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Metabolism 2 > Insulin - Counter regulatory hormone > Flashcards

Insulin - Counter regulatory hormone Flashcards

1
Q

What is the key role of insulin in controlling blood glucose levels

A

1, high glucose levels – removal of glucose from the blood (transport)

  1. Synthesis of glycogen and triglycerides to store energy
  2. Inhibition of processes that release glucose/fatty acids
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2
Q

What is the main hormone that is used in fasting to control blood glucose levels

A

Glucaogn

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3
Q

describe what metabolism is like during fasting

A
  1. Low glucose levels –No glucose transport
  2. Glycogen and triglycerides are not synthesised anymore
  3. Processes that release glucose/fatty acids are not inhibited anymore
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4
Q

describe the structure of glucagon

A
  • 29 amino acids

- one chain only

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5
Q

what islets of langhernas produce glucagon

A

alpha

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6
Q

describe how synthesis of glucagon takes place

A
  • Frist synthesised as a preproglucagon
  • Broken down into a proglucagon
  • This is then broken down into a glucagon
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7
Q

name another hormone that comes from the same precursor as glucagon

A

GLP-1

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8
Q

how low is blood glucose in order to do glucagon secretion

A
  • Stimulated by low blood glucose concentration – normal fasting levels of glucose is 80-90mg/100ml
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9
Q

what causes an increase in glucagon secretion

A
  • Exercise - In exhaustive exercise blood concentration of glucagon increases four to five fold
    (increased circulating amino acids or β-adrenergic stimulation may play a role)
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10
Q

what inhibits glucagon secretion

A
  • inulin - it breaks down cAMP by phosphodiesterase enzyme

- somatostatin (produced by delta cells in the islet of langerhans)

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11
Q

what are the effects of glucagon

A

 Increases glycogenolysis in the liver.
 Increased uptake of amino acids in the liver.
 Increases gluconeogenesis in the liver (amino acids, glycerol and lactate).
 Liver glycolysis is inhibited by inhibiting pyruvate kinase and PFK1.
 Increased lipolysis, glucagon activates hormone sensitive lipase (HSL).
 More ketogenesis is able to occur.

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12
Q

how is glucagon receptor signalled

A
  • The glucagon receptor is a G protein coupled receptor
  • GPCRs contain 7 transmembrane domains are coupled to trimeric G proteins
  • Dissociation of the trimer upon ligand binding to the receptor activates the signalling cascade
  • In the absence of glucose, it is assembled in the trimeric form and the 3 subunits are joined together
  • This activates adenylase cyclase and this activates cAMP
  • The cAMP which is produced in this reaction triggers the cascade
  • cAMP is produced and this activates PKA and then this increases phosphorylase kinase and activates the rest of the cascade causing glycogenolysis
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13
Q

what is CPT1

A

 Important enzyme in the Beta oxidation of fatty acids into Acetyl-CoA.

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14
Q

what inhibits CPT1 and what activates CPT1

A

 CPT1 is inhibited by insulin.

 It is activated by glucagon.

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15
Q

what happens in prolonged glucagon

A

 Oxaloacetate replaces amino acids as the main source for gluconeogenesis.
 Acetyl-CoA is converted into acetoacetate (ketone) via HMG-CoA.
 Glucagon inhibits HMG-CoA to prevent excess cholesterol and TGA formation.
 But, glucagon increases ketogenesis.

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16
Q

what does triglycerides break down into

A

glycerol and free fatty acids

- glycerol is used in gluconeogensis

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17
Q

what does amlonyl CoA inhibit

A
  • Malonyl-CoA inhibits transport of FFAs into mitochondria via CPT-1 therefore inhibiting β oxidation
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18
Q

what is oxaloacate used int he liver by

A
  • oxaloacetate is used by the liver as substrate for gluconeogensis
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19
Q

what is excess acetyl-CoA converted into

A
  • ketone bodies by the liver - keotgnesis
20
Q

what is ketogensis inhibited by

A
  • inhibited by insulin and activated by glucagon
21
Q

name 3 catecholamines

A
  • noradrenaline
  • adrenaline
  • dopamine

these are short term hormones

22
Q

where is adrenaline released from

A

Released from the medulla of the adrenal glands.

23
Q

what does adrenaline do

A
  • Inhibits insulin secretion
  • Stimulates glycogenolysis.
  • Stimulates glucagon secretion.
  • Increases lipolysis.
24
Q

what is adrenaline and dopamine synthesis from

A
  • Monoamines are synthesised from phenylalanine and tyrosine
25
Q

when is adrenaline released

A

 Released during stress or hypoglycaemia, also part of fight or flight response.

