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PATH30003- Frontiers in Human Disease > Lecture 12- Type 2 diabetes > Flashcards

Lecture 12- Type 2 diabetes Flashcards

1
Q

type 2 diabetes definition

A
  • metabolic disorder characterised by chronic hyperglycemia
  • relative lack of insulin action/response (insulin resistance), insulin production or both
  • leads to impaired glucose metabolism
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2
Q

3 ways to diagnose diabetes

A
  1. glycated haemoglobin test (HbA1c test)
  2. oral glucose tolerance test (oral GTT)
  3. impaired fasting blood glucose levels
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3
Q

HbA1c test

A

glycated haemoglobin test

  • measures how much glucose is bound to Hb in RBCs
  • diabetes >6.5%
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4
Q

oral glucose tolerance test (oral GTT)

A

consumption of 75g of anhydrous glucose, test plasma glucose 2 hrs later
-11.1mmol/L- diabetes

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5
Q

impaired fasting blood glucose levels

A

plasma glucose>7.0mmol/L following 8 hr fast

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6
Q

type 1 diabetes

A

autoimmune disease, immune mediated Beta cell destruction

- insulin deficiency, 5-10%

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7
Q

type 2 diabetes

A

insulin resistance and insulin deficiency, 90-95%

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8
Q

gestational diabetes

A

insulin resistance and relative insulin deficiency in pregnancy
- 3-5% of all pregnancies

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9
Q

genetic defects affecting Beta cell function

A

1-2% of cases

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10
Q

glucose homeostasis

A

balance of glucose intake/production and uptake/storage/usage

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11
Q

when high blood glucose

A

gets stored in liver and muscle (as glycogen) and fat/WAT

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12
Q

when low blood glucose

A

glucose released from stores- liver, muscle, WAT

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13
Q

where is insulin produced?

A

produced and secreted by Beta cells of pancreatic islets

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14
Q

beta cells of pancreatic islets

A

75-80% of the islet cells

produce and secrete insulin

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15
Q

glucagon

A

alpha cells in pancreatic islets

- raises blood glucose level (acts opposite to insulin)

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16
Q

somatostatin

A

gamma cells

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17
Q

insulin synthesis pathway

A
  1. genes encoding for insulin transcribed to mRNA in nucleus
  2. Pre-proinsulin synthesised (in beta cell), excision of signal peptide, formation of disulphide bonds in ER (b/w A and B chain)
  3. Transport of proinsulin to Golgi apparatus, cleaved by pro-hormone convertase
  4. Formation of separate C-peptide and mature biologically active insulin (A and B chain)
  5. Insulin stored in storage granules , secretion of insulin granules by exocytosis when calcium influx
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18
Q

Insulin secretion pathway

A
  1. glucose enters beta cells (via GLUT2 transporter)
  2. glycolysis (breakdown of glucose) increases ATP:ADP ratio, increase energy supply to beta cells
  3. Closes ATP-sensitive K channels (K cant go outside of beta cell now)
  4. increase K in cells, makes cell more positively charged, depolarisation of cells
  5. Opens voltage dependent Ca channels, influx of calcium, promotes exocytosis of insulin granules form storage granules
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19
Q

glycogen synthesis

A

convert glucose into glycogen

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20
Q

glycogenolysis

A

break down of glycogen

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21
Q

gluconeogenesis

A

production of glucose from fat

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22
Q

lipogenesis

A

convert/synthesise glucose into fat

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23
Q

Normal glucose levels- liver

A
  • increased glycogen synthesis
  • decreased glycogenolysis
  • decreased gluconeogenesis
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24
Q

