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MET2 > 8 - Insulin > Flashcards

8 - Insulin Flashcards

1
Q

Fasting glucose level

A

3.5-5 mmol/L

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2
Q

Glucose level after meals

A

<8mmol/L

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3
Q

What can the brain not do

A

Synthesise or store glucose

Extract glucose at low concentrations

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4
Q

What percent of pancreas cells are endocrine and exocrine

A

Endocrine - 2%

Exocrine - 98%

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5
Q

What do alpha cells produce

A

Glucagon

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6
Q

What do beta cells produce

A

Insulin

in islets of langerhans

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7
Q

Delta cells

A

Somatostatin

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8
Q

PP cells

A

Pancreatic polypeptide

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9
Q

Epsilon cells

A

Ghrelin

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10
Q

Structure of insulin

A

2 chains linked by 3 disulphide bonds

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11
Q

Which form of insulin is active

A

Monomer

Dimers when insulin increases

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12
Q

What is the stored form of insulin

A

Hexamer

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13
Q

What causes a dimer to hexamer

A

Zinc and pH

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14
Q

How is insulin synthesised

A

Pancreatic B cells –> preproinsulin in ER (110) –> proinsulin (86) –> indergoes maturation into active insulin via cellular endopeptidases in golgi A
o Endopeptidases cleave off C peptide from insulin by breaking the bonds between lysine 64 and arginine 55 + arginine 31 and 32 (21+30).

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15
Q

How long is preproinsulin

A

110

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16
Q

How long is proinsulin

A

86

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17
Q

What controls production of insulin

A

Transcription from insulin gene
mRNA stability
mRNA translation
post-translational modifications

18
Q

How does glucose enter B cells

A 
via GLUT 1 (humans) 
GLUT 2 (rats)
19
Q

What is the function of glucokinase

A

Acts as the glucose sensor for insulin secretion

20
Q

When is insulin secreted

A

When the levels exceed 5mm

21
Q

What is the process of insulin being secreted

A

Glucose –> G6P –> Pyruvate (glycolysis) –> Krebs cycle –> generates ATP –> increases ATP:ADP ration in the cell –> at sub-stimulatory glucose concentrations, Katp channels open –> resting potential is maintained at hyperpolarised level –> increase in Katp closing and membrane depolarisation –> voltage gated calcium channels open –> insulin secretion

22
Q

What are the 2 phases of insulin secretion

A

1) Rapid release in response to raised BG

2) Sustained, slow release of newly formed vesicles

23
Q

What other signals can potentiate insulin release

A 
Arginine
Leucine
GLP-1
Fatty Acids
Ach release via phospholipase C
CCK
24
Q

How does arginine potentiate insulin release

A

Directly depolarises the membrane

25
Q

How does leucine potentiate insulin release

A

Act through allosteric activation of glutamate dehydrogenase
can be transaminated –> KIC –> Acetyl CoA

26
Q

How does GLP-1 enhance insulin secretion

A

Inhibits glucagon
Promotes satiety
promotes B cell differentiation and can restore their function

27
Q

How can you amplify insulin secretion with amino acids

A

Intracellular catabolism of amino acids increase ATP/ADP ratio

28
Q

Incretins

A

GLP-1 secretion

GLP-1 (7-36)/exendin-4 administration stimulates insulin secretion through GPCR-1 using glucose.

29
Q

Role of phosphorylated inositol

A

Phospholipase C cleaves PIP2 to IP3 + diacylglycerol
IP3 binds to receptor protein in ER allowing for the release of calcium from ER (increases Ca –> increase insulin release)

30
Q

What activates the insulin receptor

A

Insulin
IGF-1
IGF-II

31
Q

What type of receptor is insulin receptor

A

transmembrane tyrosine kinase receptor

32
Q

Activation of insulin receptor

A

Insulin binds to extracellular alpha subunit on IR
Conformational change
Activates tyrosine kinase within the cell
Activated kinase domain autophosphorylates tyrosine residues on C-terminus of the receptor + tyrosine residues in the adaptor protein (IRS)
Relocation of IRS then phosphorylation of P13K
P13K activates and reloactes PIP2 to PIP3
causes change in Akt
phosphorylation of downstream effectors

33
Q

What does insulin do in muscles

A

Stimulate glycogen synthesis via glycogenesis

Stimulates translocation of GLUT4 to muscles

34
Q

Function of Akt

A

increases glucose transport and glycogen synthesis

  • induces translocation of GLUT4 to plasma membranes
  • phosphorylates and inactivates glycogen synthase kinase (GSK)
35
Q

How does insulin stimulate glucose uptake into adipocytes and lipogenesis

A

Glucose used for alpha glycerol phosphate that supplies glycerol to triglycerides
Insulin inhibits lipolysis
- Inhibits HSL
- Inhibits hydrolysis of triglycerides and FA release into blood

36
Q

Insulin function in the liver

A 
Enhances glucose uptake
increases glucokinase activity 
Increases glycogen synthesis (100g stored glycogen) 
Lipids exported as lipoproteins
Insulin inhibits gluconeogenesis
37
Q

Other insulin function

A 
Protein synthesis
Transports AA into cells
Increases translation of mRNA to new proteins
Inhibits catabolism of proteins
Promotes K+ uptake
38
Q

What occurs during a fast

A

Glycogen is broken down via glycogen phosphorylase
Increase in gluconeogenesis and glycogenolysis (AA and glycerol used)
Fatty acids go through B-oxidation to produce acetyl coA from acyl CoA
acetyl CoA converted into ketone bodies
Lactate to pyruvate via cori cycle

39
Q

what converts acetyl coa to ketone bodies

A

Thiolase

HMG CoA synthase

40
Q

How to turn off insulin

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 (acts on IRS)
41
Q

Insulin resistance

A
  • Reduced response in target tissue due to the IRS phosphorylating the threonine/serine instead of the tyrosine.
    o Downstream activation of PI3K does not occur

MET2 (28 decks)

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