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MEH > The Endocrine Pancreas > Flashcards

The Endocrine Pancreas Flashcards

1
Q

Describe the development of the gut

A
  • Foregut: coeliac trunk
  • Midgut: SMA
  • Hindgut: IMA
  • Pancreases is a large gland
  • develops embryologically as an outgrowth of the foregut
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2
Q

What are the functions f the pancreas

A 
• Pancreas has two functions
– produces digestive enzymes secreted directly
into duodenum (exocrine action)
• Exocrine function forms the bulk of the gland
– Alkaline secretions via pancreatic duct to duodenum
– hormone production (endocrine action)
• From Islets of Langerhans
• ~ 1% endocrine tissue, 99% exocrine tissue
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3
Q

Describe the anatomy of the pancreas

A

Has a head, neck, body, tail, hits behind the stomach, head in duodenum, in front of aorta and portal vein
Foregut derivative

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4
Q

What are important polypeptide hormones secreted by the pancreas

A 
• Important Polypeptide
hormones secreted by
pancreas - each secreted by a specified cell 
• Insulin - beta
• Glucagon - alpha
• Somatostatin - delta 
• Pancreatic polypeptide (PP) - pp cells
• Ghrelin - e cells
• Gastrin  - g cells
• Vasoactive intestinal peptide - vip cells
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5
Q

What are the major types of cell in the islets

A 
– Beta ( β)-cells - Insulin
– Alpha (α)-cell - Glucagon 
– Delta (d)-cells -Somatostatin 
– PP cells 
– e cells ghrelin
– G cells gastrin
– VIP - vasoactive intestinal peptide

The cell types in an islet all stain differently - see slide

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6
Q

Which hormonaes are involved in glucose regulation?

A

Insulin, glucagon

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7
Q

Describe the feedback look for plasma glucose regulation

A

High blood glucose islets are well perfumed with this plasma - this will stimulate the release of insulin from pancreatic beta cells. This will travel around target tissues and cause those cells to take up glucose - also stimulate the liver to produce glycogen - store. This will lower the plasma glucose levels.

Vice versa with fall- alpha - glucagon which works predominantly in liver

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8
Q

What are actions of insulin

A

Signal - feeding
Target tissues - liver (to make glycogen) adipose, skeletal muscle (take up glucose)
Affects metabolism - carbohydrates,lipids, proteins
Actions - anabolic

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9
Q

What are teh actions of glucagon

A

Signal - feeding
Target tissues - liver (break down glycogen), adipose (release sugars back into plasma)
Affects metabolism - carbs, lipids
Actions - catabolic

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10
Q

What is the importance of plasma glucose

A

• Brain uses glucose at fastest rate in body
– Relies on blood
• Sensitive to falls in glucose
• or rise = increased osmolarity
• Circulation glucose needs to be controlled
• Normally 3.3-6 mmol/L (UHL reference range)
• After a meal 7-8 mmol/L
• Renal threshold 10 mmol/L - the point at which glucose pass across filtrate in kidney and appear in urine - Elderly - higher renal threshold - longer time before it appears in urine
– Glycosuria
• Pregnancy renal threshold↓
• Elderly renal threshold↑

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11
Q

What are the properties of insulin and glucagon

A 
• Water soluble hormones:
– Carried dissolved in plasma 
– no special transport proteins 
– Short ½ life 5mins 
– interact with cell surface receptors on target cells – receptor with hormone bound can be
internalised – inactivation
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12
Q

-

A

-

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13
Q

What are properties on insulin

A
  • Action (favours storage) it is the hormone of energy storage
  • is anti-gluconeogenic – at high dosage lowers incorporation of pyruvate- into blood glucose, but also stimulated its incorporation into liver glycogen.

