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
neural conrol for maintaining A and PA states
sympathetic nervous system
26
endocrine conrol for maintaining A and PA states
pancreatic hormones (insulin & glucagon), cortisol, growth hormone, thyroid hormones etc
27
excess CHO converted to
fat
28
excess fat stored in
Adipose
29
excess AA converted to
fat
30
CHO stored as
glycogen
31
summary of PA state
gluconeogenesis fatty ocid oxidation glucose sparing through FA oxidation & AA
32
most important hormones for controlling fuel balance
glucagon & insulin
33
dominant hormone in absorptive state
insulin
34
dominant hormone in PA state
gluagon
35
where are the islet of langerhans found
pancreactic cells
36
where are plypeptide hormones made
beta and alpha cells of the prancreatic cells called the islets of langerhans
37
what stimulates insulin release
increased blood glucose
38
what does insulin inhibit
glucagon release
39
what does insulin target
targets the liver, muscle & fat to take up, utilise & store glucose
40
is insulin anabolic or catabolic
anabolic
41
when is glucagon released
when blood glucose falls, during PA state
42
what does glucagon inhibit
insulin release
43
what increases glucose oxidation, glycogen synthesis, fat synthesis and protein synthesis
insulin
44
how does insulin increase glucose uptake in the muscle and liver
increase expression of transporters
45
what transporters take up glucose in the liver
glucose kinase
46
what stimulates glycogen synthesis in the muscle & liver
insulin
47
what does insulin do to AA and protein in muscle
inreases AA uptake and protein synthesis
48
what promotoes synthesis of FA and alpha GP to form TAG in aidpose?
insulin
49
How are TAGs generated from circulatiing lipoproteins
insulin induces expression of lipoprotein lipase, which generates TAGs in the adipose from circulating LP
50
what increases anabolic actions and decreases catabolic actions
insulin
51
what catabolic actions are decreased in absorptive state
glycogenolysis in muscle and liver gluconeogenesis in the liver keton production in the liver adipocyte lipolysis
52
how is glycogenolysis in the muscle & liver inhibited
insulin inhibits glycogen phosphorylase
53
how is adipocyte lipolysis inhibited
insulin reduces intracellular lipase activity
54
summary of glucagons actions in PA state
increases glycogenolysis, gluconeogenesis and ketogenesis
55
name 3 anabolic processes that occur in PA state
glycogenolysis gluconeogenesis ketogenesis
56
what effect does glucagon have on the liver
stimulates glucose production through glycogenolysis, gluconeogenesis & ketone production
57
steroid glucocorticoid produced by the adrenal cortex
cortisol
58
what type of hormone is cortisol
steroid glucocorticoid
59
where is cortisol produced
adrenal cortex
60
does cortisol have a quick or slow time frame
slow - days to weeks
61
purpose of cortisol in fuel homeostasis
maintains liver and adipose enzymes for gluconeogenesis & lipolysis
62
disease from cortisol deficiency
addison's
63
addison's disease is caused by
cortisol deficiency
64
disease from excessive cortisol levels
cushing's syndrom
65
cushing's sydrome is caused by
excessive cortisol
66
what happens is cortisol levels are deficient
metabolic response to PA stage is prevented = addisons disease
67
what happens if cortisol levels are too high
body is in a constant PA state and opposes the effects on insulin
68
what can cushing's sydrome be mistaken for and why
diabetes because excessive cortisol levels keeps the body in a constant PA state and opposes the effects of insulin
69
what type of hormone os growth hormone
polypeptide
70
where is growth hormone produced
anterior pituitary under control of the hypothalamus
71
what hormone makea adipose more sensitive to lipolytic stimuli
growth hormone
72
what effect does growth hormone have an adipose?
makes it more sensitive to lioplytic stimuli
73
what effect does growth hormone have on the liver
increases gluconeogenesis
74
how does growth hormone effect insulin?
opposes the metabolic effects of insulin, like cortisol. Iless glucose will be uptaken by peripheral tissue
75
what do growth hormone and cortisol have in common?
both oppose the effects of insulin
76
Where are T3 and T4 produced
thyroid follicles
77
what are T3 and T4
iodinated tyrosine derivatives
78
lack of TH causes
cretinism
79
cause of cretinism
lack of TH
80
cretinism results in
severe underdevelopment of the CNS; cretinism
81
what sets the BMR of most tissues
Thyroid hormone
82
how does TH effect BMR
- 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
where does adrenaline come from
the adrenall medualla
84
what neural control switches off A and turns on PA state
adrenaline & sympathetic innervation of islets inhibit insulin and increase glucagon release
85
what stimulates the release of glucagon and inhibtion of insulin
adrenaline and sympathetic innervation of islets
86
what does adrenaine and sympathetic innervation do to islet cells
inhibits insulin release and stimulates glucogaon release. Switches from A to PA state
87
adrenaline and sympathetic innervation together affect:
islets liver adipose NOT muscle
88
how does adrenaline affect skeletal muscles
increases glycogenolysis. This is just from circulating adrenaline and s short lived response. Skeletal muscle is not stimulated by symathetic innervation
89
what does adrenaine and sympathetic innervation do to liver
directly affect liver to increase glycogenolysis and gluconeogenesis to increase plasma glucose (PA)
90
what does adrenaine and sympathetic innervation do to adipose
increase lipolysis (PA)
91
what causes neural control of fuel homeostasis
glucose receptors in the hypothalamus
92
short term mechanisms for starvation
protein catabolised to generate AA that are converted to glucose by the liver via keto acid pathway
93
long term mechanism for starvation
brain adapts to metabolise ketones as well as glucose. | Ketone production primarly from FA to spare protein, for less muscle wastage
94
how is the starvation coping mechanism efficient?
after 4 days,, blood glucose is only reduced by a few % and after 1 month only reduced by ~25%
95
what response is similar to that of the starvation response
body's response to exercise
96
what stimulates fuel release during exercise
circulating adrenaline and sympathetic innveravation will increase catabolic activity in liver, fat & muscle
97
why does glucagoon rise during exercise
counter regulatory effect because: - less glucose - increased circulatig adrenaline - increased sympathetic charge of islets
98
why does insulin fall during exercise
becuase there is less glucose, increased circualting adrenaline and increased symathetic charge of islets
99
what happens to glucagon and insulin levels in exercise
glucagon increasess and insulin decreases
100
what happens if regualtion of insulin secretion goes wrong?
diabetes mellitus
101
no or low insulin causes what to happen in the body
- 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
glycosuria
glucose in the urine when blood glucose is abover 10mM because kidneys reach max absoprtion. Diabetes M
103
polyuria and pplydypsia
excessive thrist and weeing because what is drawn out of blood into filtrate; occurs in diabetes M