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endocrine term 2 quiz 2 - julia's notes > hormonal regulation of intermediary metabolism > Flashcards

hormonal regulation of intermediary metabolism Flashcards

1
Q

glucose homeostasis

A

maintenance of concetrations within 60-150 mg/ml range is critical to survival
glucose is predominant fuel utilized by the CNS

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2
Q

hormones involved in glucose homeostasis (list)

A 
insulin
glucagon
catecholamines
growth hormone
hormones of the gut
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3
Q

what does insulin control (generally)

A

initiates events that promote removal of glucose

also fatty acids and amino acids from blood, preventing hyperglycemia

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4
Q

what do all of the glucose homeostasis hormones except for insulin control (generally)

A

all regulate biochemical processes which help to elevate the plasma glucose levels to prevent hypoglycemia

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5
Q

structure of insulin

A

2 peptide chains held together by S-S bridges
MW 6000
entire molecule needed for activity

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6
Q

synthesis of insulin

A

in beta cells of islets of langerhans
initial product of mRNA translation is pre-proinsulin
enzymatically cleaved to proinsulin
proinsulin cleaved to insulin and C-peptide

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7
Q

products secreted by beta-cells of islets of langerhans

A

insulin
c-peptide (in approximately equal amounts to insulin)
proinsulin

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8
Q

how does proinsulin compare with insulin in terms of reactivity?

A

50% of immunoreactivity of insulin

5% of its biological activity

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9
Q

how is human insulin made?

A

with recombinant DNA techniques

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10
Q

control of insulin secretion (summary card)

A

high blood glucose level is primary stimulus
modulating factors: certain AA, espec. arginine; ketones; glucagon; gut peptide hormones (stimulator); beta adrenergic receptor activation
inhibitory: catecholamines (on alpha adrenergic receptors), sympathetic nervous system, somatostatin
involves glucokinase (glucose sensor, glucose metabolism, and coupling of glucose metabolism via the ATP/ADP ratio - results in ionic events governing insulin secretion
key factor for insulin secretion is calcium ion concentration

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11
Q

stimulatory factors for insulin production

A 
certain amino acids (esp. arginine)
ketones
glucagon
gut peptide hormones
Increased plasma K
Obesity
Vagal stimulation via Ach
Beta adrenergic receptors
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12
Q

inhibitory factors for insulin production

A

catecholamines
sympathetic nervous system
somatostatin

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13
Q

key factor in insulin secretion

A

calcium ion concentration

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14
Q

inactivation of insulin and proinsulin

A

half life of insulin = ~10 minutes - degraded by hepatic proteolytic enzymes
halflife of proinsulin = 20 minutes - degraded by kidney enzymes

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15
Q

insulin mechanism of action

A

binds to cell surface receptor (TM protein)
receptor functions as tyrosine kinase
=> autophosphorylation
=> phosphorylation of docking proteins (IRS, Shc)
=> activation of series of parallel downstream events that involve cascade of covalent phos reactions and protein-protein interactions
=> modulation of specific cell functions including glucose transport, glycogen and protein synthesis and mitogenesis

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16
Q

insulin actions on muscle

A

1: stimulation of glucose transport into cell
2: enhancement of glycogen synthesis
3: stimulation of amino acid uptake
4: stimulation of protein synthesis
5: inhibition of proteolysis

note: exercise also stimulates glucose transport into muscle cells

17
Q

insulin actions on adipose tissue

A

1: stimulation of glucose uptake into the cells
2: promotion of fat synthesis
3: activation of lipoprotein lipase
4: inhibition of hormone-sensitive lipase
5: enhancement of glycogen synthesis
6: enhancement of AA uptake and protein synthesis

18
Q

insulin actions on liver

A

1: stimulation of glucokinase and glycogen synthetase activity
2: stimulation of activities of key rate limiting glycolytic enzymes (glucokinase, phosphofructokinase, pyruvate kinase, pyruvate dehydrogenase)
3: inhibition of activities of key rate-limiting gluconeogenic enzymes (glucose-6-phosphatase, fructose-1,6-diphosphate phosphatase, phosphoenolypyruvate carboxykinase, pyruvate carboxylase)
4: stimulation of FA synthesis and increase in activities of key lipogenic enzyme

19
Q

structure of glucagon

A

29 AA polypeptide chain

MW 3485

20
Q

synthesis of glucagon

A

in alpha-cells of islets of langerhans

initial product is pre-proglucagon

21
Q

stimuli for glucagon release

A 
primary stimulus = low blood glucose level
others = 
AA
gut hormones
catecholamines
22
Q

degradation of glucagon

A

degraded rapidly in liver - questionable whether any normally reaches peripheral circulation
proglucagon degraded in kidney - biological activity minimal

23
Q

glucagon receptors

A

cell surface receptors in liver, fat, myocardial cells, pancreatic islet beta-cells

24
Q

physiological actions of glucagon

A

1: stimulates hepatic glycogenolysis (most powerful hyperglycogenolytic agent known)
2: inhibits glycogen synthetase
3: stimulates gluconeogenesis
4: stimulates hepatic lipolysis
5: inhibits FA synthesis
6: increases hepatic ketogenesis

note: all of these effects are mediated via cAMP

25
Q

catecholamine synthesis

A

from tyrosine in the adrenal medulla, which primarily secretes epi
in postganglionic sympathetic nerve endings, primarily secrete norepi

26
Q

regulation of catecholamine synthesis

A

tonic inhibition by NE in cytosol - removed when nerve stimulation releases this NE
chronic nerve stimulation induces the enzymes tyrosine hydroxylase and dopamine-beta-hydroxylase (involved in synthesis)
ACTH and cortisol may enhance synthesis

27
Q

release of catecholamines

A
  • major stimulus is acetyl choline
  • induced by cold, hypoxia, stress
  • stimulation releases cat. from both adrenal gland and sympathetic nerve endings
28
Q

degradation of catecholamines

A

Degrade (plasma, liver, kidney), recycle (n. endings), or excrete (kidney)

very rapid (half-life in plasma less than one minute)
in plasma, liver, kidney
can be taken up and recycled at nerve terminals
can be excreted unchanged by kidneys

29
Q

catecholamine receptors

A

on cell surface of target cells
two categories: alpha and beta
plus lots of subtypes
both E and NE bind to all receptors, but with different affinities

30
Q

catecholamine beta receptors

A

implicated in metabolic effects

activation results in synthesis of cAMP

31
Q

catecholamine alpha receptors

A

some that release Ca++ may also be involved in metabolic effects

32
Q

effects of catecholamines on skeletal muscle

A

1: stimulation of glycogenolysis and lactate production
2: inhibition of glycogen synthesis and glucose uptake

33
Q

effects of catecholamines in adipose tissue

A

stimulation of lipolysis via the hormone-sensitive lipase

34
Q

effects of catecholamines in liver

A

1: stimulation of glycogenolysis
2: inhibition of glucose oxidation
3: inhibition of glycogen synthesis
4: stimulation of gluconeogenesis
5: stimulation of lipolysis

35
Q

actions of glucocorticoids in metabolism

A

protect body from insulin-induced hypoglycemia by:

1: stimulating hepatic gluconeogenesis
2: permissively by enhancing the stimulatory effect of glucagon and catecholamines on gluconeogenesis and glycogenolysis
3: inhibiting peripheral glucose utilization
4: promoting liver glycogen synthesis - thus storing substrate for acute responses to glycogenolytic agents

36
Q

actions of growth hormone in metabolism

A

1: stimulates lipolysis
2: inhibits tyrosine-amino transferase
3: stimulates acutely glucose uptake in muscle and fat

protect the body from insulin-induced hypoglycemia

37
Q

actions of somatostatin (SRIF) in metabolism

A

protect the body from insulin-induced hypoglycemia

inhibitor of many polypeptide hormones including:
insulin
glucagon
GH

effective as a pharmacological agent

physiological significance is unclear

endocrine term 2 quiz 2 - julia's notes (16 decks)

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