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insulin secretion and action Flashcards

(51 cards)

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1
Q

why is the brain dependent on glucose?

A

can’t store glucose

cant metabolise substrates

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2
Q

what is hyperglycaemia?

A

glucose concentrations are too high

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3
Q

what is hypoglycaemia?

A

concentration of glucose is too low

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4
Q

what is the normal fasting range of glucose?

A

3.5-5.5mmol/L

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5
Q

what is the range of glucose 2 hours after meals?

A

less than 8mmol/L

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6
Q

what organs can store glucose?

A

skeletal muscle, liver, adipose tissue

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7
Q

what molecules can glucose be converted into to be stored?

A

triglycerides and glycogen

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8
Q

when is insulin released?

A

when glucose levels are too high

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9
Q

how is the pancreas involved in glucose homeostasis?

A

o Regulates insulin secretion to promote glucose storage after meals
o Regulates glucose output from the liver during fasting

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10
Q

is the pancreas an exocrine or endocrine organ?

A

o Exocrine – can release digestion hormones

o Endocrine function – made up of islets of Langerhans (2% of the total mass of the pancreas)

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11
Q

what cells make up the islets of langerhans and what do they secrete?

A 
alpha
beta
delta
PP cells
epsilon cells
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12
Q

what do alpha cells release?

A

glucagon

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13
Q

what do beta cells release?

A

insulin

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14
Q

what do delta cells release?

A

somatostatin

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15
Q

what do PP cells release?

A

pancreatic polypeptide

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16
Q

what do epsilon cells release?

A

ghrelin

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17
Q

what is insulin?

A

Polypeptide – 2 chains linked by 3 disulfide linkages

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18
Q

what chains make up insulin?

A

o A chain – 21 amino acids

o B chain – 30 amino acids

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19
Q

when do the insulin polypeptides form dimers?

A

when insulin concentrations increase

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20
Q

when do the insulin dimers form hexamers?

A

in Zn2+ and at specific pHs

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21
Q

what is the storage form of insulin?

22
Q

what is the active form of insulin?

23
Q

what happens to insulin hexamers when they’re secreted?

Study These Flashcards
A

dissociates into monomers

24
Q

how is the endogenous production of insulin regulated?

