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Endocrinology > Biochemistry of Insulin > Flashcards

Biochemistry of Insulin Flashcards

(61 cards)

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1
Q

how you insulin kill you

A

go into hypoglycemic coma

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2
Q

what makes insulin

A

beta cells in the pancreas, islets of langerhans

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3
Q

what do alpha cells make

A

glucagon

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4
Q

what do gamma cells make

A

somatostatin

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5
Q

what do PP cells in the pancreatic islets make

A

pancreatic polypeptide

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6
Q

what is the counter hormone (starvation hormone) to insulin

A

glucagon

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7
Q

where in beta cells is insulin synthesised

A

rough endoplasmic reticulum

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8
Q

describe the process of insulin synthesis

A

starts as larger single chain preprophormone (preproinsulin)
cleaved to form insulin

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9
Q

what is the structure of insulin

A

two polypeptide chains linked by disulfide bonds

connecting C peptide (a byproduct of cleavage)

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10
Q

what preparation of insulin is ultrafast/ultra short acting

A

insulin lispro

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11
Q

what affected how long insulin lasts

A

position of amino acids- affects how stable it is

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12
Q

what is the most rapidly acting insulin

A

insulin lispro

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13
Q

how is insulin lispro used clinically

A

Injected within 15 minutes of beginning a meal

short duration of action- must be used in combination with longer-acting preparation for Type 1 diabetes unless used for continuous infusion

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14
Q

describe the structure of insulin lispro

A

monomeric, not antigenic

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15
Q

what prep of insulin is ultra long lasting

A

glargine

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16
Q

when is glargine administered

A

single bedtime dose

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17
Q

describe the action of glargine

A

Recombinant insulin analog that precipitates in the neutral environment of subcutaneous tissue

Peakless- prolonged action

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18
Q

how does glucose enter beta cells

A

GLUT2 glucose transporter (goes down concentration gradient)

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19
Q

what happens to glucose once it enters beta cells

A

phosphorylated by glucokinase

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20
Q

what senses the amount of glucose that enters a beta cell

A

glucokinase

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21
Q

what does increased metabolism of glucose lead to

A

an increase in intracellular ATP concentration

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22
Q

lists the steps of carb metabolism

A

glucose-6-P

glycolysis (also makes e- and CO2)

acetyl- CoA

TCA cycle

(e- go to oxidative phosphorylation)

=
36 ATP per glucose

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23
Q

what does ATP do in beta cells

A

inhibits the ATP sensitive K+ channel KATP- causes depolarisation of the cell membrane

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24
Q

what happens when the cell membrane of beta cells depolarises

A

voltage gates Ca2+ channels open - increase in Ca2+ conc leads to fusion of secretory vesicles within the cell membrane that release insulin

