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Endocrinology -- Freedman > Exam 2: Hormonal Regulation of Fuel Metabolism > Flashcards

Exam 2: Hormonal Regulation of Fuel Metabolism Flashcards

1
Q

How is constant supply of metabolic fuel achieved? Where is it stored?

A

storing excess CHO, protein, and fat in:

  1. liver
  2. adipose tissue
  3. skeletal muscle
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2
Q

What are the four body fuels?

A

glucose
glycogen
protein
fat

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3
Q

How do we avoid the extra weight of 22 lbs of glucose storage?

A

turn it into glycogen

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4
Q

What are the two major regulators of fuel homeostasis?

A

endocrine and ANS

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5
Q

What are the two strategies used to maintain the glucose when dietary or stored CHO is deficient?

A
  1. gluconeogenesis (from lactate, glycerol, alanine)

2. inhibition of glucose utilization by those tissues that have an alternate energy source ( FAs, lactate, ketones)

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6
Q

What are the primary fuel hormones that control fuel homeostasis?

A
  1. insulin
  2. epinephrine
  3. cortisol
  4. glucagon
  5. GH
  6. T4 (thyroxine)
  7. leptin
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7
Q

What are the three principal target tissues of primary fuel hormones to help control fuel homeostasis?

A
  1. adipose tissue
  2. liver
  3. skeletal muscle
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8
Q

What is the most abundant and efficient energy reserve?

A

fat

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9
Q

What are the problems with using fat as a metabolic fuel?

A
  1. when convert dietary CHO to fat, ~25% of energy is dissipated as heat
  2. synthesis of FA from glucose is irreversible (eat sugar, get fat)
  3. limited H2O solubility complicated transport
  4. uptake of cells occurs at cell surface after breakdown of FA by lipoprotein lipase
  5. mobilization of stored TGs requires breakdown of FA
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10
Q

How does the uptake of fat occur?

A

FA must be broken down by lioprotein lipase at the cell surface

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11
Q

How efficient is it to FA from glucose and then to make glucose from FA?

A

synthesis of glucose to FA is irreversible

only glycerol portions of TGs remain convertable back to glucose (is only 10% of mass of TGs)

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12
Q

How is fat transported?

A

has limited H2O solubility….so

packaged as LDL or chylomicrons for transport in blood to storage sites

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13
Q

What is required if we want to mobilize the stored triglycerides?

A

must breakdown FA

  • leave adipocyte as free FA
  • not very soluble in water
  • transported in blood bound to albumen (=limited access to tissues like brain)
  • oxygen required for degradation of fat, but not for glucose
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14
Q

How do RBCs get there energy?

A

from glucose (b/c they lack mitochondria and on’t use oxygen)

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15
Q

How much glucose to RBC’s collectively consume each day? What do they release in return?

A

50 grams of glucose/day and release equivalent amount of lactate

lactate readily reconverted to glucose in liver

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16
Q

What do RBCs release as they use glucose for energy? What happens to that substance?

A

release equivalent amount of lactate

–> lactate is readily reconverted to glucose in liver

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17
Q

What does the brain rely on in a healthy individual? About how much does it consume each day?

A

relies on glucose and about 150 grams/day

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18
Q

What uptakes the glucose for the brain? What does it do with it?

A

glia uptake glucose and convert it to lactate which neurons can use

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19
Q

What is the level of blood glucose when fasting? What percentage does the brain us?

A

90 mg/dl

brain extracts 10%

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20
Q

What role do the kidneys play in blood glucose regulation?

A

are capable of gluconeogenesis

- may produce 20-40% of glucose released during fasting

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21
Q

In acidosis what role do the kidneys place to help regulate blood glucose?

A

renal glucose production from glutamate accompanies production and excretion of ammonium

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22
Q

What is the Glucose Fatty Acid Cycle?

A

increase in FA to muscle limits glucose utilization (FA can decrease metabolism of glucose)

increase glucose limits FA utilization (glucose can inhibit availability and oxidation of FA

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23
Q

T/F. Glucose and FA have mutual inhibition.

