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Sem 4, case 6 (diabetes) > glucose and insulin physiology (mini learning) > Flashcards

glucose and insulin physiology (mini learning) Flashcards

1
Q

What do all tissue use glucose as ?

A

Their primary source of energy

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2
Q

What is different about the interaction between the CNS and glucose ?

A

CNS cannot substitute glucose, so delivery is therefore critical

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3
Q

How is glucose stored ?

A

as glycogen

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4
Q

Where is glycogen stored, primarily ?

A
  • the liver
  • muscle
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5
Q

What is considered the normal
a) fasting blood-glucose range ?
a) post-prandial blood glucose range ?

A
  • 4-6 mmol/L (fasting)
  • 8 mmol/L (2hrs post eating/post-prandial)
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6
Q

What blood glucose level is considered hyperglycaemia ?

A

>10 mmol/L (sustained)

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7
Q

What blood glucose level is considered hypoglycaemia ?

A

<3 or 4 mmol/L

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8
Q

How much glucose is lost via the kidneys per day ?

A

<0.3 g

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9
Q

What cells secrete insulin?

A

beta cells in islets of langerhans (pancreas)

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10
Q

What action does insulin have on blood glucose levels ?

A

decreases it

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11
Q

Which cells secrete glucagon ?

A

glucagon = alpha cells in islets of langerhans (pancreas)

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12
Q

What effect does glucagon have on blood glucose levels ?

A

glucAgon = ^ increase glucose

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13
Q

What state does insulin rectify
a) hypoglycaemia ?
b) hyperglycaemia ?

A

hyperglycaemia

insulin decreases blood glucose

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14
Q

What state does glucagon rectify
a) hypoglycaemia ?
b) hyperglycaemia ?

A

hypoglycaemia

glucagon increases blood glucose

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15
Q

What stimulates the release of glucagon ?

A

low blood glucose levels

usually the fasting state

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16
Q

What stimulates the release of insulin ?

A

high blood glucose levels

usually the post-prandial state

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17
Q

Which 2 hormones are involved in the endocrine control of glucose homeostasis ?

A
  • insulin
  • glucagon
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18
Q

What are the 3 main insulin sensitive tissues ?

A
  • liver
  • muscle
  • fat (adipocytes)
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19
Q

What are the 3 main glucagon sensitive tissues ?

A
  • liver
  • muscle
  • fat (adipocytes)
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20
Q

What are the 3 main tissues involved in glucose homeostasis ?

A
  • liver
  • muscle
  • fat (adipocytes)
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21
Q

What are levels of
a) insulin
b) glucagon
like in the fasting state ?

A

fasting

insulin = decreased
glucagon = increased

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22
Q

What are levels of
a) insulin
b) glucagon
like in the post-prandial state ?

A

post-prandial

insulin = increased
glucagon = decreased

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23
Q

What is the action of glucagon in the fasting state ?

A
  • released from alpha cells
  • acts on liver to release endogenous glucose

glucose can then travel through blood to act on necessary tissues

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24
Q

What tissue is insulin independent ?

A

the brain

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25
Q

What is the action of insulin in the ‘fed’ state ?

A
  • beta cells release insulin
  • stimulates insulin dependant tissues (muscle and fat) to increase glucose uptake
  • turns off endogenous glucose production in the liver (turns off glycogenolysis)
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26
Q

What else is involved in glucose homeostasis alongside insulin and glucagon ?

A

enteroendocrine cells in small+large intestine

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27
Q

What is the role of enteroendocrine cells in glucose homeostasis ?

A
  • stimulated by glucose/amino acids present in intestines
  • produce hormones (GLP-1)
  • GLP-1 stimulates insulin secretion via beta cells

= reduces blood glucose

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28
Q

What is the main hormone that enteroendocrine cells produce in response to glucose/amino acids in the intestines ?

A

GLP-1

glucagon-like-peptide-1

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29
Q

Where GLP-1 receptors primarily located ?

A

on beta cells in islets of langerhans

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30
Q

What are the 2 main effects that GLP-1 has on the body ?

A
  • increase insulin secretion = decrease blood glucose
  • induce feeling of ‘fullness’ after a meal
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31
Q

What 2 conditions can GLP-1 agonist drugs be used to treat ?

A
  • diabetes (decreasing hyperglycaemia)
  • obesity (inducing a feeling of fullness)
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32
Q

What causes hyperglycaemia?

A
  • impaired insulin secretion
  • impaired insulin action
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33
Q

What often causes impaired insulin secretion ?

A

loss of functioning beta cells

could be due to:
- autoimmune destruction in T1D
- surgery to remove pancreas
- damage to pancreas/pancreatitis
- generic mutations

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34
Q

What often causes impaired insulin action ?

A

reduced insulin sensitivity

occurs in type 2 diabetes

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35
Q

What is the main difference between type 1 and 2 diabetes ?

A

Type 1 = loss of insulin secretion due autoimmune destruction of beta cells

Type 2 = loss of insulin action due to defects in release, sensing and/or signalling

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36
Q

What causes hypoglycaemia ?

A
  • excessive glucose utilisation/loss
  • excessive insulin secretion levels
  • insufficient glucagon secretion levels
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37
Q

What is congenital hyperinsulinism ?

A

babies are born with either
- too many beta cells
- inability to switch off insulin when glucose is low

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38
Q

What are insulinomas ?

A

pancreatic beta cells that turn cancerous and overproduce insulin

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39
Q

What are the most common causes of hypoglycaemia in diabetes ?

A
  • patients overusing insulin
  • unawareness due to frequently low blood sugars causing a sense of de-sensitisation to the symptoms
40
Q

What are the 2 main groups of glucose transport proteins ?

A
  • SGLT
  • GLUT
41
Q

Which class of glucose transporters enable passive transport of glucose ?

A

GLUT transporters

42
Q

Which class of glucose transporters enable Na-coupled transport (co-transport) of glucose ?

A

SGLT transporters

43
Q

How do GLUT transporters work/allow glucose into cells ?

A
  • glucose binds to transporter
  • changes configuration of protein
  • allows glucose to pass through freely
44
Q

How do SGLT transporters work/allow glucose into cells ?

A
  • Na moves through protein down Na conc gradient
  • takes glucose with it into the cell
45
Q

Are SGLT transporters
a) insulin sensitive ?
b) insulin insensitive ?

A

insulin insensitive

46
Q

What does ‘insulin-sensitive transporter’ mean ?

A

the transporter requires presence of insulin in order to transport glucose across membrane

47
Q

What does ‘insulin-insensitive transporter’ mean ?

A

the transporter doesn’t require presence of insulin in order to transport glucose across membrane

48
Q

What are the 2 main SGLT proteins regarding glucose transport ? Where is each primarily found ?

A
  • SGLT1 (intestines)
  • SGLT2 (proximal tubule of kidney)
49
Q

How many molecules of Na and glucose does a SGLT2 transporter carry at once ?

A

SGLT = 1:1 ratio

= 1Na + 1glucose at a time

50
Q

How many molecules of Na and glucose does a SGLT1 transporter carry at once ?

A

SGLT 1 = 2:1 ratio

= 2Na + 1 glucose at a time

51
Q

What is the affinity *(Km) * of SGLT1 for glucose ?

A

SGLT1 Km = 2mM glucose

this means 2mM glucose fully saturates the transporter

52
Q

What is the affinity *(Km) * of SGLT2 for glucose ?

A

SGLT2 Km = 5mM glucose

this means 5mM glucose fully saturates the transporter

53
Q

Which type of diabetes are SGLT2 inhibitors approved as a treatment for ?

A

Type 2

54
Q

How do SGLT2 inhibitors help treat diabetes ?

A

prevent reabsorption of glucose within the kidneys, so it’s excreted from the body

55
Q

How many transporters are there in the GLUT family ?

A

13

56
Q

Which 3 GLUT transporters have the most major functional role in glucose homeostasis ?

A
  • GLUT1
  • GLUT2
  • GLUT4
57
Q

Which of the 3 major GLUT transporters are insulin-insensitive ?

A

GLUT1+2

58
Q

Which GLUT transporter is mainly found in the brain ?

A

GLUT1

59
Q

Where is the GLUT2 transporter mainly found ?

A
  • kidney
  • liver
  • pancreas
60
Q

Which GLUT transporter is involved in stimulating insulin secretion in the islets of langerhans ?

A

GLUT2

61
Q

Which is the main GLUT transporters is insulin-sensitive ?

A

GLUT4

62
Q

Where is GLUT4 transporter found ?

A
  • adipose tissues (adipocytes)
  • striated muscle
  • heart
63
Q

What is the affinity of GLUT1 for glucose ?

A

approx. 5mM

= conc of glucose that would fully saturate the transporter

64
Q

What is the affinity of GLUT4 for glucose ?

A

approx. 5mM

= conc of glucose that would fully saturate the transporter

65
Q

What is the affinity of GLUT2 for glucose ?

A

approx. 17mM

= conc of glucose that would fully saturate the transporter

66
Q

Which transport protein is used in the co-transport of glucose on the apical membrane of entericytes in the small intestine ?

A

SGLT1

2Na + glucose into cell

67
Q

Which transport protein is used to transport glucose out via the basolateral membrane of entericytes in the small intestine ?

A

GLUT2

68
Q

Which transport protein is found on erythrocytes (RBCs), allowing glucose to be transported in blood ?

A

GLUT1

69
Q

In a healthy kidney, is most glucose excreted or re-absorbed ?

A

about 99% is re-absorbed

70
Q

Where does the re-absorption of glucose occur in the kidney ?

A

in 2 areas of the proximal convoluted tubule

71
Q

What are the 2 parts of the proximal convoluted tubule involved in glucose re-absorption ?

