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Metabolism CC > Insulin Counter-Regulatory Hormones > Flashcards

Insulin Counter-Regulatory Hormones Flashcards

1
Q

Low Glucose levels

A

No glucose transport
Glycogen + triglycerides not synthesised
Processes releasing glucose/FAs not inhibited

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2
Q

Glucagon

A

Main hormone controlling blood glucose levels during fasting

Exact opposite to insulin

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3
Q

Glucagon make up

A

29 amino acid peptide

Release from alpha cells of islets of Langerhans when glucose levels low

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4
Q

Glucagon synthesis

A

Synthesised as large molecule= preproglucagon
Preproglucagon –> cleaved into many diff hormones depending on which cell it’s in
Cleaved into proglucagon
In pancreatic alpha cells, proglucagon –> glucagon

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5
Q

Glucagon secretion

A

Increase in intracellular Ca2+

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6
Q

Glucagon secretion stimulated by

A

Low blood glucose conc
Increased blood aa’s - especially arginine + alanine
Exercise –> in exhaustive exercise, glucagon conc increases 4-5x

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7
Q

Glucagon secretion inhibition

A

Insulin

Somatostatin - released by delta cells in pancreas

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8
Q

Glucagon receptor

A

G-protein coupled receptor

Contains 7 transmembrane domains coupled to trimeric G proteins

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9
Q

Glucagon receptor activation

A

Glucagon binds
G proteins dissociate
Subunits trigger release of cAMP
–> increases Gluconeogenesis and Glycogenolysis
–> decreases Glycolysis and Glycogenesis

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10
Q

Insulin + effect on Glucagon-depending signalling

A

Breaks down cAMP, which activates glucagon signalling cascade
Activates phosphodiesterase –> breaks down cAMP into AMP –> unable to activate signalling cascade

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11
Q

Fasting

A

No insulin secretion
Liver releases glucose into bloodstream
Triglyceride stores deplete
B-Oxidation

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12
Q

Fasting - no insulin secretion

A

cAMP downstream activates glycogenolysis

Break down of glycogen –> glucose

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13
Q

Liver + glucose release

A

Glucagon increases gluconeogenesis
Glucagon inhibits Phosphofructokinase-1 and Pyruvate kinase
–> because of this, glycolysis stopped
–> gluconeogenesis ALLOWED
–> carbon based molecules converted into glucose in liver

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14
Q

Triglyceride stores in fasting

A

Glucagon activates hormone sensitive lipase
Activates lipolysis
–> TGC –> glycerol + FAs

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15
Q

Beta Oxidation

A

Lack of Malonyl-CoA (comes from glycolysis- inhibits FFA transport into mitochondria by inhibiting CPT-1)
FFAs can be shuttled in
Glucagon stimulates CPT1
–> activates Beta Oxidation

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16
Q

Acetyl-CoA accumulation that can’t enter TCA

A

Converted into ketone bodies via Ketogenesis

Liver uses ketones to feed gluconeogenesis –> glucose for brain

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17
Q

Adrenocortical hormones short term

A

Released from adrenal medulla
Released in response to stress + hypoglycaemia
Act V quickly
Main job is to increase glucose in blood to make sure can react to stressful situation

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18
Q

Monoamines of adrenocortical hormone synthesis

A

Synthesised from phenylalanine and tyrosine

19
Q

Epinephrine

A 
Inhibits insulin secretion
Stimulates glycogenolysis in liver + muscle
Stimulates glucagon secretion
Increases lipolysis in adipose tissue
-->INCREASES BLOOD GLUCOSE + FA LEVELS
20
Q

Adrenocortical hormones long term

A

Convert proteins + fats into glucose

Increase glucose conc in blood

21
Q

Cortisol produced

A

Produced in adrenal cortex
–> Zona Fasciculatae
Derived from cholesterol

22
Q

Adrenal cortex cells

A

Have many LDL receptors, enabling cholesterol uptake for steroid hormone synthesis
Secrete glucocorticoids + other steroids

