Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

m2 > insulin secretion and action > Flashcards

insulin secretion and action Flashcards

1
Q

why is the brain dependent on glucose?

A

can’t store glucose

cant metabolise substrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is hyperglycaemia?

A

glucose concentrations are too high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is hypoglycaemia?

A

concentration of glucose is too low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the normal fasting range of glucose?

A

3.5-5.5mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the range of glucose 2 hours after meals?

A

less than 8mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what organs can store glucose?

A

skeletal muscle, liver, adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what molecules can glucose be converted into to be stored?

A

triglycerides and glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when is insulin released?

A

when glucose levels are too high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A 
alpha
beta
delta
PP cells
epsilon cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what do alpha cells release?

A

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do beta cells release?

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do delta cells release?

A

somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what do PP cells release?

A

pancreatic polypeptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what do epsilon cells release?

A

ghrelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is insulin?

A

Polypeptide – 2 chains linked by 3 disulfide linkages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what chains make up insulin?

A

o A chain – 21 amino acids

o B chain – 30 amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

when do the insulin polypeptides form dimers?

A

when insulin concentrations increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

when do the insulin dimers form hexamers?

A

in Zn2+ and at specific pHs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the storage form of insulin?

A

hexamers

22
Q

what is the active form of insulin?

A

monomers

23
Q

what happens to insulin hexamers when they’re secreted?

A

dissociates into monomers

24
Q

how is the endogenous production of insulin regulated?

A 
o	Transcription from the insulin gene
o	mRNA stability
o	mRNA translation
o	Post-translational modifications
o	Secretion
25
Q

explain the process of insulin synthesis

A

• 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
Q

how does glucose enter b cells?

A

through the GLUT1 transporter

27
Q

what does glucokinase do?

A

converts glucose into glucose-6-phosphate

28
Q

what is the mechanism of insulin secretion?

A

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
Q

how do B cells release insulin?

A

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

30
Q

what other signals can stimulate insulin release?

A
  • 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
Q

what is the insulin receptor?

A

Insulin receptor - transmembrane receptor activated by insulin, IGF-I, IGF-II - belongs to class of tyrosine kinase receptors

32
Q

how is the insulin receptor activated?

A
  • 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
Q

how does insulin signalling occur?

A
  • 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
Q

what happens to IRS, P13K and Akt when there’s no insulin? what further implications does this have?

A

they’re inactive
glucose can’t enter the cell
glucose cant be converted into glycogen

35
Q

why cant glucose cross the plasma membrane?

A

needs specific glucose transporters

36
Q

where is GLUT4 found?

A

contained in intracellular vesicles in the absence of insulin

37
Q

what does insulin-induced Akt activation lead to?

A

stimulates GLUT4 translocation to (and insertion into) the plasma membrane and ultimately glucose uptake

38
Q

how does insulin stimulate glycogen synthesis in muscles?

A

Akt phosphorylates and inactivates glycogen synthase kinase (GSK): this allows activation of glycogen synthase (GS)

39
Q

what effect does insulin have on lipogenesis and lipolysis?

A

Insulin stimulates lipogenesis in adipocytes and inhibits lipolysis

40
Q

how does insulin stimulate lipogensis and inhibit lipolysis?

A
  • 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
Q

what is the effect on;

  • glucose uptake
  • glycogen synthesis
  • lipogenesis
  • gluconeogenesis
A

enhances glucose uptake
increases glycogen synthesis
increases lipogenesis
inhibits gluconeogenesis

42
Q

what effect does insulin have on protein synthesis and storage and how?

A

• 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
Q

what effect does insulin have on K+ intracellular uptake?

A

promotes K+ intracellular uptake

44
Q

describe post-prandial metabolism

A
  • 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
Q

why does beta oxidation happen when there are reduced glucose levels?

A

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
Q

what organs can use fatty acids and what is it used for?

A

• Fatty acids can be used by most tissues to generate acetyl-CoA and therefore ATP but not by the brain

47
Q

what is glycogenolysis?

A

breaking down of glycogen

48
Q

what is gluconeogenesis?

A

synthesis of new glucose – once it’s broken down all the glycogen

49
Q

what can be used as precursors for gluconeogenesis?

A

Carbon based molecules can be used as precursors for gluconeogenesis

50
Q

what happens to accumulation of acetyl-coA that cant enter the TCA cycle?

A

converted into ketone bodies

51
Q

what are mechanisms that can switch the insulin signalling off?

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions