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Endocrinology & Reproduction > Fuel homeostasis > Flashcards

Fuel homeostasis Flashcards

1
Q

why do we need fuel homeostasis

A

we have a constant requirement of nutrients for tissues, but sporadic food intakes

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2
Q

What metabolic substrate does the CNS rely on

A

glucose, other nutrients cannot cross the BBB

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3
Q

What blood plasma [glucose] is needed to stay alive

A

above 5mM. Glucose homeostasis ensures blood plasma glucose remains between 5 and 10mM

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4
Q

which organs are involved in fuel homeostasis?

A 
Liver = major glycogen store short term & turns nearly every nutrient into glucose
Adipose = major TAG store, long term
Muscle = major consumer of fuel, with a short term glycogen store for its own use
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5
Q

What is the absorptive state

A

when ingested nutrients are enterng the blood from the GI tract; ~3 hrs after a meal

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6
Q

what happens to glucose in absorptive state

A
  • net uptake in the live, converted to glycogen and excess as alpha GP for TAG
    muscles use glucose for energy and store some as glycogen
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7
Q

what happens to FA in the absorptive state

A

in adipose FA form TAG for storage

in other organs some ingested fat is oxidesed for energy

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8
Q

what happens to amino acids in the absorptive state

A

liver: minority converted to keto aids by deamination to enter TCA cycle
skeletal muscle & other organs: use AA to synthesise proteins and replace proteins lost through catabolism

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9
Q

what is the post-absorptive state

A

when the GI tract is empty and energy is supplied by the body stores. this is the default mechanism; catabolism of stored energy

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10
Q

what is the default body state?

A

post-absorptive. Catabolism of stored energy

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11
Q

how is glucose levels maintained for CNS function

A
  • generation of glucose from stored fuels = gluconeogenesis

- glucose sparing, by utiliasation of FA and AA

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12
Q

gluconeogenesis

A

generation of glucose from stored fuels

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13
Q

fastest, most efficient way to produce glucose from stored fuels in PA state

A

glycogenolysis

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14
Q

key characteristics of glycogenolysis

A

rapid

short lived

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15
Q

what is the first repsonse to maintainng plasma glucose levels?

A

hepatic glycogenolysis

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16
Q

is glucose-6-phosphate converted to glucose in the muscle?

A

no this cannot occur. instead G6P undergoes glycolysis to produce lactate and pyruvate which circulate the liver and are coverted to glucose

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17
Q

how does muscle make glucose from G6P

A

occurs indirectly. G6P undergoes glycolysis to produce lactate and pyruvate which circulate the liver and are coverted to glucose

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18
Q

lipolysis

A

Adipose generates FA and glycerol from TAG

liver converts glycerol to glucose

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19
Q

glycogenolysis from protein

A

AA converted to glucose in the liver

short term; only 5-10% catabolised

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20
Q

what is the major source of glucose after a few hours in the PA state?

A

protein

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21
Q

glucose sparing

A

fat is utilised to spare glucose for CNS.

Organs will reduced glucose utilisation and instead oxidise FA to produce acetyla CoA to encer TCA cyle

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22
Q

fatty acid oxidation

A

produces acetyl co-a to entre TCA cycle

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23
Q

what state will the body enter in prolonged starvation

A

ketosis. In the liver, acetyl coA from FA oxidation will be converted to ketones and relesed in the blood for fuel by tissues. In extended starvation, body enters ketosis

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24
Q

two main control systems for maintaining A and PA states

A

endocrine & neural control

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25
Q

neural conrol for maintaining A and PA states

A

sympathetic nervous system

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26
Q

endocrine conrol for maintaining A and PA states

A

pancreatic hormones (insulin & glucagon), cortisol, growth hormone, thyroid hormones etc