26
Q

where are glucortoiciods produced

A

produced in the cortex

27
Q

name an example of glucoroctoids

A

cortisol

some steroids

28
Q

what causes the secretion of cortisol

A

 ACTH released in the anterior pituitary gland causes secretion of cortisol.

29
Q

is cortisol long term or short term

A

Long term = causes rapid utilisation of proteins and lipids.

30
Q

what are the actions of cortisol

A
  • It enhances gluconeogenesis
  • It inhibits glucose uptake (and utilisation)
  • It stimulates muscle proteolysis
  • It stimulates adipose-tissue lipolysis
31
Q

what can cortisol also help

A

Cortisol is important in resisting stress and inflammation

Cortisol helps maintain blood pressure and it suppresses inflammation

32
Q

what can high cortisol levels cause

A
  • Cushings sydrome

If levels of cortisol are elevated for a prolonged time they can induce proteolysis and muscle wasting

33
Q

cortisol usually does not….

A

Cortisol usually does not mobilise basic functional proteins such as muscle contractile proteins and proteins of neurons

34
Q

what do growth hormones do in

  • adipose tissue
  • liver
  • skeletal muscles
A

Adipose Tissue:
 Increases lipolysis.
 Reduces glucose uptake.
 Reduces lipogenesis.

Skeletal Muscle:
 Reduces glucose uptake.
 Increases lipoprotein lipase activity.

Liver:
 Increases VLDL secretion.
 Increases production and uptake of HDL and LDLs.

35
Q

What do thyroid hormones do

A

 T3 and T4 increase the activity and number of mitochondria, increasing the rate of
ATP synthesis.

 Increase stimulation of carbohydrate metabolism:

  • Rapid glucose uptake.
  • Enhances glycolysis and gluconeogenesis.
  • Increase insulin secretion.

 Increase stimulation of fat metabolism:
- Lipids mobilised rapidly from adipose tissue.
- Fatty acid concentration in blood increased.
 Overall effect is to increase basal metabolic rate.

36
Q

what is more potent T3 or T4

A
  • T3 is about 4 times more potent than T4

- T3 is present in the blood in much smaller quantities and persists for a much shorter time

37
Q

what are incretins

A
  • these are a group of gastrointestinal hormones
38
Q

name some examples of incretins

A

Glucagon-like peptide-1 (GLP-1)

Gastric inhibitory peptide

39
Q

what does GLP-1 do

A
  • inhibits glucagon secretion and hepatic glucose production
  • slows gastric emptying
  • promotes satiety
  • augments glucose-induced inulin secretion
  • rests beta cell function
  • increases insulin biosynthesis
  • promotes B cell differentiation
40
Q

what is hypoglycaemia

A

any abnormally low plasma glucose concentration
that exposes the subject to potential harm” with a proposed threshold
plasma glucose value <70 mg/dL (<3.9 mmol/L)

41
Q

what cause cause hypoglycaemia

A
  • can be caused by stimulation of glucose utilisation and inhibition of glucose release

High insulin doses

Alcohol excess (inhibition of gluconeogenesis)

Insulinoma (A tumour of pancreatic β cells)

Excessive exercise (Leading to increased glucose utilisation)

Reactive hypoglycaemia (Excessive insulin secretion in response to a high carbohydrate meal in the pre-diabetic condition)

42
Q

what is a major combination of type I diabetes

A
  • hypoglycaemia is a major combination of type I diabetes
43
Q

what are the symptoms of hypoglycaemia

A

Autonomic symptoms
- Include trembling palpation, sweating, anxiety, hunger, tingling

Neuroglycopenic symptom s
- Including difficulty concentration, confusion, weakness, drowsiness, vision changes, difficulty speaking, dizziness, tiredness

Severe

  • Confusion
  • Disorientation
  • Confusions
  • Fitting
  • Seizures
  • Loss of consciousness
  • Coma
44
Q

what is prolonged hypoglycaemia caused

A
  • Growth hormone and cortisol are secreted – they decrease the rate of glucose utilisation by most cells converting to fat utilisation
45
Q

what are the consequences of hypoglycaemia

A
  • Serious consequences related to neuroglycopaenia (shortage of glucose for the brain)
  • Prolonged and repeated hypoglycaemia may produce permanent brain damage
  • Loss of cognitive function, seizures and coma
46
Q

how many type 1 diabetes patients get reccurnet severe hypoglycaemia

A

Recurrent severe hypoglycaemia affects 1-3% of Type 1 diabetes patients, mostly adults having diabetes for > 10 years

Metabolism 2 (40 decks)

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