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Endocrine > Physiology: Endocrine Control of Metabolism: Nutting > Flashcards

Physiology: Endocrine Control of Metabolism: Nutting Flashcards

1
Q

What happens to insulin after a meal?

A

Increases 3-6 fold

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2
Q

What does insulin do overall?

A

Promotes utilization and storage of glucose

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3
Q

Does glucagon have any peripheral effects?

A

No, it is mainly active at the liver.

The pancreatic vein goes directly to the portal system… anatomy!

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4
Q

What does glucagon do in the liver?

A

Promote breakdown of stored products and creating new glucose

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5
Q

What is the purpose of glucagon?

A

To keep glucose constant during fasting, mainly for our nerves

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6
Q

How long would our circulating glucose last without adding to it?

A

1 hour

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7
Q

How much time would the glucose in our livers supply us?

A

1/2 day

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8
Q

How much time would the glucose in our muscles supply us?

A

1 day

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9
Q

How many g glygoen stores of glucose is stored in liver and muscle?

A

100g liver

200g muscle

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10
Q

How much time would our fat stores last us?

A

30-40 days! Fat is the most efficient storage source.

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11
Q

What cells can only live on glucose?

A

Nerves
RBC
WBC
Renal tubules

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12
Q

What proportion of the glucose do nerves take of the cells who only use glucose?

A

3/4! 150g to 50g

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13
Q

What percent is muscle of body mass?

A

50%

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14
Q

What percent of energy does muscle use at rest?

A

30%

So effecting muscle metabolism has a big effect!

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15
Q

What does muscle prefer to burn?

A

FA
Ketones
rather than glucose and AAs

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16
Q

When is muscle glycogen utilized?

A

Heavy excercise

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17
Q

What organs have glycogen?

A

liver
kidney
muscle

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18
Q

What happens with muscle glycogen is depleted?

A

It doesnt work well.

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19
Q

What organ (other than pancreas) sees the highest concentration of insulin?

A

Liver

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20
Q

What organ is most responsive to insulin?

A

Liver

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21
Q

What are the objectives of the body during feeding?

A
  1. fill Glycogen stores
  2. dont spill much glucose in urine
  3. utilize carbs and fats for energy
  4. package excess for later (aa–>protein)
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22
Q

What are the main biochemical pathways SHUT DOWN during feeding?

A 
Gluconeoenesis
Glycogenolysis
Lipolysis
Ketogenesis
Protein degradation
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23
Q

What is glucose’s effect in fat?

A

Esterify FA to store triglycerides

Stop making FA to ship

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24
Q

What are FA and ketones action in muscle during FASTING?

A

decrease Glucose utilization

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25
Q

Do FA and Ketones need insulin to get into tissues?

A

NO!

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26
Q

Why are FA stored in Fat? Why are they shipped?

A

Storage: esterified
Ship: not esterified

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27
Q

What are the objectives during fasting?

A
  1. Keep glucose constant for CNS
  2. Decrease glucose utilization elsewhere
  3. Keep some glycogen reserves
  4. Burn fat for FA and Ketones energy
  5. Utilize “sparable” proteins (AA (mainly alanine)) glycerol, and lactate, for gluconeogeneisis
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28
Q

Fat cells make FA and glycerol. What happens to they glycerol?

A

Gluconeogenesis in the liver

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29
Q

The liver makes glucose out of what in fasting?

A 
Glycogen
AA's (from muscle)
Glycerol (from fat)
-----
Lactate (from RBC)
Pyruvate
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30
Q

What do Nerves, RBC, WBC make when they eat up the glucose?

A

Lactate

Pyruvate

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31
Q

What portion of FA is burned directly by cells that can use them? What portion burned as Ketones?

A

2/3 FA

1/3 Ketones

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32
Q

How large is the glycogenolysis between meals?

A

Only SMALL… we want to keep some

Mainly lipolysis and protein degradation

33
Q

What are the short acting hormones of metabolism?

A 
Insulin
Epi
NE
Glucagon
****powerful and short=activity  +/-
34
Q

What are the long acting hormones of metabolism?

A 
GH
T3/T4
Glucocorticoids (Aldo)
Sex steroids
****weak and long lasting=efficiency
35
Q

Does GH go up or down in fasting?

A

Up

36
Q

Does cortisol go up or down in fasting?

A

About steady… slightly down. Necessary for life.

37
Q

Does SNS go up or down in fasting?

