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BIOM2012 (1, 2, 3, & 6) > 1 - endocrine > Flashcards

1 - endocrine Flashcards

1
Q

list and describe the glucose transporter family

A

transported via facilitated diffusion (down concentration gradient)

GLUT-1:

  • found in most mammalian tissues
  • involved in basal glucose uptake and maintaining blood brain barrier

GLUT-2:

  • found in liver and pancreatic beta cells
  • involved in regulation of insulin

GLUT-3:

  • found in most mammalian tissues
  • involved in basal glucose uptake and neurones

GLUT-4:

  • found in muscle and fat cells
  • traffics glucose in response to insulin

GLUT-5:

  • small intestine
  • primarily fructose transporter
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2
Q

how is glucose homeostasis achieved in the pancreas?

A

pancreatic beta cells:
- produce insulin –> induce anabolic reactions
- increases storage of glucose, fatty acids & amino acids
- signal peptide removed from linear preproinsulin
to give proinsulin –> moves from ER to golgi –> C-peptide removed to give insulin
- insulin binds to extracellular binding dimers —> activates receptor —> conformational change —> auto-phosphorylation of tyrosine kinase domain —> tyrosine kinase activated —> phosphorylates proteins (*IRS = insulin receptor substrate) —> activated IRS activates/deactivates enzymes and induces/suppresses gene expression —-> glucose homeostasis and other metabolic functions

preatic alpha cells:

  • functional antagonist to beta cells
  • produce glucagon –> catabolic reactions
  • mobilises glucose, fatty acids and amino acids from stores to blood
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3
Q

what is the absorptive state and how is glucose homeostasis achieved in this state?

A

absorptive state = following a meal

increase in glucose = increase in insulin

insulin promotes glucose uptake out of circulation and into cells/storage

decrease in blood glucose = decrease in insulin

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4
Q

how does insulin activate/stimulate glucose uptake through GLUT4?
are there other mechanisms for glucose uptake?

A

GLUT-4 stored in cytoplasmic vesicles in muscle/fat cells

insulin stimulates these vesicles to travel to membrane

vesicles under exocytosis (SNARE proteins), and GLUT-4 embeds in membrane ready to transport glucose

when GLUT-4 genes knocked out, there is still some glucose uptake into cell —> insulin can also have enzymatic effects which induces glucose uptake from other transporters - GLUT-1/3

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5
Q

what pathway does insulin activate to activate GLUT-4?

A

PI3kinase/AKT(PKB) pathway

insulin binds to tyrosine kinase receptor –> phosphorylation pathway –> PKB activates GLUT-4

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6
Q

how does insulin stimulate glucose uptake in the liver?

A

GLUT-2 found in liver but not insulin sensitive –> insulin uses enzymes such as glucokinase to stimulate glucose uptake

glucose crosses from blood stream to IS space —> then trafficked into hepatocyte via GLUT2 transporter

insulin promotes activity of glucokinase, converting glucose to glucose-6-phosphate (inhibits reconversion)

insulin promotes activity of glycogen synthase, converting glucose-6-phosphate to glucose-1-phosphate to glycogen for storage

insulin enhances enzyme activity to convert glucose-6-phosphate to pyruvate to acetyl CoA to ATP (citric acid cycle)

insulin promotes lipogenesis (acetyl CoA –> fatty acids –> triglycerols –> lipid droplets) and protein synthesis

  • draw diagram
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7
Q

how does insulin stimulate glucose uptake in muscle?

A

glucose crosses from blood stream to IS space —> then trafficked into myocyte via GLUT4 transporter

insulin promotes activity of hexokinase, converting glucose to glucose-6-phosphate (inhibits reconversion)

insulin promotes activity of glycogen synthase, converting glucose-6-phosphate to glucose-1-phosphate to glycogen for storage

insulin enhances enzyme activity to convert glucose-6-phosphate to pyruvate to acetyl CoA to ATP (citric acid cycle)

minor component: insulin promotes lipogenesis (acetyl CoA –> fatty acids –> triglycerols –> lipid droplets)
myocytes not good for fat storage

major component: protein synthesis

*draw diagram

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8
Q

how does insulin stimulate glucose uptake in fat cells?

A

glucose crosses from blood stream to IS space —> then trafficked into adipocyte via GLUT4 transporter

insulin promotes conversion of glucose to glucose-6-phosphate (inhibits reconversion)

insulin enhances enzyme activity to convert glucose-6-phosphate to pyruvate to acetyl CoA to ATP (citric acid cycle)

insulin promotes lipogenesis (acetyl CoA –> fatty acids –> triglycerols –> lipid droplets)

note: adipocytes do not store glycogen
* draw diagram

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9
Q

how is insulin secretion controlled?

A

1) pancreatic beta-cells
- control secretion for insulin, but also act as a sensor of insulin-levels
- high glucose in ECF —> glucose trafficked into cell via concentration gradient —> insulin released in cell
- insulin stimulates glucokinase: glucose —> glucose-6-phosphate —> ATP (oxidation) —> closure of K+ channel —> depolarisation (buildup of intracellular K+)
- calcium induces vesicle fusion to release insulin (SNARE proteins)

2) autonomic ns:
- sympathetic ns inhibits insulin—> don’t want glucose stored —> want high blood glucose levels
- parasympathetic ns promotes —> store glucose during digestion

3) glucagon/somatostatin:
- glucagon is a function antagonist to insulin i.e. stimulates catabolism to increase blood glucose
- stimulates insulin to maintain glucose homeostasis
- somatostatin inhibits

4) gastrointestinal hormones
- released in response to nutrients in lumen —> switch on insulin during digestion

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10
Q

describe the function of glucagon on carbs, fats and proteins.

A 
CARBS:
1. Inhibits glycogen synthesis 
2. Promotes glycogenolysis
3. Stimulates gluconeogenesis
Overall glucagon increases hepatic glucose production & release, thus increasing blood glucose
FATS:
1. Promotes lipolysis
2. Inhibits TG (triglycerol) synthesis 
3. Enhances ketogenesis
Overall glucagon increases blood FAs & ketone bodies

PROTEINS:
1. Inhibits hepatic protein synthesis
2. Promotes degradation hepatic protein
3. Stimulates gluconeogenesis (uses aa’s to produce glucose)
Overall no significant effect on blood AA levels

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11
Q

how is glucagon secretion controlled?

A

1) blood glucose
- hypoglycaemia stimulates
- hyperglycaemia inhibits

2) beta-cells
- beta-cells stimulate insulin which in turn stimulates glucagon

3) blood AA and FA
- high blood AA increase glucagon and insulin
- high protein —> don’t want all glucose stored —> glucagon counter-balances insulin action

4) sympathetic NS
- adrenaline stimulates

5) hormones
- cortisol stimulates
- somatostatin inhibits

6) infection and exercise
- stimulate glucagon to release glucose into blood

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12
Q

relationship between glucose and insulin/glucagon release

A

at low glucose levels:

  • high glucagon to mobilise glucose stores
  • low insulin

as glucose increases:
- insulin increases for storage / utilisation in cells

at high glucose levels:

  • both insulin and glucagon increase
  • paracrine infuence from beta-cells causes insulin to stimulate glucagon
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13
Q

describe what happens to insulin/glucose levels during exercise

A

during exercise, lower blood glucose inhibits insulin and stimulates glucagon secretion

sympathetic NS active:

  • noradrenaline inhibits insulin release
  • adrenaline stimulates glucagon release

acute muscle contraction stimulates GLUT-4 translocation to membrane

chronic (endurance) muscle contraction increases GLUT-4 expression

calmodulin and AMP kinase pathways also stimulate GLUT-4 translocation to membrane

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14
Q

symptoms and effects of diabetes mellitus

describe the difference between type I and type II

A

disease of impaired carbohydrate, fat and protein metabolism - characterised by HYPERGLYCEMIA

causes:

  • glucosuria (glucose in urine)
  • polyuria (frequent urination)
  • polydipsia (frequent hunger)
  • polyphagia (frequent thirst)

TYPE I:

  • —-> insulin dependent diabetes mellitus (IDDM) i.e. inadequate insulin secretion / destruction of beta cells
  • —-> early onset
  • —-> symptoms develop rapidly
  • —-> treated using insulin injections and diet management

TYPE II:

  • —-> non-insulin dependent diabetes mellitus (NIDDM) i.e. insulin resistance / insensitivity
  • —-> adult onset
  • —-> symptoms develop slowly
  • —-> treated using oral hypoglycemics, weight reduction, exercise, diet management

severe type II can lead to type I

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15
Q

how can diabetes mellitus be tested for?

A

oral glucose tolerance test

patient fasts then ingest 75g of glucose (via sugar water). plasma glucose levels are recorded to see if insulin is acting to restore homeostasis

plasma glucose levels are extremely high because insulin cannot induce uptake of glucose into storage

more insulin is required for the same glucose uptake

  • —-> pancreas forced to pump out insulin to overcome sensitivity
  • —-> pancreatic beta-cells can become damaged and fail in a chronic situation
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16
Q

what are the long term effects of diabetes mellitus?

A

chronic complications of diabetes mellitus can lower life expectancy

hyperglycaemia leads to excessive glycosylation of proteins causing:

  • —-> damage in blood vessels (atherosclerosis in peripheral vessels)
  • —-> damage kidney
  • —-> damage retina
  • —-> neuropathy in ANS fibres
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17
Q

glycolysis process

note which enzymes are regulated by insulin

A

1 glucose + 2ADP + 2Pi + 2NAD+ —-> 2 pyruvate + 2ATP + 2NADH + 2H+ + 2H2O

aerobic: 2NADH —–> 3-5 more ATP molecules in mitochondria
anaerobic: pyruvate —-> lactate

enzymes regulated by insulin:

1) hexokinase/glucokinase = glucose to gluco-6-phosphate
2) phosphofructokinase (PFK)
3) pyruvate kinase (PK)

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18
Q

gluconeogenesis process

note which enzymes are activated by glucagon

A

2 pyruvate + 4ATP + 2GTP + 2NADH + 6H2O —–> 1 glucose + 4ADP + 2GDP + 6Pi + 2H+

key products during process include glycerol and oxaloacetate

enzymes activated by glucagon:

  • phosphoenolpyruvate carboxykinase (PEPCK)
  • pyruvate carboxylase
  • oxaloacetate
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19
Q

compare the regulation of glycolysis vs gluconeogenesis

A

glycolysis occurs in cytosol
gluconeogenesis in mitochondria and ER

glycolysis = allosteric regulation i.e. regulated by ATP, not just hormones
e.g. high levels of AMP stimulate phosphofructokinase (PFK) and therefore glycolysis
high levels of ATP inhibit phosphofructokinase (PFK)

transcriptional regulation of enzymes:

  • –> insulin STIMULATES key enzymes of glycolysis (PFK / PK)
  • –> insulin INHIBITS key enzymes of gluconeogenesis (PEPCK)
  • –> glucagon INHIBITS key enzymes of glycolysis (PFK / PK)
  • –> glucagon STIMULATES key enzymes of gluconeogenesis (PEPCK)
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20
Q

gluconeogenesis process

note which enzymes are activated by glucagon

A

2 pyruvate + 4ATP + 2GTP + 2NADH + 6H2O —–> 1 glucose + 4ADP + 2GDP + 6Pi + 2H+

key products during process include glycerol and oxaloacetate

enzymes activated by glucagon:

  • phosphoenolpyruvate carboxykinase (PEPCK)
  • pyruvate carboxylase
  • oxaloacetate
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21
Q

how is fatty acid synthesised in the liver?

A

the liver can convert glucose and amino acids into fatty acids

  1. amino acids deaminated to acetyl coA and pyruvate
  2. acetyl coA and pyruvate create citrate in mitochondria
  3. citrate can travel into cytoplasm, therefore is converted to malonyl coA
  4. condensation, reduction and dehydration give palmitate (precursor for longer fatty acids)
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22
Q

how are proteins stored after a meal?

how dos insulin stimulate this process?

A
  1. high protein meal
  2. digested in gut, amino acids absorbed through gut wall into hepatic portal vein (INSULIN STIMULATED)
  3. some amino acids oxidised (pyruvate —> citric acid cycle —> G6P —> glycogen) (INSULIN STIMULATED)
  4. aa spillover into ECF
  5. aa travel into muscle to turn into protein (INSULIN STIMULATED)
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23
Q

how are fats stored after a meal?

how dos insulin stimulate this process?

A
  1. fatty meal
  2. fats broken down in gut and absorbed through lymphatics into blood (bypass liver)
  3. in blood, free fatty acids or LPL breaks down fats (INSULIN STIMULATED)
  4. these products taken up into adipocytes to create triacylglycerides —> fat storage (INSULIN INHIBITS HSL i.e. fat breakdown)
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24
Q

describe how glycogenolysis occurs in THE LIVER via the adenylate cyclase/cAMP/PKA pathway

A
  1. glucagon binds to glucagon receptor on hepatocyte
  2. Gs proteins stimulate adenylate cyclase
  3. AMP —> cAMP
  4. activates PKA
  5. PKA phosphorylates PK
  6. PK phosphorylates glycogen phosphorylase (GP)
  7. active GP catalyses breakdown of glycogen to G1P
  8. G1P converted to G6P
  9. G6P converted to glucose by G6Pase
  10. glucose released to blood
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25
Q

describe how glycogenolysis occurs in MUSCLE via the adenylate cyclase/cAMP/PKA pathway

A
  1. adrenaline binds to adrenoreceptor on myocyte
  2. Gs proteins stimulate adenylate cyclase
  3. AMP —> cAMP
  4. activates PKA
  5. PKA phosphorylates PK
  6. PK phosphorylates glycogen phosphorylase (GP)
  7. active GP catalyses breakdown of glycogen to G1P
  8. G1P converted to G6P
  9. G6P not converted to glucose, but is oxidised via glycolysis into pyruvate —> ATP —> energy for local use
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26
Q

describe how lipolysis occurs in FAT via the adenylate cyclase/cAMP/PKA pathway

A
  1. adrenaline binds to adrenoreceptor on adipocyte
  2. Gs proteins stimulate adenylate cyclase
  3. AMP —> cAMP
  4. cAMP activates hormone-sensitive lipase (HSL)
  5. HSL releases stored TAGs via hydrolysis to give fatty acids and glycerol
  6. fatty acids transported to liver and muscle
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27
Q

ketosis

A

excessive breakdown of fats occurs during states of fasting

FA converted to acyl CoA, which is then beta-oxidised to acetyl CoA
more acetyl CoA than citric acid cycle can handle
not enough oxaloacetate* to combine with excess acetyl CoA
excess acetyl coA forms ketone bodies

  • large amount of glyconeogenesis occurring to keep blood glucose levels normal —> oxaloacetate used as a substrate —> oxaloacetate deficient

ketone bodies circulate to be used as an energy source

28
Q

what is beta-oxidation?

A

2 carbons oxidised at once

yields ATP and acetyl CoA

occurs in mitrochondria of liver

fatty acids beta-oxidised in fasting states

29
Q

ketosis chemical pathway

A

2 acetyl-CoA molecules combine to give acetoacetate (ketone body) + H+ + other products

acetoacetate is either:
- reduced to beta-hydroxybutyrate
- decarboxylated to give acetone
^ both ketone bodies

this pathway is irreversible

30
Q

how are fatty acids transported in the liver?

A

1) fatty acids transported into cytoplasm
2) FAs react with CoA and carnitine
3) transported into mitochondria
4) beta-oxidised to yield ATP and acetyl CoA

31
Q

what three by-products are produced when FA oxidation is incomplete?

A

ketone bodies:

  • acetoacetate
  • b-hydroxybutyrate
  • acetone
32
Q

how and why does ketogenesis occur?

A

ketogenesis occurs during prolonged fasting, low carb diet, type 2 diabetes

FA converted to acyl CoA —> acetyl CoA, which enters citric acid cycle (CAC)

oxaloacetate + acetyl coA = citrate

very low blood glucose —> large amount of gluconeogenesis occurring to keep blood glucose levels normal —> oxaloacetate used as a substrate

not enough oxaloacetate to combine with excess acetyl CoA

excess acetyl coA forms ketone bodies:
- acetoacetate
- b-hydroxybutyrate
- acetone
these ketone bodies are produced in the liver and enter circulation, used as energy source
33
Q

describe the structure of the thyroid gland

A

located over trachea

gland is highly vascularised

made of left and right lobe

lobes contain many follicles (ring of follicular cells surrounding cholloid)

cholloid contains ECF and stores thyroid hormones

c-cells are located between follicles and produce calcitonin to ↓ calcium levels

34
Q

name and briefly describe three thyroid hormones

A

Thyroxine (T4) = predominant form in plasma

Triiodothyronine (T3) = most biologically active form

Reverse T3 = Inactive form

35
Q

describe the hypothalamus-pituitary-thyroid axis

A

hypothalamus releases TRH down pituitary stalk

TRH crosses into interstitial space and binds to GPCRs on thyrotroph in anterior pituitary