A

True (FA can decrease metabolism of glucose and glucose can inhibit availability and oxidation of FA)

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24
Q

How is depletion of energy monitored?

A

as accumulation of 5’-AMP relative to ATP

  • -> regulated by AMP:ATP ratio
  • -> the increase in the ratio of 5’-AMP to ATP activates AMPK
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25
Q

What activates AMPK (AMP activated protein kinase)?*

A

the increase of the ratio of 5’-AMP to ATP

also increased by phosphorylation

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26
Q

What does AMPK do?

A

catalyzes reactions that amplify availability of metabolic fuels and dampen ATP consumption

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27
Q

What overrides the competition b/w glucose and FA in ATP deficient states?*

A

AMPK

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28
Q

What is translocated to the cell membrane during exercise to uptake glucose?

A

GLUT 4–> therefore is insulin independent

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29
Q

Overall, what do the effects of AMPK serve to do?

A

serve to INCREASE energy production and DECREASE energy consumption

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30
Q

What will AMPK stimulate in the hypothalamus?

A

increase food intake

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31
Q

What will AMPK stimulate in skeletal muscle?

A

increase glucose transport
– translocate of GLUT 4 into cell membrane, independent of insulin during exercise

  • increase glycolysis
  • decrease glycogen synthesis
  • increase FA oxidation
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32
Q

What will AMPK stimulate in the liver?

A
  • decrease FA synthesis
  • decrease gluconeogenesis
  • increase FA oxidaiton
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33
Q

What will AMPK stimulate in adipose tissue?

A
  • decrease lipolysis
  • decrease FA esterification
  • decrease FA synthesis
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34
Q

What decreases blood glucose?

A

insulin

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35
Q

What increases blood glucose?

A
  • Epi/NE
  • Glucagon
  • Cortisol
  • GH

= counter-regulatory hormones which collectively oppose actions of insulin on blood glucose

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36
Q

What are the hormonal responses with hypoglycemia?

A

(= decrease blood glucose)
Stimulates:
- pancreatic alpha cells to release glucagon
- glucose sensing neurons in hypothalamus and hindbrain
- CRH and GHRH –> increase pituitary ACTH and GH

37
Q

During hypoglycemia, what will stimulating the glucose sensing neurons in the hypothalmus and hindbrain do?

A

they communicate and stimulate autonomic centers to activate SNS outflow to:

  • pancreatic islets of Langerhans (+ glucagon, - insulin)
  • liver (glucoenogenesis)
  • adrenal medulla (increase catacholamines–Epi)
38
Q

What hormones can offset insulin induced hypoglycemia?*

A
  • Epineprine*/NE from adrenal medulla
  • Glucagon* from pancreas
  • Cortisol* from adrenal cortex
  • GH from ant. pit. (not useful for rapid restoration of blood glucose)
39
Q

What three hormones have synergistic effect to raise blood glucose levels?*

A

Epinephrine
glucagon
cortisol

40
Q

What is the short term regulation of blood glucose conc.?

A
  • insulin
  • glucagon (lesser extent catecholamines)
  • liver glycogen is immediate source of blood glucose
41
Q

T/F. Liver is less responsive to insulin than muscle and adipose.

A

FALSE– liver is MORE responsive to insulin (but liver does NOT depend on insulin for uptake of glucose, uses GLUT 2)

42
Q

What effect does insulin have on the liver?

A

will increase glycogen synthesis forcing storage of glucose

43
Q

What occurs when hypoglycemia is perceived by pancreatic alpha cells and glucose sensing cells of the hypothalamus?

A

(short term regulation)

+ SNS –> increase glucagon; decrease insulin
+ ACTH –> cortisol
+ GHRH –> GH (delayed response)

44
Q

How is the overall regulation of blood glucose concentration done long term?