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27
Q

excess CHO converted to

A

fat

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28
Q

excess fat stored in

A

Adipose

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29
Q

excess AA converted to

A

fat

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30
Q

CHO stored as

A

glycogen

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31
Q

summary of PA state

A

gluconeogenesis
fatty ocid oxidation
glucose sparing through FA oxidation & AA

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32
Q

most important hormones for controlling fuel balance

A

glucagon & insulin

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33
Q

dominant hormone in absorptive state

A

insulin

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34
Q

dominant hormone in PA state

A

gluagon

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35
Q

where are the islet of langerhans found

A

pancreactic cells

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36
Q

where are plypeptide hormones made

A

beta and alpha cells of the prancreatic cells called the islets of langerhans

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37
Q

what stimulates insulin release

A

increased blood glucose

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38
Q

what does insulin inhibit

A

glucagon release

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39
Q

what does insulin target

A

targets the liver, muscle & fat to take up, utilise & store glucose

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40
Q

is insulin anabolic or catabolic

A

anabolic

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41
Q

when is glucagon released

A

when blood glucose falls, during PA state

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42
Q

what does glucagon inhibit

A

insulin release

43
Q

what increases glucose oxidation, glycogen synthesis, fat synthesis and protein synthesis

A

insulin

44
Q

how does insulin increase glucose uptake in the muscle and liver

A

increase expression of transporters

45
Q

what transporters take up glucose in the liver

A

glucose kinase

46
Q

what stimulates glycogen synthesis in the muscle & liver

A

insulin

47
Q

what does insulin do to AA and protein in muscle

A

inreases AA uptake and protein synthesis

48
Q

what promotoes synthesis of FA and alpha GP to form TAG in aidpose?

A

insulin

49
Q

How are TAGs generated from circulatiing lipoproteins

A

insulin induces expression of lipoprotein lipase, which generates TAGs in the adipose from circulating LP

50
Q

what increases anabolic actions and decreases catabolic actions

A

insulin

51
Q

what catabolic actions are decreased in absorptive state

A

glycogenolysis in muscle and liver
gluconeogenesis in the liver
keton production in the liver
adipocyte lipolysis

52
Q

how is glycogenolysis in the muscle & liver inhibited

A

insulin inhibits glycogen phosphorylase

53
Q

how is adipocyte lipolysis inhibited

A

insulin reduces intracellular lipase activity

54
Q

summary of glucagons actions in PA state

A

increases glycogenolysis, gluconeogenesis and ketogenesis

55
Q

name 3 anabolic processes that occur in PA state

A

glycogenolysis
gluconeogenesis
ketogenesis

56
Q

what effect does glucagon have on the liver

A

stimulates glucose production through glycogenolysis, gluconeogenesis & ketone production

57
Q

steroid glucocorticoid produced by the adrenal cortex

A

cortisol

58
Q

what type of hormone is cortisol

A

steroid glucocorticoid

59
Q

where is cortisol produced

A

adrenal cortex

60
Q

does cortisol have a quick or slow time frame

A

slow - days to weeks

61
Q

purpose of cortisol in fuel homeostasis

A

maintains liver and adipose enzymes for gluconeogenesis & lipolysis

62
Q

disease from cortisol deficiency

A

addison’s

63
Q

addison’s disease is caused by

A

cortisol deficiency

64
Q

disease from excessive cortisol levels

A

cushing’s syndrom

65
Q

cushing’s sydrome is caused by

A

excessive cortisol

66
Q

what happens is cortisol levels are deficient

A

metabolic response to PA stage is prevented = addisons disease

67
Q

what happens if cortisol levels are too high

A

body is in a constant PA state and opposes the effects on insulin

68
Q

what can cushing’s sydrome be mistaken for and why

A

diabetes because excessive cortisol levels keeps the body in a constant PA state and opposes the effects of insulin

69
Q

what type of hormone os growth hormone

A

polypeptide

70
Q

where is growth hormone produced

A

anterior pituitary under control of the hypothalamus

71
Q

what hormone makea adipose more sensitive to lipolytic stimuli

A

growth hormone

72
Q

what effect does growth hormone have an adipose?

