The Endocrine Pancreas 1 Flashcards

1
Q

Energy (food) intake is the determined by the balance of activity in what 2 hypothalamic centres?

A
  • Feeding centre: Promotes feeling of hunger and drive to eat
  • Satiety centre: Promotes feeling of fullness by suppressing the Feeding centre
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2
Q

State the “glucostatic theory”

A
  • Food intake is determined by blood glucose: as [BG] increases, the drive to eat decreases (-Feeding Centre; +Satiety centre)
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3
Q

State “lipostatic theory”

A
  • Food intake is determined by fat stores: as fat stores increase, the drive to eat decreases (-feeding centre; + Satiety Centre)

(Leptin is a peptide hormone released by fat stores which depresses feeding activity.)

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4
Q

What are the 3 categories of energy output?

A
  • Mechanical work: Movement, we can regulate this voluntarily using skeletal muscle
  • Cellular work: Transporting molecules across membranes, growth and repair, storage of energy
  • Heat loss: (half our energy output)
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5
Q

What are the 3 elements of metabolism?

A
  1. Extracting energy from nutrients in food
  2. Storing that energy
  3. Utilising that energy for work
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6
Q

Compare anabolic and catabolic pathways.

A

Anabolic pathways = Build up, synthesis of large molecules from smaller ones, usually for storage purposes

Catabolic pathways = Break down, degredation of large molecules into smaller ones, releasing energy for work

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7
Q

What is meant by:

(a) Absorptive state
(b) Post-absorptive state

A

(a) Right after a meal ingested nutrients supply the energy needs of the body and excess is stored - this is an ANABOLIC phase
(b) Between meals where the pool of nutrients from the plasma decreases and we rely on body stores to release energy - this is a CATABOLIC phase

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8
Q

The brain is an “obligatory glucose utiliser”. What does this mean?

A
  • The brain can only use GLUCOSE for energy

(execpt in extreme starvation)

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9
Q

How do we maintain blood glucose? (2)

A

BY SYNTHESISING GLUCOSE:

  • Glycogen → Glucose (glycogenolysis)
  • Amino acids → Glucose (gluconeogenesis)
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10
Q

Normal ranges of blood glucose (LATER):

A

LATER

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11
Q

The pancreas is __% exocrine and __% endocrine

A

- 99 % exocrine (acini)

- 1 % endocrine (islets of Langerhans)

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12
Q

State the 4 islet cells found in the Islets of Langerhans and state what each cells produces

A

4 types of islet cells: α, β, δ & F (hormone secreting cells)

  • α cells produce GLUCAGON
  • β cells produce INSULIN
  • δ cells produce SOMATOSTATIN

F cells produce pancreatic polypeptide

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13
Q

State the function of the peptide hormone insulin

A
  • Decreases blood glucose levels by stimulating glucose uptake by cells

(major stimulus = increase in blood glucose concentration)

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14
Q

Describe the mechanism by which a high blood glucose leads to the secretion of insulin

A
  • High abundant glucose in the blood enters the β cell through glucose transporter proteins (GLUT)
  • Metabolism increases and glucose is metabolised to produce ATP
  • ATP levels rise
  • ATP binds to K+ ion channels causing it to close
  • K+ cannot leave the cell so K+ levels in the cell build up, leading to depolarisation of the cell
  • Depolarisation of the cell causes voltage gated dependent Ca2+ ion channels to open
  • Ca2+ enters the cell and creates an intracellular signal which which triggers insulin vesicle exocytosis into the circulation
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15
Q

Descibe why, when blood gluose levels are low, why insulin is NOT secreted

A
  • When blood glucose is low, glucose does not diffuse in the β cell
  • Metabolism decreases
  • ATP production decreases
  • Low levels of ATP leave K+ ion channels open
  • K+ ions leak out, therefore positive charge is removed from the cell, hyperpolarising it
  • Therefore voltage gated Ca2+ channels remain closed and so insulin is NOT secreted
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16
Q

Describe how insulin increases the uptake of glucose by cells

A
  • After insulin is released from β cells thorugh exocytosis and is in the blood, it then leaves the blood and binds to tyrosine kinase receptors on the cell membrane of insulin-sensitive tissues
  • In muscle and adipose/fat tissue, this binding of insulin to tyrosine kinase receptors stimulates the migration of GLUT 4 transporters to the cell membrane (which normally resides in the cytoplasm of these cells)
  • GLUT 4 allows the transportation of glucose into the cell

(when insulin stimulation stops, the GLUT 4 transporters return to the cytoplasmic pool)

17
Q

Which cells in the body are insulin dependent?

A
  • Muscle cells
  • Fat cells
18
Q

Descibe the role of insulin in the uptake of glucose by hepatocytes in the fed state

A
  • In the fed state, the liver takes up glucose becuase insulin activates HEXOKINASE
  • HEXOKINASE lowers glucose levels in the cell
  • This creates a gradient, favouring glucose movement into the cells
19
Q

Descibe the role of hepatocytes in the fasted state

A
  • In the fasted state, the liver synthesis glucose via glycogenolysis (from glycogen) and gluconeogenesis (from amino acids)
  • This INCREASES glucose levels in the cell
  • This creates a gradient favouring the movement of glucose movement out of the cells into the blood
20
Q

Additional actions of insulin (LATER)

A

LATER

21
Q

Insulin has a half life of __ minutes and is principally broken down in the ______ and _______

A
  • 5 minutes
  • Liver and Kidneys
22
Q

Insulin protease (LATER)

A

LATER

23
Q

Why effect does increased glucagon have on insulin?

A
  • Stimulates insulin release
  • Glucagon causes the synthesis of glucose via gluconeogenesis in the liver
  • This glucose is released into the blood
  • So blood glucose then rises
  • And insulin does its thing to decrease blood glucose
24
Q

State the stimuli which increase insulin release

A
  • Increased blood glucose
  • Increased amino acids in the plasma
  • Glucagon
  • Other (incretin) hormones controlling GI secretion and motility e.g gastrin, secretin, CCK
  • Vagal nerve activity
25
Q

State the stimuli which inhibit insulin release

A
  • Low blood glucose
  • Somatostatin (GHIH = growth hormone inhibiting hormone)
  • Sympathetic α2 effects
  • Stress e.g hypoxia