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Pancreas Flashcards

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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
What leads to the release of insulin?
raised blood glucose, amino acids and hormones, such as GLP and nervous inputs
26
Mechanism by which insulin is release
Insulin release is diphasic
27
Explain first phase of insulin release
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
What is the affinity of GLUT2 and why is it important?
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
How else can calcium ion concentrations be increased?
activation of ryanodine receptors to release calcium from intracellular stores GPCR - phospholipase C activation- parasympathetic stimulation of pancreatic islets
30
Explain 2nd phase of insulin release
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
Explain effects of insulin
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
Stages of receptor activation
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
How are the affects of insulin halted?
degradation and endocytosis of the receptor bound to insulin dephosphorylation of the tyrosine kinase residue
34
2 more glucose transports + location and type
SGLT-1 - sodium coupled symporter- 2 sodium and one glucose/galactose. intestine and kidneys SGLT-2 one sodium one glucose- kidneys
35
What happens to these symporters during diabetes?
Become overwhelmed. Sodium driving force no longer large enough to move the increased plasma glucose out the blood
36
What is incretin?
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
A specific incretin
Glucagon-like-peptide GLP-1
38
GLP1 secretion
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
GLP1 function
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
What do alpha cells secrete?
Glucagon
41
What causes the release of glucagon?
hypoglycaemia, sympathetic nervous impulses, gastrointestinal hormones, specific amino acids, insulin- paracrine
42
Stages of glucagon action
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
Other functions of glucagon
glucose production, glycogenolysis, gluconeogenesis, non-esterified fatty acid production, lipolysis All to raise the concentration of glucose
44
Where does glucagon predominantly act?
hepatocytes and adipocytes
45
How is the secretion of glucagon regulated?
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
Somatostatin definition
Growth hormone-inhibiting hormone that regulates neurotransmission and cell proliferation via interaction with G protein coupled somatostatin receptors.
47
What does somatostatin inhibit?
insulin and glucagon secretion
48
Where is somatostatin produced?
Delta cells in the duodenum and pancreatic islets. released into the peripheral blood
49
Two forms of somatostatin
14 amino acids in brain | 28 amino acids in pancreatic islets
50
What sort of receptor is it?
Gi protein coupled receptor- inhibitory
51
Diabetes mellitus definition
Constellation of abnormalities caused y insulin deficiency
52
Diabetes insipidus definition
a deficiency in the production or action of vasopressin
53
Two types of diabetes mellitus and who is affect
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
Explain insulin resistance
Pathway's sensitivity to insulin may be blunted by free fatty acids
55
Treatment for type 1 diabetes
insulin injections after eating pancreas transplant islet cell transplant
56
Treatment for type 2 diabetes
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
Issue with transplant
rejection, so patient needs to be on immunosuppresants
58
How is type 1 diabetes diagnosed?
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
Issues with sulfonylureas
only drug that can lead to hypoglycaemia, as a result of excesses in insulin production and release
60
Why does diabetes cause neuropathy?
High blood glucose levels damage the small blood vessels that supply the nerves.
61
How is diabetes characterised?
polyuria, polydipsia, weight loss inspite of polyphagia, hyperglycemia, ketosis, acidosis, coma
62
Explain starvation in the midst of plenty
liberation of glucose into circulation from the liber, meaning there is an intracellular glucose deficiency.
63
Cancer type in the pancreas
insulinoma
64
Insulinoma definition
a tumour of the pancreas that is derived from beta cells and secretes insulin
65
Effects of insulinoma
increase in insulin, decrease in blood glucose. Patients present symptom of hypoglycemia
66
hypoglycemia symptoms
lethargy, blurred vision, diplopia (simultaneous perception of two images of a single object)

Endocrine (5 decks)

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