A

depends on action of many hormones

Direct and indirect to ensure:

  • peripheral drain on glucose reserve is minimized
  • that liver contains reservoir of glycogen to satisfy glucose demand
45
Q

What is the central event in adipose tissue metabolism?

A

cycle of FA esterfication and triglyceride lipolysis

46
Q

Under basal conditions, what percent of FAs released in lipolysis are re-esterfied to TGs?

A

20%

47
Q

What does the SNS stimulate on adipose tissue?*

A

SNS –> beta receptors–> increase cyclic AMP –> increase lipolysis

48
Q

What affect does insulin have on adipocytes?
What modulates the sensitivity of adipocytes to insulin?

What will increase lipolysis?

A

insulin decreases lipolysis
and cortisol, T3, GH modulates the sensitivity of adipocytes

catecholamines = increase lipolysis

49
Q

What effect does GH have on adipose tissue?

A
  • increase lipolysis (after 2 hour delay)

- decreases glucose utilization, insulin sensitivity, FA esterfication

50
Q

What effect does insulin have on adipose?

A
  • increases glucose uptake,FA synthesis, FA esterfication, LDL hydrolysis
  • decrease lipolysis
51
Q

What effect does cortisol have on adipose?

A
  • increase lipolysis

- decrease FA esterfication, glucose utilization, insulin sensitivity

52
Q

What effect do catacholamines have on adipose?

A
  • increase lipolysis and glycolysis
53
Q

What effect does T3 have on adipose?

A

increase glucose utilization, lipolysis

54
Q

What effect does insulin have on skeletal muscle?

A
  • increase glucose uptake, glycogen synthesis, protein synthesis
  • decreases protein degradation
55
Q

What effect does cortisol have on skeletal muscle?

A
  • increase protein degradation, fat utilization

- decreases protein synthesis, glucose utilization, insulin sensitivity

56
Q

What effect does GH have on skeletal muscles?

A
  • increases protein synthesis, fat utilization

- decreases glucose utilization, insulin sensitivity

57
Q

What effect do catacholamines have on skeletal muscle?

A

increase glycogenolysis, glycolysis

58
Q

What effect does T3 have on skeletal muscle?

A

increase glucose utilization and fat utilization

59
Q

What affect do insulin, cortisol, GHm catachlamines, and T3 have on the liver?

A

basically the same as it has on adipose and skeletal muscle

60
Q

Out of the liver, adipose, or skeletal muscle, which one does glucagon have an effect over?

A

liver!

- it increases glycogenolysis, gluconeogenesis, ketogenesis

61
Q

T/F. Glucagon can stimulate insulin secretion.

A

True (physiologically not understood though)

62
Q

What effect does insulin have of glucagon?

A

inhibits glucagon

exerts autocrine effects on beta-cells required to maintain secretory response to glucose

63
Q

What effect to NE and Epinephrine have on insulin and glucagon?

A

inhibit insulin secretion

stimulate glucagon secretion

64
Q

What effect does GH and cortisol have on beta cells?

A

increase sensitivity of beta cells

65
Q

What do 30% of inds with acromegaly or Cushing’s disease develop?

A

Type II diabetes mellitus

“diabetogenic effect”

66
Q

What occurs during the Postprandial period?

A
  • process and sequester Energy rich substances absorbed by intestines
    Insulin:
  • release beings in cephalic phase via vagal release of Ach and VIP
  • chyme in SI + incretins (GLP-1 and GIP)
  • beta-cells respond directly to increase glucose and AA in blood
67
Q

When does insulin release begin when we are eating and via what?

A

during cephalic phase via vagal release of Ach and VIP

68
Q

What does chyme in the SI simulate?

A

incretins (GLP-1 and GIP)

69
Q

What occurs during the Post absorptive period (several hours after eating)?

A
  • intestinal absorption completed
  • body draws on fuel stores
  • insulin levels decrease due to glucose levels decreasing (glucagon effects prevail now)
  • GH and cortisol secreted at low basal rates
  • 75% glucose used in BRICKLE/glut 2 tissues
  • blood FFA increases as insulin restraint on adipose increases
  • glycogen storage in liver gradually depleted
70
Q

What occurs during Initial Fasting (>24 hrs after last meal?

