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Endocrinology and Reproduction > Growth Hormone and IGF-1 > Flashcards

Growth Hormone and IGF-1 Flashcards

1
Q

Mediates growth and metabolic functions to include cell proliferation and differentiation, and serum glucose concentrations

A

Growth Hormone

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2
Q

GH is an anabolic hormone. In so doing, it

  1. ) Increases
  2. ) Lowers
A
  1. ) Urinary nitrogen retention

2. ) Serum urea

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3
Q

Target tissues for GH expression express a cell surface receptor consisting of an extracellular ligand binding and cytoplasmic signaling domains. This receptor is the

A

GH receptor

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4
Q

The anabolic actions of GH result from its stimulatory effects on which three things?

A
  1. ) Cellular amino acid uptake
  2. ) Increased gene transcription
  3. ) De novo protein synthesis
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5
Q

GH is an antagonist to the catabolic effects of

A

Glucocorticoids

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6
Q

Promotes lipolysis and this increases the availability of glycerol and free fatty acids as fuel for muscle work

A

GH

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7
Q

During periods of metabolic demand, GH shunts the matabolic pathways from glycogenolysis to the metabolism of FFA into

A

Acetyl-CoA

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8
Q

This increased production of acetyl-CoA is used to produce

A

ATP

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9
Q

GH thus supports the conservation of glycogen stores while decreasing the cellular uptake of

A

Glucose

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10
Q

There are strong relationships between GH and

A

Glycemic status and insuln

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11
Q

GH is the only

A

Proglycemic hormone

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12
Q

Designed to preserve plasma glucose levels by 1) directly blocking glucose uptake by skeletal muscle (promoting insulin resistance), and 2) shunting muscle energy expenditure away from the utilization (oxidation) of glucose to the oxidation of FFA

A

GH

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13
Q

This glucose conservation is of benefit during periods of fasting/starvation when muscle catabolism would be generated by

A

Glucocorticoids

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14
Q

Promote muscle catabolism during periods of fasting/starvation to free up amino acids that can be used to generate ATP

A

Glucocorticoids

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15
Q

Thus acts as a counter modulator to the catabolic actions of glucocorticoids in skeletal muscle

A

GH

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16
Q

GH secretion is suppressed by

A

Acute hyperglycemia

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17
Q

After a meal, insulin is released to promote glucose uptake. The insulin-induced drop in blood glucose in turn stimulates

A

GH secretion

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18
Q

GH tends to slightly raise

A

Blood glucose levels

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19
Q

Should GH remain elevated, we will likely see an increase in the secretion of

A

Insulin

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20
Q

Antagonizes insulin sensitivity in the liver and especially in skeletal muscle

A

GH

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21
Q

This induces an insulin resistant state which maintains

A

Blood glucose

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22
Q

Since elevated GH impairs insulin sensitivity, a subsequent glucose challenge during this insulin resistant period would result in

A

Hyperinsulinemia

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23
Q

Chronic elevation of GH can result in a pathologic condition of

A

Insulin resistance and accompanying hyperglycemia

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24
Q

Work in conjunction under physiologic conditions to stimulate anabolism in bone and muscle tissue

A

GH and Insulin

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25
Q

Insulin and GH each stimulate the cellular uptake of

A

Amino acids and subsequent protein synthesis

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26
Q

A member of the insulin family, and mediates the growth-promoting effect of GH

A

Insulin-like growth factor (IGF-I)

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27
Q

Regulates IGF-I gene transcription

A

GH

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28
Q

Exerts negative feedback on GH secretion

A

IGF-I

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29
Q

Circulating isoforms of truncated IGF-I and GH respectively

A

IGF binding proteins (IGFBPs) and GH binding proteins (GHBPs)

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30
Q

These are produced mainly in the liver, are carrier proteins which extend the half-life of circulating GH and IGF-I, and aid in the delivery of these hormones to target tissues

A

IGFBPs and GHBPs

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31
Q

By extending the half-life of GH, GHBP dampens acute changes in serum GH levels, in part by reducing

A

Renal clearance of GH

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32
Q

Are GH and IGF-I bioactive when they are bound to their respective binding proteins?