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25
what blood glucose level should cause insulin to be released
>5 mM
26
how does the secretion of insulin related to the tyeps of diabetes
type 1 loss of beta cells other types beta cells lose the ability to sense changes in glucose (due to hyperglycaemia takin glucose conc outwith the Km of glucokinase)
27
describe the flow of the release of insulin
is biphasic- as only 5% ready for immediate release (first phase) reserve pool must become mobilised to be released in the second phase
28
what happens to the biphasic release of insulin in poorly controlled T2DM- why
becomes flattened | - down regulation of the sensing process
29
what drug can mimic the action of ATP to depolarise beta cells (and cause release of insulin) by inhibiting KATP
sulphonylurea (SURs)
30
what two proteins make up the KATP channels
Kir6- inward rectifier subunit (pore) SUR1- sulphonylurea receptor (regulatory subunit)
31
what stimulates KATP (inhibits the secretion of insulin)
diazoxide
32
when are SURs used
for patients who cant inject insulin (second line therapy as makes beta cells work very hard) or patients who have improved their glucose control
33
what can mutations in Kir6.2 and SUR1 cause
Kir6.2- neonatal diabetes (constantly active KATP channels) Kir6.2 or SUR1 mutations- congenital hyperinsulinism
34
what is MODY
maturity onset diabetes of the young (familial form of type 2 diabetes) monogenic diabetes with genetic defect in beta cell function
35
what happens to glucokinase in MODY2
glucokinase activity impaired | glucose sensing defect- threshold for insulin release increased
36
what are the roles of HNF transcription factors
play key roles in pancreas foetal development and neogenesis regulate beta cell differentiation and function
37
what is the important of genetic screening to differentiate MODY from type 1 diabetes
allows treatment of MODY with sulphonylurea rather than insulin as MODY patients have some beta function available
38
name the diabetes: | loss of insulin secreting beta cells
type 1
39
name the diabetes: | defective glucose sensing in the pancreas and/ or loss of insulin secretion
MODY
40
name the diabetes: | intially hyperglycemia with hyperinsulinemia so primary problem is reduced insulin sensitivity in tissues
type 2 diabetes
41
what does insulin 'turn on'
``` amino acid uptake in muscle DNA synthesis protein synthesis growth responses glucose uptake in muscle and adipose tissue lipogenesis in adipose and liver cells glycogen synthesis in liver and muscle ```
42
what does insulin 'turn off'
lipolysis | gluconeogenesis in liver
43
what receptor does insulin bind to
receptor tyrosine kinases
44
what happens when insulin binds to the alpha subunits of tyrosine kinases
beta subunits dimerise and phosphorylate themselves (autophosphorylation) e.g. activate the catalytic activity of the receptor
45
what does insulin prevent
hyperglycemia
46
what causes insulin resistance
reduced insulin sensing and/ or signalling associated with obesity and complete lack of adipose tissue can occure in monogenic diabetes due to mutation
47
why is type 2 diabetes polygenic
as has input from environmental causes
48
what is leprechaunism - donohue syndrome
autosomal recessive mutation in the gene for the insulin receptor - severe insulin resistance - developmental abnormalities (elfin facial appearance, short stature, absence of fat and muscle mass)
49
what causes leprechaunism
defects in insulin binding or insulin receptor signalling
50
what rabson mendenhall syndrome
autosomal recessive trait severe insulin resistance, hyperglycemia and compensatory hyperinsulinemia -developmental abnormalities -acanthosis nigricans (hyperpigmentation) -fasting hypoglycaemia -diabetic ketoacidosis
51
what are the symptoms of diabetic ketoacidosis
vomiting, dehydration, increased heart rate, acetone smell on breath
52
where and how are ketone bodies formed
in liver mitochondrian derived from acetyl-CoA beta oxidation of fatty acids yields acetyl-CoA which enters TCA cycle (when fat and carb degeneration balanced) if no oxaloacetate (e.g. due to no glycolysis) then acetyl CoA diverted to ketones
53
what is the role of ketone bodies
diffuse into the blood stream and to peripheral tissues important molecule of energy metabolism for heart muscle and renal cortex emergency energy supply for brain during fasting
54
what prevents ketone body overload
low levels of insulin inhibit lipolysis
55
when is DKA at risk in T1DM
if insulin supplementation is missed
56
when is DKA at risk in T2DM
rarer- can happen as insulin resistance and deficiency increases- alongside increase in glucagon
57
how does DKA happen
Oxaloacetate is consumed for gluconeogenesis When glucose is not available-fatty acids are oxidised to provide energy Excess acetyl-CoA is converted to ketone bodies Accumulation of ketone bodies can lead to acidosis High glucose excretion causes dehydration, exacerbates acidosis Coma, death
58
what do ketone bodies do to the pH of the blood
decrease it
59
when is ketosis seen
in glucose limiting conditions
60
how do you treat DKA
insulin and rehydration
61
what is the only hormone that can maintain euglycema following food ingestion
insulin

Endocrinology (46 decks)

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