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Hormonal regulation of intermediary metabolism III Flashcards

1
Q

I. Hormonal regulation of intermediary metabolism
1. What are 1 & 2?

A

1/ Beta cell
2/ Insulin

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2
Q

I. Hormonal regulation of intermediary metabolism
2. What are 1 & 2?

A

1/ Blood glucose
2/ Plasma FFA & ketone body

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3
Q

I. Hormonal regulation of intermediary metabolism
3. What are the 2 things that are increased?

A

1/ Increase glucose uptake and utilization (muscle and adipose)
2/ Increase hepatic conversion of glucose to glycogen and lipids

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4
Q

I. Hormonal regulation of intermediary metabolism
4. What is the thing that is decreased?

A

Decrease hepatic glucose production

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5
Q

I. Hormonal regulation of intermediary metabolism
5. What are the 2 things that are inhibited?

A

1/ Inhibit hepatic ketogenesis
2/ Inhibit HSL and decrease release of FFAs from adipose

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6
Q

I. Hormonal regulation of intermediary metabolism
6. What are happening here?

A

1/ Stimulate secretion
2/ Decrease level
3/ Decrease level

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7
Q

I. Hormonal regulation of intermediary metabolism
2A. If blood glucose level is decreased, what will happen?

A
  • blood glucose level is decreased
    -> alpha cells are stimulated to secrete glucagon
    -> Glucagon:
    1) Stimulate beta cells
    2) Increase hepatic glucose production via glycogenolysis and gluconeogensis
    3) Decrease hepatic conversion of glucose to glycogen or lipids
    4) Increase hepatic ketogenesis
    => Blood glucose, FFA and ketone bodies levels will be increased
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8
Q

I. Hormonal regulation of intermediary metabolism
2B. Which factor inhibit alpha cells to secrete glucagon?

A

Insulin

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9
Q

I. Hormonal regulation of intermediary metabolism
3A. How does decreasing blood glucose level affect sympathoadrenal activity?

A
  • decreasing blood glucose level inhibit sympathoadrenal activity to secrete catecholamines:
    1/ Decrease glucose uptake by adipose and muscle
    2/ Increase release of gluconeogenic substrates from muscle and adipose
    3/ Increase HSL and release FFAs from adipose
    4**/ Stimulate alpha cells to secrete glucagon
    => Increase blood glucose level
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10
Q

II.
1. Which condition that fits these charts?

A
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11
Q

II. Draws the chart that demonstrate plasma cortisol level that corresponds to stress

A
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12
Q

III. Other hormones
1A. What are the effects of glucocorticoids in case of stress?

A

CNS in respond to stress
-> ACTH
-> Glucocortidcoids
-> Effects:
1/ Proteolysis ↑
2/ Insulin sensitivity↓
3/ Potentiation of epinephrine and glucagon effect
4/ Gluconeogenesis (enzyme expression)

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13
Q

III. Other hormones
1B. Glucocorticoids can cause Insulin sensitivity↓. How?

A

– IR kinase activity ↓
– Plasma membrane GLUT-4 ↓
– Phosphodiesterase inhibition

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14
Q

III. Other hormones
1C. Glucocorticoids can causePotentiation of epinephrine and glucagon effect? How?

A

Phosphodiesterase inhibition

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15
Q

III. Other hormones
1D. What happen in fasting? (glucocorticoids (cortisol))

A

In fasting, its basal level is necessary for the effects of hypergylcemic hormons

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16
Q

III. Other hormones
1E. What are permissive effects of glucocorticoids (cortisol)?

A

1/ β-receptor
2/ glucagon secretion
3/ cAMP signal transduction

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17
Q

III. Other hormones
1F1. Draw a schematic diagram explaining effect of cortisol in skeletal muscle?

A
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18
Q

III. Other hormones
1F2. Draw a schematic diagram explaining what happen if we there is no cortisol in skeletal muscle?

A
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19
Q

III. Other hormones
1G1. Draw a schematic diagram explaining effect of cortisol in fat tissue?

A
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20
Q

III. Other hormones
1G2. Draw a schematic diagram explaining what happen if we there is no cortisol in fat tissue?

A
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21
Q

III. Other hormones
1H1. Draw a schematic diagram explaining the effects of cortisol in the liver

A
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22
Q

III. Other hormones
1H2. Draw a schematic diagram explaining what happen if there is no cortisol in liver?

A
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23
Q

III. Other hormones
2. What are the acute effects of high cortisol level on the intermediary metabolism (fasting/acute
stress)

A

Potetiation of epinephrine and glucagon effects
* Permissive effect for β-receptor and glucagon expression
* Augmentation of cAMP signal transduction– PDE inhibition

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24
Q

III. Other hormones
3A. What are the Effects of chronic elevation in cortisol on intermediary metabolism?

25
Q

III. Other hormones - Effects of chronic elevation in cortisol on intermediary metabolism
3B. What happens here?

A

Plasma glucose ↑
Plasma FFA ↑

26
Q

III. Other hormones - Effects of chronic elevation in cortisol on intermediary metabolism
3C. What happens here?

A

1/ Plasma insulin ↑
2/ BUT Plasma glucose ↑
3/ Plasma FFA ↑ persist

27
Q

III. Other hormones - Effects of chronic elevation in cortisol on intermediary metabolism
3D. What happens here?

A

1/ Synergic effects with insulin
2/ Lipogenesis in central fat tissues ↑

28
Q

III. Hormones - Effects of chronic elevation in cortisol on intermediary metabolism
3E. What happen here?

A

1/ Fat cell differentiation↑; Lipogenesis ↑
2/ Glycogen synthesis in the liver

29
Q

III. Other Hormones - Effects of chronic elevation in cortisol on intermediary metabolism
3F. What happen here?

A

1/ Liver gluconeogenesis ↑
2/ Muscle, fat insulin sensitivity ↓
3/ Muscle, fat glucose uptake ↓
4/ Lipolysis ↑
5/ Proteolysis ↑

