yana-notes

Growth Hormone

links: Hormones reference:

Growth Hormone (GH) #

Released by the Pituitary Gland.

  • Estrogen causes growth hormone to increase Peat
  • Opposes Insulin.
  • Anti-aging: increases hair growth, improves complexion
  • Increases bone density, quality/duration of heart, kidneys,
  • Knockout mice to not have age-related degeneration in Testosterone secretion.
  • Transgenic overexpression of growth hormone in mice promotes significantly faster cognitive aging with 5 month old transgenic gh overexpression mice having the cognitive function of 25 month old wild type mice
  • Spatial memory is enhanced in long-living Ames dwarf mice and maintained following kainic acid induced neurodegeneration
    • Ames dwarf mice have no decline in cognitive function with age and live 70% longer than wild type.
  • https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/ames-dwarf-mouse
    • Ames dwarf mice are almost completely lacking in Pituitary Gland somatotropes, lactotrophs, and thyrotropes.
  • Effects of Growth Hormone on Glucose and Fat Metabolism in Human Subjects
    • It therefore was unexpected when Beshyah and colleagues observed an increased prevalence of abnormal glucose tolerance among GH-deficient adults as compared with healthy, age- and sex-matched con-trol.
    • Jessen and colleagues [34] were unable to demonstrate any significant suppressive effect of GH on PI3 kinase activity in normal subjects even though GH significantly stimulated lipolysis and in-duced insulin resistance.
    • Endogenous GH secretion in normal subjects is stimulated during fasting and is accompanied by low levels of insulin. Concomitantly, substrate metabolism is shifted toward lipid oxidation. When glycogen stores are depleted, glucose oxidation relies on gluconeogenesis from protein. In a series of studies Norrelund and colleagues [28] have demonstrated that in the fasting state (42 hours) GH is essential for the ongoing release and oxidation of FFA [28]. At the same time GH reduces insulin sensitivity as indicated by muscle uptake of glucose. These effects translate into reduced protein breakdown in muscle and at the whole-body level. The lipolytic effects of GH during fasting, which could be considered the natural domain of GH, thus seem to result in protein sparing.
  • [Effects of growth hormone on glucose metabolism and insulin resistance in human]
    • Increased the mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and Glucose 6-Phosphatase, in mouse hepatocytes
    • Increased hepatic Glycogen content (and therefore one would assume synthesis)
    • Stimulates Lipolysis via increasing Hormone-sensitive lipase in visceral adipose, increasing FFA flux from adipose to circulation.
  • Effects of growth hormone on glucose metabolism
    • There is however evidence that GH acutely decreases glucose oxidation (secondary to an increase in lipid oxidation) and suppresses muscle uptake of glucose, suggesting that GH redistributes glucose fluxes into a non-oxidative pathway, which could be a build up of glycogen depots through gluconeogenesis.
    • Under pathological conditions of GH excess (e.g. acromegaly, poorly controlled tp. 1 diabetes or high dose GH treatment) the diabetogenic actions of GH become apparent