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Endocrine > Pancreas > Flashcards

Pancreas Flashcards

1
Q

Which organ is especially sensitive to low glucose levels?

A

The brain, as it cannot use triglycerides

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2
Q

Why is the pancreatic tumour the most difficult to operate on?

A

pancreas is placed just anterior to the aorta and portal vein

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3
Q

what innervates the pancreas?

A

vagus nerve

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4
Q

Endocrine cells in pancreas

A

islets of Langerhans

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5
Q

What four regulatory polypeptides do they secrete?

A

Insulin, glucagon, somatostatin and pancreatic polypeptide

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6
Q

Structures of islets of Langerhans

A

clusters of around 1000 endocrine cells

make up 1-2% of pancreatic volume

organised as a rosetta cell, with a large variety of cells

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7
Q

cells in rosetta + function

A

alpha cells- secrete glucagon

beta cells- secrete insulin

delta cells- secrete somatostatin

F cells- secrete pancreatic polypeptide

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8
Q

Rough organisation of cells in rosetta

A

60-75% beta of the centre of each islet

20% alpha- tend to surround beta

less common delta and F cells surround that

surrounded by pancreatic acini

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9
Q

Function of pancreatic acinar cells

A

exocrine function, that produce and transport enzymes that are passed into the duodenum where they assist in the digestion of food

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10
Q

Two main functional components of the pancreas explained

A

exocrine- acinar cells secerete digestive enzymes

endocrine- islets of Langerhans secrete hormones

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11
Q

Experiment to determine the organisation of cells in the rosetta

A

fluorescently tag proteins that bind to the different, specific receptors

able to visualise

humans have scattered, mice have predominantly ring of glucagon and large centre of insulin

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12
Q

secretion of insulin stages

A
  1. Synthesised in the rough ER of B cells
  2. transported to golgi where it is packaged into membane bound granules
  3. granules move to plasma membrane via microtubules
  4. granules removed by exocytosis, where insulin then enters blood stream via fenestrated capillaries
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13
Q

Biosynthesis of insulin stages

A
  1. synthesised as a part of a larger preprohormone
  2. preproinsulin is produced by the ER
  3. molecule is then folded and disulfide bridges form to make proinsulin
  4. The connecting C peptide is cleaved in the golgi
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14
Q

Why is the preprohormone secreted?

A

More stable

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15
Q

How much insulin is released per secretory granule?

A

8fg

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16
Q

Structure of B cell granules

A

packets of insulin found in the cytoplasm

shape of packets varies dependent on species

insulin molecules form complexes with zinc

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17
Q

Half life of insulin

A

5 minutes

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18
Q

What type of function?

A

endocrine

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19
Q

How fast is insulin action?

A

It can be fast, intermediate or slow

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20
Q

Different glucose transporters + where they act

A

GLUT1- plasma membranes of all cells, associated with basal uptake of glucose

GLUT2- small intestine, renal tubules, hepatocytes, brain and B cells

GLUT3- ubiquitous

GLUT4- skeletal and cardiac muscle, adipose tissue

GLUT5- mainly gut

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21
Q

What is transported by each GLUT channel?

A

GLUT1- glucose, galactose, mannose

GLUT2- glucose, fructose

GLUT3- glucose

GLUT4- glucose

GLUT5- fructose

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22
Q

What leads to sugar toxicity?

A

Specificity of channels. Fructose cannot be taken up by muscle tissue and adipose, therefore must be broken down by liver. If too much, can lead to toxic effects

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23
Q

Which Glucose transporter is under the control of insulin?

A

GLUT4

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24
Q

Why is the cleaved C protein very important?

A

Longer half life than insulin and produced in the same quantities, so can be measured in the blood, to determine whether an individual lacks insulin- may suggest diabetes mellitus 1

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25
Q

What leads to the release of insulin?

