1.3 Endocrine Regulation of Growth Flashcards
What is/isn’t the definition of growth?
- Progressive increase in the size of an organism, requiring net synthesis of proteins
- NOT increase in mass associated with fluid retention
How does the predominance of certain hormones during growth change from foetal/infancy/childhood/puberty?
Foetal: IGF-1 and 2
Infancy: GH and thyroxine
Childhood: GH-IGF-1 axis and thyroxine
Puberty: androgens added in
Why might somatostatin be released by the pancreas (hint: what’s detecting it?) What effects might it exert on the endocrine pancreas itself?
- Inhibits the release of pancreatic hormones
- Therefore, can be triggered by insulin when blood sugar is low, and triggered by glucagon when blood sugar is high
This cell type makes up about half of all cells in the anterior pituitary…
Somatotrope (cells that release Growth Hormone)
Role of IGF-1 vs IGF-2
IGF-1: Exerts effect on most tissues in body (stimulates cell growth, inhibits apoptosis)
IGF-2: Promotes growth during gestation
List some factors that can increase secretion of growth hormone
- Decreased blood sugar
- Sleep
- Exercise
- Stressors / excitement / trauma (of certain levels)
- Increased blood amino acids (GH will pull them into muscle)
- Grehlin release
What is grehlin? When is it released?
- Grehlin is a hormone
- It is released in response to an empty stomach; sometimes called “hunger hormone”
Which negative feedback loops/factors might decrease GH release?
- High somatomedins/GH
- High blood sugar
- High blood fatty acids
- Obesity
List as many actions of somatomedins as you can think of
- Hypertrophy + hyperplasia
- Interstitial bone growth
- Increased protein synthesis
- Epiphyseal plate proliferation
List as many actions of GH as you can think of
- Amino acids pulled into muscle
- Gluconeogenesis
- Lipolysis
- Increased blood sugar
What is the receptor type of GH receptors? What is the outcome of this similar to?
- JAK/STAT receptors
- Outcome is altered gene transcription (and therefore protein synthesis)
- Similar in outcome to steroid receptors (but extracellular)
Acromegaly vs gigantism
Both involve hypersecretion of growth hormone.
If in childhood; bone keep growing in proportion length-wise, so this results in gigantism (Yao Ming). Also increased risk of diabetes (high blood sugar, insulin resistant)
If after childhood; body resorts to appositional growth, so this results in thickening of bones and acromegaly (like Grawp)
How is acromegaly/gigantism treated?
- Somatostatin analogues (decrease GH)
- Surgery to remove tumour on anterior pituitary
Why can negative psychological factors decrease GH release?
- The hypothalamus is circumventricular (exposed to substances outside the blood brain barrier)
- Therefore, if stress hormones are high, can damage hypothalamus
- In this case, less ability to produce GHRH; therefore less GH release