Study These Flashcards
A 
o	Transcription from the insulin gene
o	mRNA stability
o	mRNA translation
o	Post-translational modifications
o	Secretion
25
explain the process of insulin synthesis
• Initially synthesised as preproinsulin in pancreatic B-cells • 5-10mins after assembly in the ER, preproinsulin is processed into proinsulin • Proinsulin matures into active insulin via action of cellular endopeptidases within the Golgi apparatus • Endopeptidases cleave off C peptide from insulin o Break bonds between lysine 64 and arginine 65 and arginine 31 and 32 • Insulin and C-peptide are then stored awaiting for secretion
26
how does glucose enter b cells?
through the GLUT1 transporter
27
what does glucokinase do?
converts glucose into glucose-6-phosphate
28
what is the mechanism of insulin secretion?
Glucose enters B cells through GLUT1 transporter • Glucose is converted to G6P and to pyruvate through glycolysis • Pyruvate generates ATP through the Krebs cycle and the ETC • Causes a rise in ATP:ADP ratio within the cell • At sub-stimulatory glucose concentrations, K-ATP channels are open – resting membrane potential is maintained at hyperpolarised level (-70mV) • Increased ATP:ADP ration causes closure of K-APT channels and membrane depolarisation • Voltage gate calcium channels open  intracellular concentration of calcium increases  insulin secreted
29
how do B cells release insulin?
o 1st phase – release is rapidly triggered in response to blood glucose levels o 2nd phase – sustained, slow release of newly formed vesicles
30
what other signals can stimulate insulin release?
* Intracellular catabolism of amino acids increases the intracellular ATP/ADP ratio * Leucine acts through allosteric activation of glutamate dehydrogenase (GDH) – can be transaminated to a-ketoisocaproate (KIC) – converted to acetyl-CoA * Amino acids e.g. arginine can directly depolarise the plasma membrane * Gastrointestinally-derived incretins glucagon-like peptide-1 (GLP-1) * Glucose-dependent insulinotropic peptide (GIP) * Fatty acids * Parasympathetic release of acetylcholine (via phospholipase C) * Cholecystokinin (CCK, via phospholipase C)
31
what is the insulin receptor?
Insulin receptor - transmembrane receptor activated by insulin, IGF-I, IGF-II - belongs to class of tyrosine kinase receptors
32
how is the insulin receptor activated?
* Insulin binds to the extracellular portion of the alpha subunits * Causes conformational change that activates the tyrosine kinase domain on the intracellular portion of the beta subunits * Activated kinase domain autophosphorylates tyrosine residues on the C-terminus of the receptor + tyrosine residues within the adptor protein IRS
33
how does insulin signalling occur?
* Receptor becomes phosphorylated when the insulin binds * IRS from the cytoplasm can now bind to the receptor * IRS becomes phosphorylated by the receptor * Bc IRS is phosphorylated, P13K can bind to IRS at the membrane * Lipid gets phosphorylated * Akt can now bind to the lipid and trigger reactions e.g. translocation of the transporter of glucose into the membrane * ATP needed to move the receptor * ATP is only activated when the insulin binds
34
what happens to IRS, P13K and Akt when there's no insulin? what further implications does this have?
they're inactive glucose can't enter the cell glucose cant be converted into glycogen
35
why cant glucose cross the plasma membrane?
needs specific glucose transporters
36
where is GLUT4 found?
contained in intracellular vesicles in the absence of insulin
37
what does insulin-induced Akt activation lead to?
stimulates GLUT4 translocation to (and insertion into) the plasma membrane and ultimately glucose uptake
38
how does insulin stimulate glycogen synthesis in muscles?
Akt phosphorylates and inactivates glycogen synthase kinase (GSK): this allows activation of glycogen synthase (GS)
39
what effect does insulin have on lipogenesis and lipolysis?
Insulin stimulates lipogenesis in adipocytes and inhibits lipolysis
40
how does insulin stimulate lipogensis and inhibit lipolysis?
* Insulin inhibits hormone sensitive lipase * Inhibits hydrolysis of triglycerides and release of FFAs into the circulating blood * Malonyl-CoA inhibits transport of FFAs into mitochondria via CPT-1 therefore inhibiting beta oxidation
41
what is the effect on; - glucose uptake - glycogen synthesis - lipogenesis - gluconeogenesis
enhances glucose uptake increases glycogen synthesis increases lipogenesis inhibits gluconeogenesis
42
what effect does insulin have on protein synthesis and storage and how?
• It stimulates transport of amino acids into the cells o Valine, leucine, isoleucine, tyrosine, phenylalanine • It increases translation of mRNAs - Synthesis of new proteins • It inhibits catabolism of proteins - It decreases aminoacids release from cells (muscle)
43
what effect does insulin have on K+ intracellular uptake?
promotes K+ intracellular uptake
44
describe post-prandial metabolism
* High glucose will stimulate insulin release from the pancreas * Acts on the liver to convert glucose to glycogen * Glucose is also converted to triglycerides in the liver * Gluconeogensis in the liver is inhibited * Breaking down of glycogen and triglycerides is inhibited
45
why does beta oxidation happen when there are reduced glucose levels?
When there are reduced glucose levels, no insulin is secreted  HSL no longer inhibited  triglycerides are broken down into glycerol and fatty acids  beta oxidation
46
what organs can use fatty acids and what is it used for?
• Fatty acids can be used by most tissues to generate acetyl-CoA and therefore ATP but not by the brain
47
what is glycogenolysis?
breaking down of glycogen
48
what is gluconeogenesis?
synthesis of new glucose – once it’s broken down all the glycogen
49
what can be used as precursors for gluconeogenesis?
Carbon based molecules can be used as precursors for gluconeogenesis
50
what happens to accumulation of acetyl-coA that cant enter the TCA cycle?
converted into ketone bodies
51
what are mechanisms that can switch the insulin signalling off?
* Endocytosis and degradation of the receptor bound to insulin * Dephosphorylation of the tyrosine residues by tyrosine phosphatases * Decrease in the number of receptors also leads to reduced insulin signalling * Serine/Threonine kinases reduce the activity of insulin receptor

m2 (24 decks)

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