• Insulin is Anabolic
– anti-gluconeogenic
– anti-lipolytic and anti-
ketogenic

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14
Q

Describe this islats o langerhans

A

See slide

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15
Q

Why does the endocrine pancreas tissue have a good blood supply

A

Production of hormones - quickly taken up by blood supply and transported around

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16
Q

Describe the structure of insulin

A

• Insulin is a big peptide
with an alpha helix structure (3bits)
• consists of two un- branched peptide chains which are connected by 2 disulfide bridges this ensure stability (hold chains together)
– 51 amino acids
– 2 polypeptide chains
– (A = 21, B = 30)
– 2 disulphide bridges: = rigid structure

17
Q

Outline the formation of insulin a

A
  1. Pre-proinsulin translation, signal cleavage, proinsulin folding
  2. Proinsulin is transported to Golgi
  3. Proinsulin is cleaved to produce insulin and C- peptide
    See mcbg
    In vesicle - marginate to surface - collect here
    When there is a signal from influx of calcium - vesicles fuse with membrane - contents released
18
Q

What transporter toes glucose enter through

A

GLUT2

19
Q

Describe the action of KATP channels

A

Glucose closes K ATP channels in pancreatic beta cells - When glucose added - channel activity gone - no longer effluxing potassium - no longer hyperpolarised - now depolarised
Metabolic inhibition reopens K ATP channels - Hyperpolarisation - membrane potential closer to Ek
Cell-attached patch recordings, high external K -60mV

Makes the link between electrical excitability and metabolism. It cellis able to metabolise, it is able to make ATP, channels are inhibited in presence of ATP

20
Q

Describe the release of insulin.

A

If metabolism is low, low atp, high adp, channels open, membrane hyperpolarised
When insulin perfumes cell eg after meal, glucose taken up through GLUT2, cell increase metabolic rate, produce ATP, inhibit K ATP channels, beta cell memb potential +ve - depolarise. On the cel surface there is a VOCC - depolarisation opens this - Ca2+ enters the cell down conc grads. Influx of Ca2+ triggers fusion of vesicles to B cell memb - release of insulin

21
Q

What are the metabolic effects of insulin

A

• Insulin…. What does it do?

• increases glucose uptake into target cells and glycogen synthesis (insertion of Glut 4 channel - glucose enters target cells)
- no insulin - no signal - no glut 4 - no glucose uptake
– in the liver it increases glycogen synthesis by stimulating glycogen formation and by inhibiting
breakdown
– in muscles it increase uptake of AA promoting protein synthesis
– in liver inhibits breakdown of AA – in adipose tissue increases the storage of
triglycerides
• inhibits breakdown of fatty acids

22
Q

Describe the insulin receptor.

A

– Insulin binds to the insulin receptor on cell surfaces
– receptor is a dimer
– two identical subunits spanning the cell membrane.
– two subunits are made of one α-chain and one β- chain, connected together by a single di-sulfide bond.
– α-chain on exterior of the cell membrane,
– β-chain spans the cell membrane in a single segment,

23
Q

What is glucagon

A 
• Hormone that opposes insulin
– acts to raise blood glucose levels
– It is glycogenolytic
– gluconeogenic
– lipolytic
– ketogenic 
• it mobilizes energy release
If patient has low levels of glucose - can give glucagon if unable to rally take it 
Normally would cause hyperglycaemia unless levels low
24
Q

How is glucagon secreted

A

• Secreted by α- cells
• Secreted due to low glucose levels in α-cells
• Synthesized in Rough ER transported to Golgi - folded and a bit cleaved
• package in granules
• Effect mainly in the liver
• Granules move to cell surface
– Margination – movement of storage vesicles to cell
surface
– Exocytosis – fusion of vesicle membrane with plasma
membrane with the release of the vesicle contents.
C peptide MIGHT have a physiological effect - probably for a reason that affects smal vessels

25
Q

What is the structure of glucagon

A
  • 29 amino acids in 1 polypeptide chain
  • No disulphide bridges: =flexible structure
  • Simpler synthesis
26
Q

What are the effects of glucagon

A

• In the liver increases the rate of glycogen
breakdown (glycogenolysis)
• Stimulates the pathway for synthesis of glucose from AA (gluconeogenesis) • Net effect is a rise in blood glucose levels
• Stimulates lipolysis to increase plasma fatty acid