GPCR uses Gq —> phospholipase C —> calcium release —> exocytosis of TSH

TSH goes into circulation and binds to receptors on follicular cells of thyroid gland

synthesis and secretion of thyroid hormone (T3 and T4) from thyroid gland

these hormones regulates basal O2 use and metabolism and consequent heat production

36
Q

do we need both tyrosine and iodine in our diet to synthesise thyroid hormones?

how is iodine synthesised into the thyroid hormone?

A

no, only iodine is essential in diet

low iodine —> low thyroid hormone —> low metabolic rate

1) uptake and concentration of iodide (I-)
2) incorporation of I- into phenol ring of tyrosine
3) coupling of two iodinated tyrosine molecules to form T4 or T3

37
Q

how is thyroid hormone synthesised?

A

TG = large molecule with MIT, DIT, T3 + T4 residues

TG comes from follicular cell via normal production of any protein (amino acids, transcription, translation, packed into vesicles and secreted into lumen through apical membrane)

iodide transported into follicular cell on basal membrane (active transport - Na/I transporter), known as iodide “trapping” mechanism

iodide exported through apical membrane into lumen

iodide added to TG in lumen

molecule taken into cholloid via pinocytosis (i.e. no receptor)

thyroid hormones released from molecule via association with lysosome and diffuse out of follicular cell via basal membrane

some MIT and DIT residues are recycled
– iodide cleaved out and recycled
– efficient mechanism ∴ can go for a sufficient period of time without ingesting iodine from diet

38
Q

TRUE OF FALSE

T4 converted to T3 in the liver

A

true :)

39
Q

in what form do thyroid hormones circulate?

A

> 99% circulating thyroid hormones are bound to plasma proteins e.g. TBG

“free” fraction of THs is important, that that is the portion available to bind to receptors

40
Q

are thyroid hormones fast or slow acting?

A

slow, up to days

41
Q

what are the actions of thyroid hormones?

A

1) THERMOGENIC EFFECT
– stimulates O2 consumption in most cells = heat production

2) GROWTH AND DEVELOPMENT
– essential normal somatic growth and neural development
– myelination of axons

3) METABOLISM
– multifaceted
– in general increase favours catabolism

4) CARDIOVASCULAR
– increases response to catecholamines
– enhances beta-adreno receptor responses

5) SKELETAL MUSCLE
– abnormal levels = muscle weakness

42
Q

create a table describing the different effects of hyperthyroid vs hypothyroid

A

HYPERTHYROID:
basal metabolic rate: ↑
carbohydrate metabolism: ↑ gluconeogenesis, glycogenolysis. normal glucose
protein metabolism: ↑ synthesis, proteolysis, muscle wasting
lipid metabolism: ↑ lipogenesis + lipolysis, ↓ cholesterol
thermogenesis: ↑
autonomic nervous system: ↑ expression of beta-adrenoreceptors

HYPOTHYROID:
basal metabolic rate: ↓
carbohydrate metabolism: ↓ gluconeogenesis, glycogenolysis. normal glucose
protein metabolism: ↓ synthesis, proteolysis
lipid metabolism: ↓ lipogenesis + lipolysis, ↑ cholesterol
thermogenesis: ↓
autonomic nervous system: normal

43
Q

what is euthyroidism

A

normal levels free TH

44
Q

what is hypothyroidism?

describe the causes, symptoms and associated diseases

A

hypothyroidism = deficiency of TH secretion (T4 in particular)

causes:
• immune system attacks follicular cells —> cannot produce hormones
• failure of gland (Hashimoto’s autoimmune thyroiditis)
• secondary to deficiency TRH, TSH
• inadequate supply of iodine

symptoms:
• reduced basal metabolic rate poor resistance to cold
• excessive weight gain
• easily fatigued
• slow weak pulse
• slow mentation & reflexes

myxoedema:
• oedema of skin and tissues
• “tragic facial expression”

cretinism:
• hypothyroidism since birth
• usually iodine deficiency
• mental retardation, small stature, low MR, sexual immaturity

45
Q

how is hypothyroidism treated?

