3.6.4.2 Control of blood glucose concentration Flashcards

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1
Q

Glycogenesis

A

Formation of glycogen from glucose

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2
Q

Glycogenolysis

A

breakdown of glycogen to glucose

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3
Q

Gluconeogenesis

A

formation of NEW glucose from non carbohydrates

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4
Q

Response when blood glucose is too high

A
  • Insulin releases by beta cells in the Islets of Langerhans in the pancreas into the blood
  • Insulin travels to effectors liver and muscle cells and bind to receptors on cell surface membrane
  • It increases the permeability of target cells to glucose by increasing the number of channel proteins to increase rate of facilitated diffusion of glucose into target cells down concentration gradient
  • Insulin also activates enzymes that catalyse glycogenesis
  • stimulates lipid formation from glucose
  • Insulin increases rate of respiration in muscle cells so more glucose is used - less glucose in cell, increases gradient, increases rate of F.D.
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5
Q

Response when blood glucose is too low

A
  • Glucagon secreted by alpha cells in Islets of Langerhans into the blood, where it travels to liver effector cells and binds to receptors
  • This activates enzymes in the liver to catalyse glycogenolysis and gluconeogenesis
  • Glucagon reduces the rate of respiration in liver cells
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6
Q

Effect of adrenaline

A
  • released from adrenal glands during stress or exercise
  • increases glucose
  • binds to receptors on liver cells
  • activates glycogenolysis (glucagon secretion)
  • inhibits glycogenesis (inhibits insulin secretion and ability to bind to receptors)
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7
Q

What does a second messenger do?

A

Amplifies the signal (internal signal)

Activates enzymes for glycogenolysis

  • Adrenaline and glucagon act via a second messenger cAMP
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8
Q

Stages of second messenger model

A
  1. Adrenaline binds to complementary receptors on cell membrane
  2. This activates adenylate cyclase
  3. Adenylate cyclase converts ATP into cAMP
  4. cAMP activates protein kinase A
  5. Protein kinase A activates a chain of reactions - glycogenolysis

no cAMP - no glycogenolysis nor gluconeogenesis

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9
Q

Type 1 diabetes

A
  • Insulin not produced
  • Genetic - gene must be triggered
  • Autoimmune - antibodies produced by plasma cells destroy insulin producing beta cells
  • Treated with insulin therapy
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10
Q

Type 2 diabetes

A
  • may produce less insulin but most display lower sensitivity of target receptors to insulin
  • Can be reversed
  • Insulin injections usually ineffective as this won’t alter receptors
  • Treated with diet and exercise
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11
Q

How is glucose reabsorbed?

A
  1. Sodium pumped out of the proximal convoluted tubule cell using the Na+/K+ pump
  2. This reduces the [Na+] in the cell, creating a Na+ concentration gradient
  3. Na+ is drawn into the cell by the PCT down its concentration gradient, it moves through a co-transport protein with glucose
  4. Glucose moves out of the cell by facilitated diffusion into the capillaries
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12
Q

What affects the rate of glucose absorption?

A
  • required transport proteins
  • the number of transport proteins is a limiting factor
  • if there is a higher than normal glucose concentration in the filtrate it cannot all be absorbed and is lost in the urine
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13
Q

How does urea change?

A
  • concentration of urea increases due to loss of water from filtrate
  • but the amount (mol) of urea doesn’t change as it isn’t reabsorbed
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14
Q

How do concentrations of glucose, urea and salt ions change as distance increases across PCT?

A
  • Glucose - ALL of the glucose leaves the glomerular filtrate by co transport
  • Salt - most of the salts leave the filtrate by active transport and facilitated diffusion
  • Urea - concentration increases due to the loss of water from the filtrate into the blood, but the amount of urea doesn’t change as it is not reabsorbed
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