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Yr 2 - GI & Metabolism > Acute Regulation of Glucose > Flashcards

Acute Regulation of Glucose Flashcards

1
Q

What does plasma glucose conc need to stay between?

A

3 and 10 mM

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2
Q

After a meal, what can portal vein glucose reach?

A

20mM (between meals it can decline to almost 0)

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3
Q

What can the liver make ketone bodies from?

A

Lipid

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4
Q

How can the liver make glucose?

A
  • From glycogen (glycogenolysis)

- From amino acids (gluconeogenesis)

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5
Q

What is glycogenolysis?

A

Breakdown of glycogen into glucose

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6
Q

What is gluconeogenesis?

A

Forming glucose from non-carbohydrate molecules (e.g. amino acids)

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7
Q

What is glycogenesis?

A

Forming glycogen from glucose

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8
Q

What are the sodium/glucose co-transporters?

A

SGLT1 and SGLT2 (active carrier transport)

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9
Q

What do SGLT1 and SGLT2 take up?

A

Glucose at the apical brush border

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10
Q

Where does SGLT1 work?

A

Small intestine, kidney tubules

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11
Q

Where does SGLT2 work?

A

Kidney proximal tubule

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12
Q

What do SGLT1 and SGLT2 transport along with glucose?

A

Sodium

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13
Q

What is an enterocyte?

A

A cell of the intestinal lining

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14
Q

What does SGLT1 pick up at the brush border?

A

Glucose or galactose

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15
Q

What picks up fructose at the brush border?

A

GLUT5

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16
Q

What then transports glucose/galactose/fructose from inside the enterocyte (or other tissues) into the capillary?

A

GLUT2

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17
Q

What are the glucose transporters?

A

GLUT1-12 (all use facilitated diffusion to transport monosaccharides)

Allow glucose across membranes

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18
Q

Where does GLUT2 work?

A

Kidney, ileum, liver, pancreatic beta cells

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19
Q

Does GLUT2 have a low or high affinity?

A

Low (as glucose levels rise, it will very effectively transport more glucose)

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20
Q

Where is GLUT4 found?

A

Skeletal muscle, heart, adipocytes

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21
Q

What is job of GLUT2?

A

Takes sugar that has been taken up by gut and transports it out of cells and into circulation

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22
Q

Where does GLUT1 work?

A

Brain, red cells, endothelium, beta cells (a transporter we use where we always need some uptake of glucose)

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23
Q

What is GLUT4 induced by?

A

Insulin (when insulin levels are high, cells put this transporter into the membrane so they can take up glucose)

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24
Q

Where does GLUT3 work?

A

Neurones, placenta

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25
Q

Where does GLUT5 work?

A

Widely distributed (picks up fructose)

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26
Q

Are the Islets of Langerhans exocrine or endocrine glands? Why?

A

Endocrine as secreting directly into bloodstream

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27
Q

Describe the blood supply to the Islets of Langerhans?

A

Arterioles run into the centre of these Islets and then the blood passes through capillaries into the periphery (middle to outside)

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28
Q

What do the beta cells of the pancreas produce?

A

Insulin

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29
Q

What do the alpha cells of the pancreas produce?

A

Glucagon

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30
Q

What do the delta cells of the pancreas produce?

A

Somatostatin

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31
Q

Where are beta cells of the pancreas found?

A

Mainly central, most abundant

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32
Q

Where are alpha cells of the pancreas found?

A

At the periphery (i.e. blood picks up insulin at centre then glucagon)

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33
Q

What is a key element of the beta cells of the pancreas regarding insulin secretion?

A

Have an ATP gated K+ channel in the cell membrane

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34
Q

What happens when lots of ATP is around the beta cells of the pancreas?

A

K+ channel is not open –> cell depolarises (K+ does not flow out) –> secretes insulin

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35
Q

How does glucose enter the beta cells of the pancreas?

A

GLUT2 transporter (mediates facilitated diffusion of glucose into cell)

As glucose levels rise, they will transport more glucose in

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36
Q

As glucose is transported into the beta cells of the pancreas, what happen?

A

Glucose –> ATP (and NADH) (glycolysis and TCA)

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37
Q

What does this increase in ATP (and NADH) inhibit in the beta cells of the pancreas?

A

Inhibits the K+ channel which causes Vm (membrane potential) to become more positive –> depolarisation

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38
Q

What does the depolarisation (beta cells of the pancreas) activate?

A

A voltage gated Ca2+ channel in the plasma membrane –> Ca2+ influx

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39
Q

What does Ca2+ influx cause (beta cells of the pancreas)?

A

Secretion of insulin (by exocytosis)

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40
Q

How do insulin levels differ between oral glucose and injection of glucose?

A

Much higher spike in insulin if oral, despite lower plasma [glucose]

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41
Q

How do other modulators of secretion of glucose (in beta cells of pancreas) act?