A

thyroxine therapy: thyroxine converted to T4

iodine administration

46
Q

what is hyperthyroidism?

describe the causes, symptoms and associated diseases

A

hypothyroidism = overproduction of TH (thyrotoxicosis)

causes:
• graves disease (autoimmune - production of antibodies that act like TSH)
• excess TRH or TSH (result from tumour in hypothalamus or in thyrotrophs of pituitary)
• hypersecreting thyroid tumour (most common)

symptoms:
• elevated basal metabolic rate
• excessive sweating & heat intolerance
• weight loss despite increase appetite
• muscle weakening (tremor)
• excessively alert, irritable, anxious, emotional
• heart palpitations
• bulging eyes (orbital muscles have TH receptors - common in graves disease)

47
Q

what is a goitre and when does it occur?

A

goitre = enlargement of the thyroid gland

OCCURS WHEN THERE IS INCREASED TSH
– TSH drives cell division and hypertrophy of follicular cells

can occur in hypothyroid OR hyperthyroid states

hypothyroid:
deficient in thyroid hormone = reduced long loop negative feedback = release TSH to stimulate synthesis and secretion of thyroid hormone

hyperthyroid:
tumour in hypothalamus or in thyrotrophs of pituitary results in excess TSH

goitres commonly results from iodine deficiency and graves disease

48
Q

structure of adrenal gland

A

adrenal gland consists of adrenal cortex and medulla

adrenal cortex (80%):

  • zona glomerulosa (outermost)
  • zona faciculata
  • zona reticularis (innermost)

cortex produces steroid hormones (e.g. cortisol)

49
Q

classes of steroid hormones

A

• gonadal or sex steroids
e.g. progesterone, testosterone, oestradiol

• glucocorticoids
e.g. cortisol, corticosterone

• mineralocorticoids
e.g. aldosterone

50
Q

describe how gluccocoritcoids are regulated via the HPA axis (include the near, medium and long term effects)

A

HPA axis becomes activated under stress

hypothalamus releases CRH

CRH travels down pituitary stalk to ant. pituitary

ant. pituitary release ACTH into circulation

ACTH binds to receptor on adrenal cortex and signals through cAMP

near term:
• increases cholesterol transport into mitochondria
• increases cholesterol binding to P450 side-chain cleaving enzyme (rate-limiting) —> increase pregnenolone (precursor)

medium term:
• increase gene transcription of side-chain cleaving enzyme
• increases transcription of LDL receptor

long term:
• trophic to cell (size and number)
• enhances functionality of organelles

adrenal cortex releases cortisol into circulation where it acts on target cells

51
Q

TRUE OR FALSE

in the morning, more ACTH is synthesised and released in due to the circadian clock ∴ higher cortisol levels in the morning

A

FALSE

ACTH levels are not regulated by circadian clock

ACTH levels normal but cortisol IS INCREASED in the morning

the circadian clock enhances the response of the adrenal gland in the morning

52
Q

describe six different actions of cortisol

A

1) FUEL METABOLISM:
• in peripheral tissues, cortisol is catabolism:
–– stimulates lipolysis in adipocytes to mobilise FA → used for energy
–– in muscle, decrease AA uptake (oppose insulin)
• in liver, cortisol is anabolic:
–– stimulates gluconeogenesis
–– increase glucose and AA storage (↑ glycogen + protein)

2) PERMISSIVE EFFECTS:
• metabolic reactions & vascular reactivity

3) WATER METABOLISM
• necessary for normal water excretion

4) RESISTANCE ADAPTION TO STRESS
• preserves blood glucose

5) NERVOUS SYSTEM
• regulates mood and behaviour

6) REDUCE RESPONSE TO INFLAMMATORY STIMULI AND IMMUNOSUPPRESSION

53
Q

what is addison’s disease?

A

addison’s disease is chronic failure of the adrenal cortex

causes:
• autoimmune
• no ACTH
• adrenalectomy

symptoms:
• loss of gluccocorticoids = reduction in stress response and metabolism abnomalities (hypoglycemia)
• loss of aldosterone = massive electrolyte imbalance, dehydration and hypotension

FATAL IF UNTREATED

54
Q

what is cushing’s syndrome?