A
  • insulin decreased, glucagon and GH increased, intially cortisol follows its basal diural rhythm (peak 7am, trough 2am)
  • cortisol and GH exert restrain on glucose metabolism in muscle and adipose
  • lipolysis increases
  • low insulin permits breakdown of muscle protein –> AAs (alanine) –> gluconeogenesis
71
Q

What occurs during Prolonged Fasting (>3 days)?

A
  • decrease insulin, increase GH–> therefore increase mobilization of FFA
  • cortisol level remain unchanged or slightly decrease
  • ketogenesis driven by glucagon on liver (form ketone bodies from FFA)
  • N excretion low but steady
  • Glycerol liberated from TGs
72
Q

What can occur in extremely obese individuals that are in the Prolonged fasting (>3 days)?

A

slow protein depletion can lead to death before adipose is depleted

73
Q

Even tough cortisol levels do not rise and may actually until late in starvation, why are they still essential for survival?

A

with lack of glucocorticoids, mechanisms for producing and sparing CHO are virtually inoperable –> death from hypoglycemia

74
Q

What happens to the plasma levels of T3 during fasting? what may occur?

A

from decrease conversion of T4 to T3 OR T4 conversion to rT3(inactive form)

–> decreases metabolism

75
Q

What is exaggerated during fasting of the rate of GH secretion?

A

the pusatile pattern is exaggerated

- increase lipolysis, decrease glucose utilization in muscle/adipose, increase glucose production by liver

76
Q

What may happen to individuals that with GH deficiency during fasting?

A

may become hypoglycemic

77
Q

What is our long-term fuel storage?

A

adipose–> adipocytes receive signals to store or mobilize TGs

78
Q

How do adipocytes play a role in communication for long-term fuel storage?

A

secrete hormones that notify brain and other body parts about there state of fullness

79
Q

What may occur when there is an increase number in adipocytes and they are filled to excess?

A

role in development of pathology:

  • –> Metabolic syndrome
  • insulin resistance (type II DM)
  • hypertension
  • atherosclerosis
80
Q

What does adipose secrete?

A

over 50 biologically active peptides = adipokines

–> produced by adipocytes, stromal cells, vascular elements, macrophages, other immune cells

81
Q

What will the secretion of adipokines from adipose be associated with?

A

inflammation, hemostasis and blood pressure regulation

82
Q

What endocrine organ has control over appetite and food intake?

A

hypothalamus

83
Q

We know the hypothalamus controls appetite and food intake, what three things stimulate appetite?

A
  • NPY (neuropeptide Y)
  • AGRP (agouti-related protein)
  • MCH (melanin concentration hormone)
84
Q

We know the hypothalamus controls appetite and food intake, what two things decrease appetite?

A
  • CART (cocaine and amphetamine regulated transcript)

- POMC (proopiomelanocortin)

85
Q

What are hormones whose production and actions are associated with monitoring the mass of adipose stores and have input into hypothamus?

A

adiposity signals:

  • Leptin
  • insulin
  • adipokines (TNF, IL-6, Adiponectin)
86
Q

What are three adipokines?

A

TNF
IL-6
Adiponectin

87
Q

What peripheral satiety signals (GI hormones and neural mechanisms) regulate fuel intake and have effect on hypothalamus?

A

ghrelin

88
Q

What peripheral satiety signals (GI hormones and neural mechanisms) regulates but inhibiting food uptake?

A
  • CCK
  • GLP-1
  • oxyntomodulin
  • Peptide YY
  • Pancreatic polypeptide
  • amylin
89
Q

What three things have peripheral input to hypothalmic feeding and satiety neurons?

A
  1. Adiposity signals
  2. Periphral satiety signals
  3. Circulating nutrients monitored by hypothalamic neurons which provide input into energy homeostasis

Endocrinology -- Freedman (14 decks)

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