A
  • early proximal
  • late proximal
72
Q

Which glucose transport protein is found in the early proximal convoluted tubule ?

A

early = SGLT2

73
Q

Which glucose transport protein is found in the late proximal convoluted tubule ?

A

late = SGLT1

74
Q

Which section of the proximal convoluted tubule is responsible for the majority of glucose reabsorption ?

A

> 90% reabsorbed in early tubule

75
Q

What is the mechanism of glucose absorption in the primary convoluted tubule ?

A

same as in ileum = co-transport

  • SGLT1/SGLT2transports Na and glucose into cell
  • GLUT1/GLUT2 transports glucose out into blood
  • Na-K pump maintains conc gradient
76
Q

Why does glucose reabsorption not work well in a person with diabetes ?

A

absorptive capacity of glucose transporters is overwhelmed

77
Q

What does glucose in the urine result in ?

A

an osmotic gradient, pulling large amounts of water into urine

78
Q

How does glucose stimulate insulin release from the beta cells ?

A
  • GLUT1+2 take glucose into beta cells
  • glucose is metabolised, generating ATP
  • ATP closes a K channel in the memebrane
  • depolarises the cell = causes influx of Na and Ca
  • Ca influx results in exocytosis of insulin
79
Q

What are the 6 simplified steps of glucose-stimulated insulin release ?

A
  1. uptake
  2. metabolism
  3. K channel closure (via ATP)
  4. depolarisation
  5. Ca channel open/influx
  6. exocytosis/release of insulin
80
Q

What happens in GLP-1 mediated insulin release from the beta cells ?

A

GLP-1 produced when high blood glucose

  • GLP-1 binds to receptor on membrane
  • increases cAMP levels in cell
  • cAMP activates PKA (protein kinase A)
  • causes exocytosis of insulin
81
Q

Is insulin a growth hormone ?

A

yes

82
Q

What processes is insulin involved in ?

A
  • glucose homeostasis
  • lipid metabolism
  • protein metabolism
  • growth
  • reproduction
  • cognition
83
Q

Which metabolic pathways does insulin stimulate/up-regulate ?

A
  • glycolysis
  • glycogenesis
  • glucose uptake
  • lipogenesis
  • amino acid uptake
  • protein synthesis
  • DNA synthesis
84
Q

Which metabolic pathways does insulin inhibit/down-regulate ?

A
  • gluconeogenesis
  • lipolysis
  • apoptosis
  • autophagy (reusing old cell parts)
85
Q

Where in the cell do most of the effects of insulin take place ?

A

in the cytoplasm

86
Q

Can insulin impact gene expression ?

A

Yes

87
Q

Which glucose transporter does insulin have an up-regulatory effect on the production of within cells ?

A

GLUT4

88
Q

Is GLUT4 insulin sensitive or insensitive in the transport of glucose ?

A

insulin sensitive

89
Q

How does insulin interact with GLUT4 to stimulate glucose transport into cells ?

A
  • insulin binds to receptor on cell membrane
  • **activates tyrosine kinase ** component of the receptor
  • tyrosine kinase triggers signalling cascade
  • results in translocation of GLUT4 from vesicles inside cell into membrane
  • GLUT4 efficiency is therefore increased
90
Q

How does metformin increase sensitivity of the body to insulin ?

A

acts on the insulin-GLUT4 pathway to increase expression of GLUT4 in membrane

stimulates signalling cascade that results in translocation of GLUT4 into membrane

91
Q

What happens to blood glucose levels when there is an insulin-sensing defect ? why?

A

blood glucose levels rise = hyperglycaemia

because…
- pathways stimulated by insulin are not responding (e.g glycogenesis) so glucose isn’t being removed
- pathways inhibited by insulin aren’t responding (e.g gluconeogenesis) so more glucose is being created and released

92
Q

What are the short-term complications of hyperglycaemia ?

A
  • glucosuria (glucose in urine)
  • polyuria (more urine production)
  • dehydration
  • ketoacidosis
93
Q

What are the long-term complications of hyperglycaemia ?

A

glucotoxicity in neural cells/capillary endothelial cells manifesting as…
- peripheral vascular disease
- peripheral neuropathy
- kidney disease

94
Q

What does the body do to compensate for insulin insensitivity in type 2 pre-diabetes ?

A

produces more insulin to counteract the resistance of the insulin sensitive organs

95
Q

What is the pathophysiology of type 2 diabetes ?

A
  • genetic defects causing minor insulin resistance paired with a bad lifestyle
  • leads to raised insulin resistance
  • pancreas secretes more insulin to counteract this, but this cannot be maintained forever without intervention
  • leads to hyperglycaemia = diabetes
96
Q

Which glucose transporter is involved in insulin-mediated glucose uptake ?

A

GLUT4

97
Q

True or false, GLP1R agonists are used as a treatment for diabetes ?

A

true

Sem 4, case 6 (diabetes) (4 decks)

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