A

Up

38
Q

Does T3 go up or down in fasting?

A

Down.

This is a protective action to decrease metabolism use of glucose.

39
Q

What is normal fasting insulin level?

A

10

40
Q

What is normal fed insulin level?

A

90

41
Q

At what level does glucose equalize during fasting?

A

70

42
Q

What happens to SNS during a meal?

A

Goes down

43
Q

What hormones increase protein synthesis during a meal?

A

T3
GH
*insulin obviously…

44
Q

What is very important about cortisol during fasting?

A

Is is PERMISSIVE to gluconeogenesis with Insulin/NE/E

45
Q

What is important about GH during fasting?

A

It is permissive to lipolysis with NE/E

46
Q

What synergizes with GH/Epi/NE to allow lipolysis during fasting?

A

T3

47
Q

What short hormone is active in a meal?

A

Insulin

48
Q

What decreases insulin secretion during a fast?

A

Epi and NE (not glucagon??)

49
Q

What short hormone is active in a fast?

A

Glucose

NE/E

50
Q

What are the moderators of Glucose production in liver?

A

+: NE/E/Glucagon/Glucocorticoids

-: Insulin

51
Q

What are the moderators of glucose consumption in the muscle and fat?

A

+: insulin
-: Glucocorticoids/GH weak
(NOT E/NE/Glucagon!!!!)

52
Q

What is effect of cortisol on glucose? TEST

A

Not direct. Weak alone. Permissive!

53
Q

What is the effect of NE/E on glucose?

A

Increase more than glucagon

54
Q

What is the effect of glucagon on glucose?

A

Increase more than cortisol

55
Q

What is the effect of E/Glucagon

A

Synergistically higher

56
Q

What is the effect of Cortisol/E/Glucagon

A

Permissively more synergistically higher! Highest!

57
Q

Why is it so important to have cortisol once a day?

A

To allow glucagon and epinephrine to work to keep glucose levels high

58
Q

What are the major lypolytic hormones?

A

NE/E–>cAMP–>lipase–>FA

59
Q

What is the major antilipolytic hormone?

A

Insulin–>decrease cAMP

60
Q

What makes NE/E more effective lipolitic? TEST

A

T3/T4
Cortisol
GH

61
Q

What moderates glucose conversion to alpha glycerol (which becomes TG in fat)?

A

+: Insulin

-: GH, Cortisol (NOT T3…)

62
Q

Decrease activity of Hormone sensitive lipase to do what?

A

Decrease FA production, decrease ketones

63
Q

How long does lipolysis take via NE/E? GH?

A

NE/E=mins

GH=hours

64
Q

How do Glucocorticoids promote permissiveness in the liver?

A 
Increased syn: 
    Glycogen synthetase
    G6Phosphatase
    PEP CK
    PE Carboxylase (PC)  (shung Pyruvate up)
    Transaminase (shunt AAs up)
65
Q

How do Glucocorticoids promote permissiveness in the periphery?

A

Muscle: Increase AA release by decreased PS
Fat: increase Glycerol release (works with GH and T3)

66
Q

What do PEPCK and PC do in liver?

A

Shunt pyruvate back up to G6P for gluconeogenesis ship out

67
Q

What does G6Pase do in liver?

A

Locks G in, sends G out

68
Q

What does Glucocorticoid increase in AA breakdown cause?

A

Urea formation: increase BUN

69
Q

Glucocorticoids in liver are permissive for:

A

Gluconeogenesis

Lipolysis

70
Q

What happens to plasma glucose in exercise?

A

Stays same

71
Q

What happens to muscle glucagon in exercise?

A

Down

72
Q

What happens to FA in exercise?

A

UP

73
Q

What happens when you “hit the wall” in exercise?

A

Muscle is out of glycogen

74
Q

What are the hormone changes in extended moderate exercise?

A

+: Up: GH, Cortisol, Glucagon, NE, Epi

-: Down: Insulin

75
Q

Test: What keeps us from dying of hypoglycemia?

A
  1. Eat

2. Get glucose into cells: insulin

76
Q

What glucose level stops insulin? Starts G/G/E? C? Symptoms?

A

80
70
60
50

77
Q

Cortisol is increased by what 2 hormones?

A

CRH

ACTH

78
Q

At what glucose level does the liver increase gluconeogenesis even without hormones?

A

47… 45 is cognition error…

Endocrine (15 decks)

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