A

raised blood glucose, amino acids and hormones, such as GLP and nervous inputs

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26
Q

Mechanism by which insulin is release

A

Insulin release is diphasic

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27
Q

Explain first phase of insulin release

A

Rapidly triggered in response to increased blood glucose levels and lasts about 10 minutes

  1. Glucose enters the B cells through glucose transporters via GLUT2
  2. Glucose is phosphorylated to glucose 6-phosphate by hexokinase IV
  3. Glucose enter the glucolytic pathway and then via pyruvate enters oxidative phosphorylation where high energy ATP is produced, leading to a rise in ATP:ADP
  4. An increased ATP:ADP leads to the closing of ATP potassium channels, preventing the potassium ions from leaving the cell. Leads to a buildup of intracellular potassium ions, causing the cell to become less negative- depolarisation
  5. Upon depolarisation, voltage gated calcium ion channels open, allowing calcium ions to move into the cell by facilitated diffusion
  6. the significant increase in calcium ions in the cytoplasm causes the release of secretory vesicles containing insulin
28
Q

What is the affinity of GLUT2 and why is it important?

A

Has a relatively low affinity for glucose, thus ensures that the rate of glucose entry into beta cells is proportional to the extracellular glucose concentration

29
Q

How else can calcium ion concentrations be increased?

A

activation of ryanodine receptors to release calcium from intracellular stores

GPCR - phospholipase C activation- parasympathetic stimulation of pancreatic islets

30
Q

Explain 2nd phase of insulin release

A

Sustained, slow release of newly formed vesicles triggered independently of sugar- peaking at 2-3 hours.

Oscillates with a period of 3-6 minutes

31
Q

Explain effects of insulin

A

insulin binds to a receptor present in the cell membrane

This leads to the insertion of GLUT4 glucose transporters into the cell membranes of muscle and fat cells

leads to conversion of glucose into insoluble glycogen- glycogenesis

conversion of glucose into triglycerides and protein, decreased lipolysis

decreased glucineogenesis and glycogenolysis

enhances anabolism

32
Q

Stages of receptor activation

A
  1. Insulin binds to receptor present on cell membrane
  2. Receptor is an alpha, beta homodimer.
  3. Insulin binds to the alpha subunits of the homodimer, which faces the extracellular side of the cell
  4. The beta subunit has tyrosine kinase enzyme activity which is triggered by the insulin binding.
  5. leads to autophosphorylation of the beta subunit and subsequently the phosphorylation of proteins inside the cell known as insulin receptor substrates
  6. activates a signal transduction cascade, that leads to the activation of other kinases.
  7. MAPK, PIK, PKB and GFPB activated, which lead to intracellular enzyme activation
33
Q

How are the affects of insulin halted?

A

degradation and endocytosis of the receptor bound to insulin

dephosphorylation of the tyrosine kinase residue

34
Q

2 more glucose transports + location and type

A

SGLT-1 - sodium coupled symporter- 2 sodium and one glucose/galactose. intestine and kidneys

SGLT-2 one sodium one glucose- kidneys

35
Q

What happens to these symporters during diabetes?

A

Become overwhelmed. Sodium driving force no longer large enough to move the increased plasma glucose out the blood

36
Q

What is incretin?

A

A group of metabolic hormones that stimulate a decrease in blood glucose levels. Released after eating and augment the secretion of insulin.

Some may also inhibit glucagon release from alpha cells

37
Q

A specific incretin

A

Glucagon-like-peptide GLP-1

38
Q

GLP1 secretion

A

Produced and secreted by intestinal enteroendocrine L-cells in the distal ileum, colon, jejunum and duodenum.

Packaged in secretory granule and secreted into the hepatic portal system.

released in a biphasic pattern

39
Q

GLP1 function

A

Promotes insulin secretion in a glucose dependent manner.

As GLP1 binds to receptors expressed on pancreatic beta cells, the receptors couple to G proteins, activating adenylate cyclase that increases the production of CAMP

leads to PKA activation and increases cytosolic Ca2+ so enhances exocytosis of insulin containing granules

also ensures that b cell insulin stores are replenished by promoting insulin gene transcription, mRNA stability and biosynthesis

decreased appetite (Ghrelin)

40
Q

What do alpha cells secrete?

A

Glucagon

41
Q

What causes the release of glucagon?