A

Act via the adenylyl cyclase-cAMP-protein kinase A pathway and phospholipase C-phosphoinositide (PLC) pathway

These increase exocytosis of insulin

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42
Q

How does the parasympathetic NS affect insulin secretion?

A

Increases

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43
Q

How does the sympathetic NS affect insulin secretion?

A

Inhibits

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44
Q

What are incretins?

A

Gut hormones that stimulate insulin secretion (along with high glucose)

45
Q

What is insulin produced as?

A

A preprohormone which is quickly cleaved to the prohormone

Internal disulphide bonds fold it up (due to cysteine)

46
Q

During processing in the Golgi, what is insulin cleaved to give?

A

A and B chains, which are linked, and a free C peptide

47
Q

What is the free C peptide a marker of?

A

Inactive peptide but is a useful marker of endogenous insulin production

48
Q

What is the insulin receptor?

A

Tyrosine kinase receptor (enzyme linked)

  1. Insulin binds to receptor
  2. Turns on tyrosine kinase
  3. These start to phosphorylate lots of things
49
Q

What are the 2 main pathways for insulin signalling?

A
  1. Fast pathway –> PI3K and PKB phosphorylate proteins, altering activity (and inserting GLUT4)
  2. Slow pathway –> MAPK pathway alters gene expression
50
Q

What are both insulin signalling pathways mediated by?

A

Insulin Receptor Substrates (IRS)

51
Q

What does the fast insulin pathway control?

A

Controls metabolism

52
Q

What does the slow insulin pathway control?

A

Longer term growth type changes

53
Q

Does the liver have insulin receptor?

A

Yes

54
Q

Why is the liver always permeable to glucose?

A

Due to GLUT2

55
Q

Is there GLUT4 in the liver?

A

No

56
Q

What is effect of insulin on the liver?

A

Increased uptake of glucose:

  • Movement of glucose down glycolysis pathway and then into mitochondria favoured
  • Glycogen storage increased
  • VLDL production increased
  • Gluconeogenesis inhibited
  • Ketone body production inhibited
57
Q

What happens when glucose is moved down glycolysis pathway and then into mitochondria in the liver? What then happens?

A

Acetyl CoA is made –> make it into fatty acids and triglycerides

Liver then packages those as VLDL (storing energy in form of fat)

58
Q

Is GLUT4 present in muscle?

A

Yes –> insulin receptors trigger insertion of GLUT4 into membrane and favours use of glucose

59
Q

Are insulin receptors present in muscle?

A

Yes

60
Q

What is effect of insulin on muscle?

A

Favours glucose over using fatty acids as foodstuff

  • Used in TCA to make lots of ATP
  • Glycogen, triglyceride, protein synthesis increase
61
Q

What is effect of exercise on GLUT4?

A

Via adrenaline, induces GLUT4 and synergises with insulin

62
Q

Is GLUT4 present in fat?

A

Yes - insulin receptors trigger insertion of GLUT4 into membrane and favours glucose uptake

63
Q

What is effect of insulin on fat?

A
  • Triglyceride storage increased (glucose –> fat by stealing Acetyl CoA)
  • Export of FFA and glycerol reduced
  • Increased expression of LPL which extracts FFA from VLDL
64
Q

Do type 2 diabetics produce C peptides?

A

Yes –> still produce insulin but just faulty receptors

65
Q

Does injected insulin (for type 1 diabetics) contain C peptides?

A

No

66
Q

How does insulin affect potassium?

A

Insulin also increases the permeability of many cells to potassium. Insulin activates sodium-potassium ATPases in many cells, causing a flux of potassium into cells.

67
Q

What is hyperkalaemia?

A

High levels of potassium

68
Q

What are the ranges of normal potassium?

A

3.5-5.0 mmol/L

69
Q

What can hyperkalaemia cause?

A

Slow heartbeat and weak pulse, may result in heart stopping

70
Q

How can hyperkalaemia be treated?

A

Give them glucose and insulin –> will load potassium into cells (decreasing plasma [K])

71
Q

What can hypokalaemia cause?

A

Cardiac arrhythmias, cardiac arrest

72
Q

What must you be careful of when seeing a hypoglycaemic patient?

A

First thought is to load with glucose (especially if they have lots of insulin)

BUT be careful of [K+] levels as glucose will further decrease [K+] levels –> will have to give them K as well if K+ levels are already low

73
Q

What is glucagon release antagonised by?

A

Glucose

74
Q

What is glucagon release driven by?

A

Amino acids

75
Q

What is the glucagon receptor in the liver? What does this receptor active?

A

GPCR, linked to Gs

Activates adenyl cyclase and activates protein kinase A

PKA then phosphorylates enzymes involved in glycolysis and gluconeogenesis

76
Q

What is effect of glucagon in the liver?