23
Q

Cortisol secretion

A

In response to adrenocorticotrophic hormone (ACTH) from pituitary, with a negative feedback loop
V strictly regulated
Stops its own release

24
Q

Cortisol metabolic action long term

A

Enhances gluconeogenesis
Activates transcription of new genes for protein synthesis
Inhibits glucose uptake + utilisation
Stimulates muscle proteolysis
Stimulates adipose tissue lipolysis
–> rapid mobilisation of AA’s and FAs from cellular stores

25
Q

Cortisol in resisting stress + inflammation

A

Helps maintain BP + Suppresses inflammation

26
Q

Elevated cortisol levels for prolonged time

A

Can induce proteolysis + muscle wasting

27
Q

Growth hormones

A

Can stimulate liver to produce insulin-like growth factor
Act at level of:
–> liver- gluconeogenesis
–> adipose - lipolysis

28
Q

Thyroid hormone mechanism

A

Similar to cortisol –> long term response

Activate nuclear receptors + transcription of large number of genes

29
Q

Thyroid hormone release

A

very strictly controlled

30
Q

Iodinated thyronines

A

Tetraiodothyronine, thyroxine (T4)

Triiodothyronine (T3)

31
Q

Thyroid hormone bioactivity

A

Regulated by controlling conversion of T4–>T3 into target tissues
T3= 4x more potent than T4

32
Q

T3 in blood

A

Present in much smaller quantities than T4

Persists for much shorter time

33
Q

Thyroid hormone Metabolic Actions

A

Increases no. + activity of mitochondria –> increases ATP synthesis rate
Stimulation of carbohydrate metabolism
–> rapid glucose uptake, enhances glycolysis + gluconeogenesis, increased insulin secretion
Stimulation of fat metabolism
–> lipid mobilised rapidly from fat tissue, increased FA concentration in plasms
Increased basal metabolic rate

34
Q

Incretins

A

Group of gastrointestinal hormones
GLP-1
Gastric inhibitory peptide
Come from preproglucagon as well

35
Q

GLP-1 Function

A

Inhibit glucagon secretion + hepatic glucose production
Augments glucose-induced insulin secretion
Increases insulin biosynthesis
Slows gastric emptying
Promotes satiety

36
Q

Hypoglycaemia

A

Any abnormality low plasma glucose concentration that exposes the subject to potential harm
Proposed Threshold plasma glucose value <70mg/dL

37
Q

Hypoglycaemia reasons

A

Stimulation of glucose utilisation

Inhibition of glucose release

38
Q

Hypoglycaemia causes

A 
High insulin doses
Alcohol excess (inhibition gluconeogenesis)
Insulinoma
Excessive exercise
Reactive hypoglycaemia
39
Q

Mild hypoglycaemia symptoms

A 
<70mg/dL causes autonomic symptoms
Trembling
Palpitations
Sweating
Anxiety
Hunger
Tingling
40
Q

Moderate hypoglycaemia symptoms

A 
<55mg/dL cause autonomic symptoms + neuroglycopaenic symptoms
Difficulty concentrating
Confusion
Weakness
Drowsiness
Vision changes
41
Q

Severe hypoglycaemia symptoms

A 
<40mg/dL is MEDICAL EMERGENCY
Confusion
Disorientation
Convulsion
Fitting
Seizures
loss of consciousness
coma
42
Q

Prolonged hypoglycaemia

A

Growth hormone + cortisol secreted

  • -> decrease rate of glucose utilisation by most cells
  • -> Convert to fat utilisation
43
Q

Prolonged hypoglycaemia consequences

A

Serious consequences related to neuroglycopenia (shortage of glucose for brain)
Permanent brain damage
Loss of cognitive function, seizures + coma

44
Q

Severe Hypoglycaemia

A 
Diabetic emergency
Can occur in patients using blood glucose lowering medication or prandial glucose regulators 
Missed or delayed meal
Overdose on medication
Exercise without medication adjustment
Alcohol consumption

Metabolism CC (29 decks)

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