A

cuchsing’s syndrome is an excess of gluccocorticoids

causes:
• very rare ACTH secreting tumour
• adrenal tumour (hypersecrete cortisol)
• over-medication with anti-inflammatory steroids

symptoms:
• extra gluccocorticoids have catabolic effects
• protein depletion
• immune deficiency
• thin skin and hair
• body fat redistributed (obesity) 
• insulin-resistant diabetes
55
Q

what are adrenal androgens?

what are diseases associated with abnormal levels of adrenal androgens?

A

hormones which control early maturation before ovaries/testes have fully matured

synthesis of adrenal androgens is regulated by ACTH

very important:
• in fetus
• during childhood in both sexes “adrenarche”
• in females throughout life
• in adult males, not so important due to excess
gonadal androgens

high levels leads to:
• precocious pseudopuberty in males
• pseudohermaphroditism in females

56
Q

give a brief summary of GH action

A

in child, GH causes true growth and has metabolic effects

in adults, GH maintains muscle mass and retains same metabolic functions

muscle:
• ↑ AA uptake
• ↓ glucose uptake
• ↓ protein breakdown
• ↑ muscle mass

adipose tissue:
• ↓ glucose uptake
• ↑ fat breakdown

liver:
• ↑ protein synthesis
• ↑ gluconeogenesis

57
Q

describe the signalling mechanism used by GH

A

GH signals through JAK/STAT pathway

1) GH binds and receptor dimerises
2) JAK molecules phosphorylate each other
3) active JAK molecules phosphorylate receptor to create SH2 binding domains
4) STAT molecules bind to SH2 domain
5) JAK phosphorylates STAT
6) STAT molecules disassociate and dimerise
7) STAT dimer translocates to nucleus to induce transcription of target proteins

58
Q

how does GH act during fasting?

A

GH is the only “anabolic hormone” to increase during fasting (insulin and IGF-I levels decrease)

Catabolic hormones increase (glucagon, adrenaline and cortisol)

GH works to preserve muscle mass

59
Q

how does GH act during moderate exercise?

A

GH stimulates of lipolysis (FA as energy source)

protein and glucose metabolism remain unaffected

60
Q

compare the three different energy sources for muscle contraction

A

1) immediate
• power events
• ADP and phosphocreatine generate ATP

2) oxidative
• sprints
• anaerobic glycolysis
• glycogenolysis provides glucose 
• fastest pathway

3) non-oxidative
• >2 mins
• oxidation of fat and glucose
• most efficient pathway

61
Q

how does the body respond to exercise?

A 
↑ adrenaline
↑ glucagon
↑ cortisol
↑ GH
↓ insulin

Glucose decreases but doesn’t deplete

Glycerol and free fatty acids increased – you start mobilising fat reserves which are used to produce energy

Glycerol required for gluconeogenesis

62
Q

how does the body respond to an overnight fast

A

reduced glucose uptake + no exercise = less trafficking

low insulin, increased glucagon, increased GH

reduced glucose uptake in skeletal muscle and adipose tissue

shift to FA oxidation

increased:
• glycogenolysis
• gluconeogenesis
• lipolysis

63
Q

how does the body response to a prolonged fast (starvation)

A

shift from enhanced gluconeogenesis of protein stores to ketogenesis from fat

ketone bodies used as fuel for brain, muscle and other tissues

stress response:
↓ insulin, thyroxine
↑ glucagon, adrenalin, cortisol, GH

liver becomes site for gluconeogenesis

kidney becomes site for ketogenesis —> uses various aa’s as precursors for glucose

eventually, ketone bodies converted back into acetyl CoA
– decrease gluconeogenesis in liver
– enhanced gluconeogenesis in kidney
– increased ketogenesis in liver

64
Q

how is lactate utilised during exercise?

A

lactate is produced in the muscle fibres during contraction and afterwards is released into circulation where it is taken up by the liver and used to produce glucose in gluconeogenesis

65
Q

what are the two main priorities during exercise?

A
  1. Maintain blood glucose for brain function
    – CNS main energy source
    – Other tissues are capable of oxidation of FAs
  2. Maintain protein reserves
    – Contractile proteins, enzymes, nervous tissue

BIOM2012 (1, 2, 3, & 6) (4 decks)

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