A

Glycogen breakdown and increases gluconeogenesis (opposite of insulin)

Liver also breaks down some glucagon

77
Q

How is glucose exported from the liver?

A

G6Pase

78
Q

What are fatty acids used by the liver for?

A

Energy source and ketone body production

79
Q

What is effect of high levels of glucagon on adipocytes?

A

Lipolysis

80
Q

What is effect of high levels of glucagon in muscle?

A

Proteolysis (releasing AA for gluconeogenesis)

81
Q

How is most glucagon largely cleared?

A

By liver (1st pass metabolism)

82
Q

Where are very high levels of glucagon normally seen?

A

Pathologically –> ketoacidosis, sepsis etc

83
Q

What is the shift in metabolism in fat and muscle largely due to?

A

Decrease in insulin as glucose levels fall

84
Q

What is somatostatin?

A

Peptide hormone

85
Q

Where is somatostatin released from?

A

D cells of stomach, duodenum and pancreas

86
Q

What is somatostatin release stimulated by?

A

Lumenal [H]+

87
Q

What is somatostatin release inhibited by?

A

ACh

88
Q

What are effects of somatostatin?

A
  • Acts on G cells to inhibit gastrin

- Inhibits CCK and secretin (and sometimes insulin and glucagon)

89
Q

During exercise, what is effect of adrenaline on liver?

A

Adrenaline signals via cAMP to enhance:

  • Glucose production in liver from gluconeogenesis
  • Glycogen breakdown
90
Q

What is effect of adrenaline on muscle? Where do waste products go?

A

Glycolysis (to make ATP)

Type 2 muscle –> Pyruvate and lactate go back to liver for gluconeogenesis (Cori cycle)

Type 1 muscle –> uses pyruvate in TCA cycle, takes lactate from type 2 and turns into pyruvate to be used

91
Q

What is effect of adrenaline on adipocytes?

A

Triacylglycerol breakdown (fatty acid release)

92
Q

What are effect of diabetes mellitus?

A
  • Polyuria
  • Polydipsia (excessive thirst due to dehydration)
  • Weight loss (due to peeing out sugar and energy)
  • Blurred vision
  • Ketoacidosis (type 1) (due to lack of insulin so livers are fooled into starvation so lots of production of ketone bodies)
93
Q

What is ketoacidosis?

A

Ketoacidosis is a metabolic state caused by uncontrolled production of ketone bodies that cause a metabolic acidosis. While ketosis refers to any elevation of blood ketones, ketoacidosis is a specific pathologic condition that results in changes in blood pH and requires medical attention.

94
Q

What is the primary defect in type 1 diabetes?

A

Inability to produce enough insulin –> autoimmune disease in which beta cells of pancreas are destroyed

Lots of food around but cells can’t use it

95
Q

In type 1 diabetes, what can excess glucagon or insulin:glucagon imbalance lead to?

A
  • Lipolysis
  • Proteolysis
  • Gluconeogenesis and ketogenesis in liver
96
Q

What is the primary defect in type 2 diabetes?

A

Can make insulin but impaired cellular response to insulin

  • Receptor downregulation
  • Reduced signalling
97
Q

What is type 2 diabetes strongly associated with?

A

Obesity

98
Q

Difference in type 1 and 2 diabetes onset time?

A

1 –> Early onset (10-14 years)

2 –> Late onset (40s-60s)

99
Q

Describe weight of typical type 1 and 2 diabetes patients?

A

1 –> Generally lean

2 –> Generally overweight

100
Q

Describe onset of type 1 and 2 diabetes?

A

1 –> Rapid onset (days to weeks)

2 –> Gradual onset (years_

101
Q

Which type of diabetes presents autoantibodies?

A

Type 1

102
Q

Which type of diabetes are HLA markers present?

A

Type 1

103
Q

Describe the insulin conc in type 1 and 2 diabetes?

A

1 –> low plasma insulin conc

2 –> insulin resistance (plasma insulin conc may be low, normal or high)

104
Q

What can trigger type 2 diabetes?

A

Poor diet / lack of exercise

105
Q

Describe incidence of ketoacidosis in type 1 and 2 diabetes?

A

1 –> Ketoacidosis is common

2 –> Ketoacidosis unusual

106
Q

Which type of diabetes requires exogenous insulin?

A

Type 1

107
Q

What drugs are used in type 2 diabetes?

A
  • To enhance insulin secretion
  • To enhance insulin sensitivity
  • To inhibit gluconeogenesis
108
Q

Can diet transform type 2 diabetes?

A

Yes –> healthy eating and exercise

109
Q

What is effect of insulin on lipolysis and proteolysis?

A

Reduces

Yr 2 - GI & Metabolism (51 decks)

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