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Metabolism CC > Insulin > Flashcards

Insulin Flashcards

1
Q

Normal glucose before meals

A

3.5-5.5 mmol/L

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2
Q

Normal glucose 2 hours after meals

A

Less than 8mmol/L

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3
Q

Pancreas in Glucose Homeostasis

A

Regulation of insulin secretion to promote glucose storage after meals
Regulation of glucose output from liver during fasting

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4
Q

Where is insulin synthesised

A

Islets of Langerhans

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5
Q

Endocrine part of pancreas

A

2% of total pancreas mass

1-3 million islets of Langerhans

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6
Q

Pancreas is primarily a

A

Exocrine gland

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7
Q

PP cell

A

Produces pancreatic polypeptide

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8
Q

Acinar cells

A

Exocrine

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9
Q

Alpha cell

A

Glucagon producing

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10
Q

Delta cell

A

Somatostatin producing

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11
Q

Epsilon cells

A

Produce ghrelin

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12
Q

Insulin

A

Two chain linked by 3 disulphide linkings

Monomer is its active form

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13
Q

Insulin conc. increases

A

Monomers tend to form Dimers

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14
Q

Presence of zinc + specific pH

A

Dimers form hexamers (storage form of insulin)

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15
Q

Insulin synthesis step 1

A

Initially synthesised as Preproinsulin in pancreatic Beta cells

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16
Q

Insulin synthesis step 2

A

After 5 mins of assembly in endoplasmic reticulum, preproinsulin –> proinsulin

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17
Q

Insulin synthesis step 3

A

Proinsulin matures into insulin

Through action of cellular endopeptidases within Golgi apparatus

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18
Q

Endopeptidases function

A

Cleave off C peptide from insulin

Break bonds between lysine 64 + arginine 65, and between arginine 31 + 32

19
Q

Mechanism of insulin secretion

A

Glucose enters Beta cell through glucose transporter GLUT1
Initiation of insulin secretion by glucose occurs only when glucose >5mM
Glucose –> G6P –> pyruvate
Pyruvate, through Krebs cycle + ETC, generates ATP
–> ATP:ADP ratio in cell rises
Results in closure of KATP channels + membrane depolarisation
Voltage gated Ca2+ channels open
–> intracellular Ca2+ rises
–> insulin secretion

20
Q

Insulin release first phase

A

Release is rapidly triggered in response to increased blood glucose levels

21
Q

Insulin release second phase

A

Sustained, slow release of newly formed vesicles

22
Q

Amino acids + insulin release

A

Mainly leucine + arginine

Intracellular catabolism of amino acids increases intracellular ATP/ADP ratio

23
Q

Leucine

A

Acts through allosteric activation of glutamate dehydrogenase (GDH)
Can also be transaminated to alpha-ketoisocaproate (KIC) that is converted into acetyl-CoA

24
Q

Arginine

A

Can directly depolarise plasma membrane

25
Q

Other molecules that stimulate insulin release

A 
GLP1
Glucose-dependent insulinotropic peptide (GIP)
FAs
Parasympathetic release of acetylcholine
Cholecystokinin
26
Q

Insulin-responsive cells

A

Express a specific receptor at plasma membrane

27
Q

Insulin receptor

A

Transmembrane receptor
Belongs to large class of TKIs
Activated by insulin, IGF-I, IGF-II

28
Q

Insulin receptor activation

A

Insulin binds to extracellular portion of Alpha subunits

  • -> conformational change
  • -> activates tyrosine kinase domain, residing on intracellular portion of beta subunit
29
Q

Signalling pathway activated by insulin- when NO INSULIN

A

IRS, PI3K and Akt are inactive
Glucose cannot enter cell
Glucose cannot be converted into glycogen

30
Q

Signalling pathway activated by insulin- when INSULIN PRESENT

A

IRS, PI3K and Akt are active
(phosphorylated)
Glucose can enter cell
Glucose can be converted into glycogen

31
Q

Insulin + muscles and adipocytes

A

Stimulates glucose uptake
GLUT4 contained in intracellular vesicles in absence of insulin
Insulin-induced Akt activation stimulates GLUT4 translocation to plasma membrane

32
Q

Insulin stimulates glycogen synthesis in muscles

A

Akt activated by insulin
Akt phosphorylates + therefore inactivates glycogen synthase kinase (GSK)
–> allows activation of glycogen synthase
–> GLYCOGENESIS

33
Q

Insulin + lipogenesis

A

Stimulates lipogenesis in adipocytes

34
Q

Insulin + lipolysis

A

Insulin inhibits hormone sensitive lipase

–> inhibits hydrolysis of triglycerides + release of FFAs into circulating blood

35
Q

Malonyl-CoA

A

Inhibits transport of FFAs into mitochondria via CPT-1

–> inhibits Beta Oxidation

36
Q

Beta oxidation

A

FAs broken down to produce acetyl-CoA

37
Q

Insulin + liver

A

Enhances glucose uptake (increases glucokinase activity)
Increases glycogen synthesis
Increase lipogenesis
Inhibits gluconeogenesis

38
Q

Other insulin functions

A

Promotes protein synthesis + storage
Stimulates AA transport into cells
Increases translation of mRNAs (synthesis new proteins)
Inhibits catabolism of proteins (decreases aa release from cells)
Promotes K+ intracellular uptake

39
Q

During fasting

A

No insulin secretion
Glycogenolysis- breaking down of glycogen
Hormone sensitive lipase no longer inhibited, so fat –> glycerol + FAs
No malonyl-CoA –> FAs into cell, allows Beta oxidation

40
Q

Fasting

A

Liver releases glucose into bloodstream
AAs and glycerol can be used as precursors for gluconeogenesis
Lactate can be used for gluconeogenesis

41
Q

Accumulation Acetyl-CoA that can’t enter TCA

A

Converted into Ketone bodies

42
Q

Ketone bodies

A

Main source of energy during prolonged fasting

43
Q

Mechanisms that can switch insulin signalling off

A

Endocytosis + degradation of receptor bound to insulin
Dephosphorylation of tyrosine residues by tyrosine phosphatases
Decrease in number of receptors
Serine/Threonine kinases reduce insulin receptor activity

44
Q

Insulin resistance

A

Reduced response to insulin in target tissues
–> hyperglycaemia + dyslipidaemia
Due to tyrosine residues not phosphorylated

Metabolism CC (29 decks)

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