A

makes it more sensitive to lioplytic stimuli

73
Q

what effect does growth hormone have on the liver

A

increases gluconeogenesis

74
Q

how does growth hormone effect insulin?

A

opposes the metabolic effects of insulin, like cortisol. Iless glucose will be uptaken by peripheral tissue

75
Q

what do growth hormone and cortisol have in common?

A

both oppose the effects of insulin

76
Q

Where are T3 and T4 produced

A

thyroid follicles

77
Q

what are T3 and T4

A

iodinated tyrosine derivatives

78
Q

lack of TH causes

A

cretinism

79
Q

cause of cretinism

A

lack of TH

80
Q

cretinism results in

A

severe underdevelopment of the CNS; cretinism

81
Q

what sets the BMR of most tissues

A

Thyroid hormone

82
Q

how does TH effect BMR

A
  • sets BMR in most tissues
  • increases mitochondrial oxidative phosphorylation to regualte fuel usage
  • increases plasma membrane Na/K ATPase activity
  • regulates the expression of many enzymes involved in metabolic processes
83
Q

where does adrenaline come from

A

the adrenall medualla

84
Q

what neural control switches off A and turns on PA state

A

adrenaline & sympathetic innervation of islets inhibit insulin and increase glucagon release

85
Q

what stimulates the release of glucagon and inhibtion of insulin

A

adrenaline and sympathetic innervation of islets

86
Q

what does adrenaine and sympathetic innervation do to islet cells

A

inhibits insulin release and stimulates glucogaon release. Switches from A to PA state

87
Q

adrenaline and sympathetic innervation together affect:

A

islets
liver
adipose
NOT muscle

88
Q

how does adrenaline affect skeletal muscles

A

increases glycogenolysis. This is just from circulating adrenaline and s short lived response. Skeletal muscle is not stimulated by symathetic innervation

89
Q

what does adrenaine and sympathetic innervation do to liver

A

directly affect liver to increase glycogenolysis and gluconeogenesis to increase plasma glucose (PA)

90
Q

what does adrenaine and sympathetic innervation do to adipose

A

increase lipolysis (PA)

91
Q

what causes neural control of fuel homeostasis

A

glucose receptors in the hypothalamus

92
Q

short term mechanisms for starvation

A

protein catabolised to generate AA that are converted to glucose by the liver via keto acid pathway

93
Q

long term mechanism for starvation

A

brain adapts to metabolise ketones as well as glucose.

Ketone production primarly from FA to spare protein, for less muscle wastage

94
Q

how is the starvation coping mechanism efficient?

A

after 4 days,, blood glucose is only reduced by a few % and after 1 month only reduced by ~25%

95
Q

what response is similar to that of the starvation response

A

body’s response to exercise

96
Q

what stimulates fuel release during exercise

A

circulating adrenaline and sympathetic innveravation will increase catabolic activity in liver, fat & muscle

97
Q

why does glucagoon rise during exercise

A

counter regulatory effect because:

  • less glucose
  • increased circulatig adrenaline
  • increased sympathetic charge of islets
98
Q

why does insulin fall during exercise

A

becuase there is less glucose, increased circualting adrenaline and increased symathetic charge of islets

99
Q

what happens to glucagon and insulin levels in exercise

A

glucagon increasess and insulin decreases

100
Q

what happens if regualtion of insulin secretion goes wrong?

A

diabetes mellitus

101
Q

no or low insulin causes what to happen in the body

A
  • increased catabolism
  • anabolism cannot occur
  • acidoses due to build up of ketones
  • glucose in urine because kidneys reach saturation of 10 mM
  • water drawn out of blood to filtrate
  • water and salt depletion lead to CVS collapes
102
Q

glycosuria

A

glucose in the urine when blood glucose is abover 10mM because kidneys reach max absoprtion. Diabetes M

103
Q

polyuria and pplydypsia

A

excessive thrist and weeing because what is drawn out of blood into filtrate; occurs in diabetes M

Endocrinology & Reproduction (15 decks)

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