A

hypoglycaemia, sympathetic nervous impulses, gastrointestinal hormones, specific amino acids, insulin- paracrine

42
Q

Stages of glucagon action

A
  1. glucagon binds to GPCR located in plasma membrane
  2. leads to the activation of adenylate cyclase, cAMP and then PKa
  3. pKa activates a phosphorylase kinase, which then phosphorylates glycogen phosphorylase b
  4. this activates it, turning it into phosphorylase a
  5. The phosphorylated phosphorylase then clips glucose units from glycogen
43
Q

Other functions of glucagon

A

glucose production, glycogenolysis, gluconeogenesis, non-esterified fatty acid production, lipolysis

All to raise the concentration of glucose

44
Q

Where does glucagon predominantly act?

A

hepatocytes and adipocytes

45
Q

How is the secretion of glucagon regulated?

A

Pancreatic B cells contain GABA receptors, which are chloride channels.

Increased insulin production leads to GABA being released, binds to GABAa receptors, which causes the hyperpolarisation of the cells

stimulation of beta adrenergic receptors increases secretion

alpha adrenergic inhibits secretion

46
Q

Somatostatin definition

A

Growth hormone-inhibiting hormone that regulates neurotransmission and cell proliferation via interaction with G protein coupled somatostatin receptors.

47
Q

What does somatostatin inhibit?

A

insulin and glucagon secretion

48
Q

Where is somatostatin produced?

A

Delta cells in the duodenum and pancreatic islets. released into the peripheral blood

49
Q

Two forms of somatostatin

A

14 amino acids in brain

28 amino acids in pancreatic islets

50
Q

What sort of receptor is it?

A

Gi protein coupled receptor- inhibitory

51
Q

Diabetes mellitus definition

A

Constellation of abnormalities caused y insulin deficiency

52
Q

Diabetes insipidus definition

A

a deficiency in the production or action of vasopressin

53
Q

Two types of diabetes mellitus and who is affect

A

Type 1, insulin-dependent - lack of production of insulin, younger. Autoimmune condition where the B cells are destroyed

Type 2, non insulin dependent- beta cells unresponsive to insulin. Insulin resistance in peripheral tissues such as skeletal muscle, brain and liver

54
Q

Explain insulin resistance

A

Pathway’s sensitivity to insulin may be blunted by free fatty acids

55
Q

Treatment for type 1 diabetes

A

insulin injections after eating

pancreas transplant

islet cell transplant

56
Q

Treatment for type 2 diabetes

A

metformin- inhibition of glucagon induced cAMP levels with reduced action of PKA- decreases gluconeogenesis

exercise, eating healthier, less carbohydrates and sugars

sulphonylureas- increase insulin release from beta cells in the pancreas. Bind to and close K-ATP channels, depolarising the membrane, leading to a rise in intracellular calcium.

57
Q

Issue with transplant

A

rejection, so patient needs to be on immunosuppresants

58
Q

How is type 1 diabetes diagnosed?

A

When diabetic ketoacidosis occurs, which is when there is not enough insulin in the body, causing insulin to spill into the urine, causing osmotic diuresis.

Absence of insulin also causes release of fatty acids from adipose tissue, which are converted into ketone bodies during beta oxidation

ketone bodies cause the blood to turn acidic

59
Q

Issues with sulfonylureas

A

only drug that can lead to hypoglycaemia, as a result of excesses in insulin production and release

60
Q

Why does diabetes cause neuropathy?

A

High blood glucose levels damage the small blood vessels that supply the nerves.

61
Q

How is diabetes characterised?

A

polyuria, polydipsia, weight loss inspite of polyphagia, hyperglycemia, ketosis, acidosis, coma

62
Q

Explain starvation in the midst of plenty

A

liberation of glucose into circulation from the liber, meaning there is an intracellular glucose deficiency.

63
Q

Cancer type in the pancreas

A

insulinoma

64
Q

Insulinoma definition

A

a tumour of the pancreas that is derived from beta cells and secretes insulin

65
Q

Effects of insulinoma

A

increase in insulin, decrease in blood glucose. Patients present symptom of hypoglycemia

66
Q

hypoglycemia symptoms

A

lethargy, blurred vision, diplopia (simultaneous perception of two images of a single object)

Endocrine (5 decks)

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