30
Q

III. Other Hormones
4. Explain Glucocorticoid metabolism in central fat tissues

31
Q

III. Other Hormones
5. Draw a schematic diagram explaining hypoglycemia and plasma growth hormone level

32
Q

III. Other Hormones
6. What happen if growth hormone is inhibited?

33
Q

III. Other Hormones
7. What are direct effects of GH?

34
Q

III. Other Hormones
8. What are INdirect effects of GH?

35
Q

III. Other Hormones
9. What are the thresholds for the effects of hyperglycemia?

36
Q

III. Other Hormones
10A. What is ketogenic diet?

A

Ketogenic diets: from cancer to mitochondrial diseases and beyond

37
Q

III. Other Hormones
10B. What are the consequences of ketogenic diets?

A

1/ Increasing mitochondrial function
2/ Increasing mitochondrial biogenesis
3/ Decreasing oxidative stress
4/ decreasing MtD pathogenic mutation

38
Q

III. Other Hormones
10C. Identify

39
Q

III. Other Hormones
10D. Identify

40
Q

III. Other hormones
11A. How do thyroid hormones affect glucose level?

A

1/ Glucose uptake by intestine (liver) (GLUT-2) ↑
2/ Gluconeogenesis ↑
3/ Glycogenolysis ↑
4/ Glycolysis ↑
5/ Glucose turnover ↑

41
Q

III. Other hormones
11B. How do thyroid hormones affect fatty acids level?

A

1/ Lipolysis ↑
2/ FFA synthesis ↑
3/ FA oxidation ↑
4/ Lipid turnover ↑

42
Q

III. Other hormones
11C. How do thyroid hormones affect protein level?

A
  • Proteolysis ↑
  • Protein synthesis ↑
    Protein turnover ↑
43
Q

III. Other hormones
11D. What are other effects of thyroid hormone?

A
  • ß-receptor expression (permissive effect) adrenergic effect augmentation
    • glucagon, GH, cortisol effect augmentation
44
Q

III. Other hormones
12. What is the role of androgens? (sex steroids)

A

1/ Protein synthesis ↑
2/ Lipolysis ↑
3/ Lipogenesis ↓
4/ Fat accumulation in central fat tissues ↑
5/ Insulin sensitivity ↑ (in man)

45
Q

III. Other hormones
13. What is the role of Estrogens/progesteron? (sex steroids)

A

1/ Protein synthesis ↑
2/ Lipolysis ↑
3/ Lipogenesis ↓
4/ Fat accumutaion in subcutaneous fat tissues ↑
5/ Insulin sensitivity ↑ (estrogen)
6/ BUT Insulin sensitivity ↓ (progesteron)

46
Q

III. Other hormones
14. Draw the schematic diagram explaining PCO?

47
Q

IV. Role of fat tissues in energy metabolism
1. What is the Role of fat tissues in energy metabolism?

A
  1. Triglyceride storage
  2. Production of peptide mediators; adipocytokines/adipokines
48
Q

IV. Role of fat tissues in energy metabolism
2. How is the production of adipokines regulated?

A

The production of adipokines is substantially regulated by the triglyceride content of fat
cells, the general nutritional status

49
Q

IV. Role of fat tissues in energy metabolism
3. Where is adipokines regulated?

A

Adipokines produced by fat cells

50
Q

IV. Role of fat tissues in energy metabolism
4. Make a schematic diagram explaining effects of adipokines

51
Q

IV. Role of fat tissues in energy metabolism
5. Make a schematic diagram explaining effects of adipokines in the liver

52
Q

IV. Role of fat tissues in energy metabolism
6. Make a schematic diagram explaining effects of adipokines on insulin and glucagon production

53
Q

IV. Role of fat tissues in energy metabolism
7. What is the role of leptin?

A

1/ reduces apetite
2/ inhibits insulin secretion
3/ insulin resistency ? (in fat)
4/ increases fatty acid oxidation

54
Q

IV. Role of fat tissues in energy metabolism
8A. What is the role of Adiponectin?

A

1/ Subcutaneous fat storage
2/ Other tissues (liver, muscle, pancreatic islets)
3/ Insulin sensitivity increases
4/ Reduces TNFα and IL-6 production

55
Q

IV. Role of fat tissues in energy metabolism
8B. Adiponectin also affects Subcutaneous fat storage
-> What are the effects involved?

A

– Fat tissue hyperplasia
– Activity of LPL is increased
– Increased lipid storage

56
Q

IV. Role of fat tissues in energy metabolism
8C. Adiponectin also affects Other tissues (liver, muscle, pancreatic islets)
-> What are the effects involved?

A

– Reduced lipid level
– Reduced ectopic fat storage

57
Q

IV. Role of fat tissues in energy metabolism
8D. Adiponectin also increase Insulin sensitivity increases
-> What are the effects involved?

A

– Plasma glucose level decreases
– Plasma FFA level decreases

58
Q

IV. Role of fat tissues in energy metabolism
8F. Adiponectin also Reduces TNFα and IL-6 production
-> What are the effects involved?

A

Anti-inflammatory effect (important in the prevention of atherosclerosis)

59
Q

IV. Role of fat tissues in energy metabolism
9. What is the role of PPARγ
(peroxisome proliferator activated receptor γ)?

A Physiology (20 decks)

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