagon levels are abnormal?

A
  • Insulin:

I. High – hypoglycaemia

II. Low – hyperglycaemia (diabetes mellitus)

  • Glucagon:

I. High – worsens diabetes

II. Low – may contribute to hypoglycaemia

24
Q

Diabetes Mellitus is a group of metabolic disorders resulting from abnormal insulin levels.

What is it characterised by?

A
  • Chronic hyperglycaemia
  • Long-term clinical complications
  • Elevated glucose levels in urine
25
Q

How is Diabetes Mellitus diagnosed?

A

Diagnosis is based on venous plasma glucose concentration:

  • Fasting ≥ 7.0mM
  • Random ≥ 11.1mM
26
Q

What is the cause of Diabetes in Type I Diabetes Mellitus?

A

Type I – absolute insulin deficiency due to the autoimmune destruction of Pancreatic β- cells

27
Q

What is insulin deficiency?

A

Insulin deficiency is the failure to secrete adequate amounts of insulin from β-cells

28
Q

What are the two types of insulin deficiency?

A
  • Absolute – destruction of pancreatic β- cells
  • Relative – abnormally slow/small secretory response of β-cells
29
Q

What change occurs in KATP channels in relative insulin deficiency?

A
30
Q

What is the cause of Diabetes in Type II Diabetes Mellitus?

A

Type 2 – normal insulin secretion but relative peripheral insulin resistance

31
Q

What are the three possible manifestations of insulin resistance

A
  • Defective insulin receptor mechanism – change in receptor number and/or affinity
  • Defective post-receptor events – tissues become insensitive to insulin
  • Excessive glucagon secretion
32
Q

Insulin resistance involves the main sites of glucose utilisation showing decreased response to normal circulating concentrations of insulin

What are the causes of this?

A

Results from combination of:

  • Genetic factors
  • Environmental factors e.g. obesity, sedentary lifestyle
33
Q

Explain how insulin resistance present before 12+ years leads to the onset of hyperglycaemia and development of overt Type II Diabetes

A
  • Initially: β-cells compensate by increasing insulin production – maintains normal blood glucose
  • Eventually: β-cells unable to maintain increased insulin production – impaired glucose tolerance
  • Finally: β-cell dysfunction leads to relative insulin deficiency – overt Type II Diabetes

(LUSUMA) Metabolism, Endocrinology & Haematology (20 decks)

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