A

No

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33
Q

Have been observed with malnutrition, chronic liver disease, and short stature

A

Low GHBP levels

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34
Q

Together, stimulate skeletal muscle growth and proliferation, as well as the growth and deposition of bone

A

GH and IGF-I

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35
Q

In long bones, GH/IGF-I exert mitogenic effects in chondrocytes within the

A

Epiphyseal cartilages (epiphyseal lengthening)

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36
Q

Also promote osteoblast activity, and in so doing, support the deposition of Ca2+ phosphate salts in bone

A

GH and IGF-I

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37
Q

Epiphyseal lengthening has a limited life span, and stops late in adolescence when epiphyseal plates fuse due to rising

A

Estradiol-17B production

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38
Q

The neuroendocrine control of GH secretion resides within the

A

Hypothalamus and anterior pituitary

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39
Q

The ventromedial nucleus of the hypothalamus houses neurons which produce

A

Growth Hormone Releasing Hormone (GHRH)

40
Q

A stimulatory factor that is secreted into the hypophyseal portal vessels

A

GHRH

41
Q

GHRH stimulates the production and release of GH by the

A

Somatotropes (in the anterior pituitary)

42
Q

Express receptors for GHRH, GH secretagogue (stimulatory), dopamine (stimulatory), and somatotroph-release inhibiting factor (SRIF, aka somatostatin, inhibitory), which together represent a few of the central factors that control the secretion of GH

A

Somatotropes

43
Q

GH secretogues and dopamine stimulate the secretion of

A

GH

44
Q

What inhibits the secretion of GH?

A

Somatotroph release inhibiting factor (SRIF)

45
Q

A hormone secreted by the gastric mucosal neuroendocrine cells and the hypothalamus which stimulates GH secretion

A

Ghrelin

46
Q

Hypoglycemia and depressed serum concentrations of certain amino acids also signal the neuroendocrine release of

A

GH

47
Q

Acute hyperglycemia lowers GH secretion, however, GH secretion is stimulated by

A

Chronic Hyperglycemia

48
Q

GH secretion can also be transiently stimulated by high protein meals and the amino acids

A

Arginine and Lysine

49
Q

In general, metabolic and/or physical stress (to include trauma, hypovolemic shock, sepsis, and exercise) stimulate

A

GH secretion

50
Q

Will control GH secretion based upon the central (i.e. hypothalamic) receptor isoform that is most activated

A

Heightened SNS tone

51
Q

Results in stimulation of GH secretion, likely by inhibiting the secretion of somatostatin while increasing seratonin

A

a2 adrenergic response

52
Q

Are coupled to the release of somatostatin and thus down-regulate GH secretion

A

B2 adrenoreceptors

53
Q

There is also a circadian rythm for GH secretion, and this results in an increase in serum GH concentrations during the first hours of

A

Deep (REM) sleep

54
Q

The production of GH is greatest in the child (and through puberty), and following age 20, GH production begins to wane by about

A

14% per decade

55
Q

By approximately 50-60 years of age. GH secretion can be reduced by 60%. This process is called

A

Somatopause

56
Q

Has a short half-life; thus, catching peak versus nadir levels is tricky

A

GH

57
Q

Testing for abnormalities in the GH system relies upon the principles of stimulation and suppression; these are forms of

A

Endocrine dynamic testing

58
Q

Has been shown to be a fairly reliable marker of GH excess

A

Serum IGF-I

59
Q

If GH excess is suspected, we rely upon the suppression of GH by glucose as a form of

A

Suppression testing

60
Q

To conduct this evaluation, the patient is given an oral glucose load (the oral glucose tolerance test, OGGT), and blood GH is drawn at timed intervals after the

A

Glucose load

61
Q

Failure to lower GH below 2ng/mL shows

A

Loss of negative feedback (indicates positive test for GH excess)

62
Q

If GH deficiency is suspected, testing relies upon known mechanisms for the stimulation of GH, so called

A

Stimulation testing

63
Q

Uses insulin tolerance, arginine, GHRH, and exercise to test for GH deficiency

A

Stimulation testing

64
Q

A disease resulting from the abnormal production of GH/IGF-I

A

Acromegaly (hypersomatotrophism)

65
Q

Affects roughly equal numbers of men and women and is often diagnosed in the early-mid4th decade of life

A

Acromegaly

66
Q

Presenting symptoms often include headache and visual field defects (resulting from compression of the neural visual tracts by expanding pituitary mass), and/or a host of reproductive endocrine manifestations ranging from amenorrhea, oligomenorrhea, or galactorrhea to loss of libido and impotence