normal glucose levels- muscle

A
  • increased glucose uptake

- increased glycogen synthesis

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25
normal glucose levels- WAT/fat
- increased glucose uptake | - increased lipogenesis
26
vagus nerve
parasympathetic control of digestive tract e.g. liver
27
high glucose levels- pancreas
decrease beta cell function
28
normal glucose levels- brain
decrease appetite
29
high glucose levels- liver
- decreased glycogen synthesis | - increased gluconeogenesis
30
high glucose levels- muscle
- decreased glucose uptake | - decrease glycogen storage
31
high glucose levels- WAT/fat
- decrease fat/TG storage - increased lipolysis - increase FFA in blood
32
lipolysis
breakdown of fats and other lipids by hydrolysis to release FAs
33
high glucose levels- insulin
- lots produced but not used by liver, muscle, WAT or brain
34
high glucose levels- brain
increased appetite
35
GLUT4 vesicle
used in glucose uptake by fat, muscle
36
Akt
responsible for increasing glycogen synthesis | - Akt activates FOXO and GLUT4 vesicle
37
FOXO
decreases gluconeogenesis in liver
38
PI3K
activates Akt-->FOXO and GLUT4 vesicle
39
how does insulin lead to changes in glucose production in organs and tissues?
insulin receptor (IR) binds to IRS (insulin receptor substrate)-->PI3K-->Akt--> 1. GLUT4 vesicle- increase glucose uptake 2. increased glycogen synthesis 3. FOXO- decrease gluconeogenesis
40
chronic inflammation
triggers recruitment of immune cells-->increase pro inflammatory cytokine levels (IL-1, IL-18, TNF) in affected tissues (muscle, liver, islets, adipose tissue) - islets (resident macrophages become activated, increased immune T and B cells)
41
anti- inflammatory drugs
TNF, IL-1 blockers- beneficial for T2D- clinical trial
42
ER stress
chronic overnutrition and increased FA (due to adiposity)-->accumulation of unfolded/misfolded proteins in ER lumen -->ER stress
43
ER
central organelle in which trans-membrane and secretory proteins are synthesised and folded
44
unfolded protein response- UPR
mitigate ER stress - reduces protein synthesis through (PERK/ATF4) - increase ER molecular chaperones through (ATF6) - Activation of ER-associated degradation proteins through (IRE1/XBP1) - CHOP- apoptosis
45
PERK/ATF4
reduces translation, protein synthesis to reduce ER stress
46
ATF6
increases ER molecular chaperones
47
IRE1/XBP1
activates ER-associated degradation proteins (ERAD)
48
CHOP
apoptosis of unfolded/misfolded proteins in ER
49
BiP/GRP78
ER chaperones
50
therapeutic potential for ER stress
chemical chaperones to reduce ER stress- clinical trial
51
risk factors for T2D
lifestyle, age, genetics, history of gestational diabetes
52
hallmarks of T2D
insulin resistance hyperinsulinemia hyperglycemia
53
acute complications of T2D
hyperglycemic hyperosomlar state (HHS) | - high blood glucose levels-->high osmolarity-->extreme dehydration (dry skin, drowsy)
54
chronic complications of T2D
micro- diabetic retinopathy/nephropathy/neuropathy macro- stroke, heart disase, peripheral vascular disease
55
key principle in treatment of T2D
control blood glucose levels
56
3 key components of T2D treatment
1. lifestyle modification 2. oral glucose-lowering therapy 3. insulin therapy
57
lifestyle modification
diet- healthy eating | exercise- reduce weight to improve insulin sensitivity and glucose uptake
58
oral glucose lowering therapy
metformin - safe, cheap, first line oral treatment (mono/combo therapy) - activates AMP-activated kinase (AMPK)
59
metformin
activates AMP-activated kinase (AMPK) - liver- suppresses gluconeogenesis and lipogenesis - skeletal muscle- increases insulin sensitivity and glucose uptake - side effects- liver disease and GIT issues (diarrhoea)
60
lipogenesis
formation of fat
61
metformin- liver
suppresses gluconeogensis and lipogenesis
62
metformin- skeletal muscle
increases insulin sensitivity and glucose uptake
63
metformin side effects
liver disease and GIT issues
64
incretin hormones
stimulate insulin production and trigger insulin release in response to meals
65
GLP-1
gut derived glucagon peptide 1 | - rapidly degraded by DPP-4
66
function of GLP-1
activates GLP-1R-->decrease blood glucose levels and improve glycemic control
67
DPP-4
degrades GLP-1 within minutes
68
GLP-1R action on brain
decrease appetite
69
GLP-1R action on stomach
decrease gastric emptying
70
GLP-1R action on pancreas
- increase insulin secretion/synthesis - decrease glucagon secretion - increase beta cell proliferation - decrease beta cell apoptosis
71
GLP-1R agonists/ DPP-4 inhibitors
act on GLP-1R and DPP
72
GLP-1R agonist
Exenatide - inject subcutaneously - side effects- hypoglycemia (act directly on beta cells)
73
DPP-4 inhibitor
Gliptin - Tablets, reduce GLP-1 degradation - side effects- sinusitis, nausea, allergic issues
74
sulfonylureas
safe, cheap, second generation | e.g. glimepiride, glipizide, glyburide
75
function of sulfonylureas
- inhibit opening of ATP-sensitive K channels (no K goes out) - increase Ca influx-->depolarisation - increase insulin release from beta cells in pancreas side effects-- hypoglycemia, weight gain
76
acarbose
alpha glucosidase inhibitor | - cheap, effective
77
function of acarbose
lowers blood glucose, prevent T2D - reduces rate of digestion of carbs in intestine-->less glucose is absorbed - side effects- flatulence, diarrhoea
78
alpha glucosidase
intestinal enzyme that breaks down carbs into glucose
79
future therapies
prevention- public health policies, lifestyle modification basic science- further understanding for causes of diabetes

PATH30003- Frontiers in Human Disease (20 decks)

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