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MET2 > Insulin > Flashcards

Insulin Flashcards

1
Q

What is glucose used for?

A

By cells to synthesise ATP

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2
Q

What are the words used to describe when blood glucose levels are too high and too low?

A

Too high - hyperglycaemia

Too low - hypoglycaemia

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3
Q

What are normal fasting blood glucose concentrations?

A

3.5-5.5 mmol/L

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4
Q

What is glucose used for post feeding?

A 
ATP formation (powers cellular functions)
Stored in specific organs then converted into molecules which can be stored (glycogen, triglycerides)
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5
Q

What organs store glucose?

A

Skeletal muscle
Liver
Adipose tissue

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6
Q

How is glucose metabolised during starvation?

A

Glycogen broken down into glucose

TG broken down into glycerol and free fatty acids -> Glycerol converted into glucose

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7
Q

What organ is the most important in glucose homeostasis? What is its role?

A

Pancreas - regulates insulin secretion to promote glucose storage after meals, vs glucose output from liver during fasting

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8
Q

Where is insulin synthesised?

A

In the pancreas within the islets of langerhans

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9
Q

What do the islets of Langerhans contain?

A 
alpha cells - produce glucagon
beta cells - produce insulin
delta cells - produce somatostatin
PP cells - produce pancreatic polypeptide
epsilon cells - produce ghrelin
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10
Q

What are the properties of insulin?

A
  • 2 chains (one 21 aa, one 20 aa) linked by 3 disulphide bridges
  • monomers form dimers when insulin conc increases and when released
  • in presence of Zn2+ and at specific pH dimers form hexamers (storage form of insulin)
    once hexamers secreted insulin dissociates into monomeric form
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11
Q

How is insulin synthesised?

A

Initially in preproinsulin in pancreatic beta cells
peproinsulin processed into proinsulin about 5-10 mins after assembly in endoplasmic reticulum
proinsulin undergoes maturation into active insulin through endopeptidases within Golgi
endopeptidases cleave off C peptide from insulin by breaking bonds between peptides

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12
Q

How is endogenous insulin production regulated?

A
  • transcription from insulin gene
  • mRNA stability
  • mRNA translation
  • post-translational modifications
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13
Q

How is insulin synthesis and insulin secretion independent?

A

insulin and C-peptide are stored after synthesis awaiting secretion

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14
Q

How is insulin secreted?

A
  • glucose enters beta cells through GLUT 1 transporter
  • glucokinase converts glucose into glucose-6-phosphate and acts as glucose sensor for insulin secretion
  • Km of glucose carrier and glucokinase ensures initiation of insulin secretion by glucose occurs only when glucose levels are higher
  • glucose is converted to glucose-6-phosphate and pyruvate (glycolysis)
  • pyruvate through Krebs cycle and ETC generates ATP leading to rise in ATP:ADP ratio within cell
  • Katp channels open so resting membrane potential is maintained at hyperpolarised level (-70mV)
  • increased ATP/ADP ratio results in Katp closure and membrane depolarisation
  • voltage gated Ca2+ channels open, intracellular concentration of Ca2+ increases and so insulin secretion triggered
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15
Q

How do pancreatic beta cells release insulin in phases?

A

1st phase - release is rapidly triggered in response to increased blood glucose levels
2nd - sustained slow release of newly formed vesicles

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16
Q

How do amino acids potentiate insulin release?

A
  • increased intracellular catabolism of amino acids increases ATP/ADP ratio
  • leucine acts through allosteric activation of glutamate dehydrogenase and transaminated to be converted into acetyl-coA
  • amino acids such as arginine can directly depolarise plasma membrane
17
Q

What other signals potentiate insulin release?

A
  • fatty acids
  • PS release of acetylcholine
  • cholecystokinin
  • gastrointestinally derived incretins glucagon like peptide 1
  • glucose dependent insulinotropic peptide
18
Q

What is special about insulin responsive cells?

A
  • insulin responsive cells express specific receptor at plasma membrane
  • insulin receptor is a transmembrane receptor, activated by insulin, IGF-I and IGF-II, belong to large class of tyrosine kinase receptors
19
Q

How is the insulin receptor activated?

A
  • insulin binds to extracellular portion of alpha subunits
  • causes conformational change activating tyrosine kinase domain residing on intracellular portion of beta subunits
  • this autophosphorylated tyrosine residues on C-terminus of receptor and within adaptor protein
20
Q

How does insulin stimulate glucose uptake in muscles and adipocytes?

A
  • glucose cannot cross plasma membrane and uptake requires specific transporters
  • GLUT4 contained in intracellular vesicles in absence of insulin
  • Akt activation due to insulin stimulates GLUT4 translocation to plasma membrane = glucose uptake
21
Q

How does insulin stimulate glycogen synthesis in muscles?

A

Akt phosphorylates and inactivates glycogen synthase kinase allowing activation of glycogen synthase

22
Q

What is the effect of insulin on fats?

A
  • stimulates lipogenesis in adipocytes (TG break down into glycerol and fatty acids)
  • inhibits lipolysis by inhibiting hormone sensitive lipase
23
Q

What is the function of malonyl-CoA?

A

inhibits transport of free fatty acids into mitochondria via CPT-1 (inhibits Beta oxidation)

24
Q

What effect does insulin have in the liver?

A
  • enhances glucose uptake (increases glucokinase activity)
  • increases glycogen synthesis
  • increases lipogenesis (lipids exported as lipoproteins)
    (essentially inhibits gluconeogenesis)
25
Q

What other functions does insulin have?

A
  • promotes protein synthesis and storage
  • stimulates transport of amino acids into the cells
  • increases translation of mRNAs
  • inhibits catabolism of proteins
  • promotes K+ intracellular uptake
26
Q

How does metabolism change during fasting?

A
  • no insulin secretion = reduced blood glucose levels
  • liver releases glucose into bloodstream
  • amino acids and glycerol used as precursors for gluconeogenesis
  • other metabolic adaptations provide substrates for gluconeogenesis (lactate from Cori cycle)
  • acetyl-CoA accumulation that cannot enter TCA cycle converted into ketone bodies
27
Q

What mechanisms can switch insulin signalling off?

A
  • endocytosis and degradation of receptor bound to insulin
  • decrease in number of receptors -> reduced insulin signalling
  • dephosphorylation of tyrosine residues by tyrosine phosphatases
  • serine/threonine kinases reduce activity of insulin receptor

MET2 (26 decks)

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