A

Acromegaly

67
Q

The pathogenesis of acromegaly most commonly results from a

A

GH-producing pituitary tumor

68
Q

Disproportionate thickening of bone tissue can occur,
and this is especially apparent in the jaw (mandible overgrowth), forehead (frontal skull bossing, cranial
ridging), nose, hands, and feet of the adult if there is

A

Abnormally elevated levels of GH in acromegaly

69
Q

Often times, the first signs of acromegaly are

-caused by excess GH targeting essentially all systems with GH and IGF-I receptors

A

Metabolic and cardiovascular problems

70
Q

Can include enlargement of organs, glands, and soft tissues such as the heart, thyroid, spleen, tongue, liver, and kidneys

A

Acromegaly

71
Q

Can increase cardiomyocyte contractility by enhancing intracellular Ca2+

-also induces cardiomyocyte hypertrophy

A

Excess GH

72
Q

GH increases lean body mass by promoting the expansion of total body water (i.e. fluid retention). Second, GH alters vasomotor function, likely due to changes in endothelial structure and function which increase vascular resistance. Thus, GH excess often results in

A

Hypertension

73
Q

Early on in acromegaly, GH-induced increases in HR raise

A

Cardiac output

74
Q

Over time, GH can stimulate the formation of

-leads to Heart failure

A

Biventricular hypertrophy

75
Q

Owing to its stimulatory effect on blood glucose levels, chronic GH in acromegaly can lead to impaired

A

Glucose tolerance, insulin resistance, and diabetes mellitus

76
Q

GH induces volume expansion, resulting in reduced

A

PRA

77
Q

Increases in total body water may be linked with a GH-directed rise in aldosterone levels that has been observed in

A

Acromegaly

78
Q

Results from abnormally elevated levels of GH and IGF-I during childhood and puberty

-essentially the development of acromegaly in children

A

Gigantism

79
Q

Often caused by GH secreting tumores and is linked with insulin resistance and hyperglycemia

A

Gigantism

80
Q

What are two non surgical options to treat gigantism or acromegaly?

A
  1. ) Somatostatin analogue (octreotide)

2. ) GH-R antagonist (pregvisomant)

81
Q

In about 20-30% of certain somatotroph adenomas, GH secretion can be reduced by

A

Dopamine agonism

82
Q

Dopamine receptor agonists which can be effective in the management of some forms of acromegaly

A

Bromocriptine and cabergoline

83
Q

It is believed this mechanism results from a common embryonic lineage of these tumors which couples the mechanism of GH secretion to that of

A

Prolactin (PRL)

84
Q

Dopamine is a potent inhibitor of

A

Prolactin (PRL)

85
Q

Realize though that under normal physiologic conditions, dopamine STIMULATES

A

GH secretion

86
Q

In children, short stature, central obesity, and high pitched voice are signs of

A

GH deficiency

87
Q

In adults, decreased bone density, central obesity, depression, and an abnormal lipid profile are clues to the presence of

-also comes with cardiovascular consequences

A

GH deficiency

88
Q

Conditions of isolated GH deficiency are very rare. Rather GH deficiency is usually associated with

A

Hypopituitarism

89
Q

This condition often manifests with signs resembling

that of metabolic syndrome: central obesity, insulin resistance, dyslipidemia, and atherosclerosis

A

Hypopituitarism

90
Q

When present in children and/or for prolonged duration, GH deficiency can lead to decreased

A

Left ventricular wall thickness and ejection fraction

91
Q

In additional to its purported performance-enhancing actions, GH has been historically difficult to detect since some exogenous GH preparations have a chemical signature that is virtually indistinguishable from that of

A

Endogenous GH

92
Q

What is the half-life of GH?

A

15-20 minutes

93
Q

Data show that while GH replacement does improve physical performance parameters in GH-deficient
adults (e.g., muscle mass; strength; and aerobic capacity, VO2max), studies have indicated that it
probably has no significant performance-enhancing effect in

A

Healthy individuals

94
Q

Increased by GH

A

Lean body mass (LBM)

95
Q

The main performance enhancing benefit of GH

A

It’s lipolytic properties

96
Q

Thus GH is really only beneficial to

A

Body builders

Endocrinology and Reproduction (15 decks)

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