27
Q

Why is glucagon clinically important

A

Glucagon in emergency medicine is used
when a person with diabetes is
experiencing hypoglycaemia and cannot
take sugar orally

28
Q

Describe the opposition of insulin and glucagon

A

See slide
Eg an increase in amino acids - stimulates insulin AND glucagon - in the presence of pure AA - protein dominant diet with no carbs - stimulates both but as soon as u add any carb, stop stimulating glucagon

29
Q

Give a summary of carb metabolism

A

Glucose uptake in muscle & adipose - insulin positive glucagon negative = rapid
Glycolysis - insulin positive glucagon negative
Gluconeogenesis - increase glucagon - minutes or delay
Gyro Genesis I - insulin positive effect - intermediate
Glycogenolysis - glycogen positive effect

30
Q

Give a summary of lipid metabolism

A

Lipogenesis - insulin positive - delayed
Lipolysis - glucagon - rapid
Ketogenesisi - glucagon

31
Q

Give a summary of AA metabolism

A

AA uptake - insulin - rapid

Protein synthesis - insulin - intermediate few minutes

32
Q

What happens with abnormal insulin or glucagon

A

• Insulin
– High – hypoglycaemia.
– Low – hyperglycaemia -diabetes mellitus

• Glucagon
– High – makes diabetes worse
– Low – may contribute to hypoglycaemia

33
Q

Give an overview of blood glucose disorders

A

• Diabetes mellitus
• Group of metabolic diseases
• Affect >2% of population in UK
• Characterised by
– chronic hyperglycaemia mellitus (L) = honeysweet (prolonged elevation of blood glucose)
– leading to long-term clinical complications
• Associated with elevated glucose levels in urine

34
Q

How is diabetes mellitus diagnosed

A

• Diagnosis basis of venous plasma glucose
concentration:
• normal range 3.3-6mmol/L plasma glucose (UHL reference range)
• if fasting ≥ 7.0mM significant
• not fasting, random ≥ 11.1mM significant

35
Q

What is diabetes mellitus type 1 caused by

A 
• Diabetes mellitus  is caused by: 
• Type 1 – absolute insulin
deficiency (Autoimmune
destruction of Pancreatic b-
cells).
– Absolute – pancreatic b-cells
destroyed 
– Relative – secretory response of b-cell is abnormally slow or small (Insulin deficiency – failure to secrete adequate amounts of insulin from b-cells (defective b-cells or b-cell loss).
36
Q

Describe K atp channels in insulin deficiency

A

Made up of 4 subunits with hole in the middle of them to make the channel
KIR and SUR subunits
With some mutations to KIR6.2 leads to loss o ATP sensitivity in these channels. Rather than being affected by changes in metabolism they become ineffective - mutation occurs - one way of explaining why pancreatic beta cells become less sensitive or ess efficient at releasing insulin

37
Q

What is the cause o type 2 diabetes

A

• Type 2 – normal ? secretion but relative peripheral insulin resistance.
– Defective insulin receptor mechanism
– change in receptor number and/or affinity.
– Defective post-receptor events
• Insulin resistance – tissues become insensitive to insulin.
– Or Excessive or inappropriate glucagon secretion

38
Q

What is insulin resistance

A 
• Main sites of glucose utilisation (adipose, liver &
skeletal muscle) show decreased response to normal circulating concentrations of insulin. 
• Affects:
– ~ 25% of general population 
– ~ 92% of patients with type 2 diabetes
• Results from combination of:
– genetic factors 
– environmental factors including:
• obesity
• sedentary lifestyle
39
Q

Describe insulin resistance in the young

A

• Insulin resistance present before ( 12+ years) onset of hyperglycaemia & development of overt type 2 diabetes.
• Initially:
– β-cells compensate by increasing insulin production - maintains normal blood glucose.
• Eventually:
– β -cells unable to maintain increased insulin production - cant work at unregulated level - impaired glucose tolerance.
• Finally:
– β -cell dysfunction leads to relative insulin deficiency - overt type 2 diabetes

MEH (21 decks)

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