Case 4 - Male Repro and Bone Growth Flashcards
what are the hormonal changes at the onset of puberty?
kisspeptin stimulated - increases GNRH
endocrine cells in APG more sensitive to GNRH =
rise in FSH and LH
ovarian and testicular cells more sensitive to FSH
what is leptin
adipose tissue produces it
feedback control of appetite
adipose tissue absorbs glucose and lipids
releases leptin into blood
leptin binds to HT neurones = suppression of appetite
how is leptin involved in puberty
increase in GNRH dependent on leptin = low levels of leptin = delayed puberty
HCG effects in male fetuses
interstitial cell stimulating effect on testes of male fetus
= production of testosterone in male fetuses until birth
hence grows male organs
7th month = testosterone secreted by fatal testes causes them to descend into scrotum
6 functions of bones
support; skeleton
protection
movement; muscle attached to bone
blood cell production: red and yellow.
triglyceride storage = yellow marrow, pot energy reserve
mineral homeostasis; calcium, phosphate stays within a certain limit
which are the types of bones and an example
flat: frontal in skull
long: humerus
irregular: facial
short: cuboidal, carpal
sesamoid: wherever tendon crosses over at end of bone
define osteoprogenitor cell
flat, elongated uncles
bone stem cell
define osteblast
cuboidal, builds bone
osteoclasts
remove dead bone cells
osteocyte
circular, sits in lacuna. maintains bone homeostasis
what is intramembranous ossification
when compact and spongy bone develops directly from mesenchymal connective tissue. flat bones formed
endochondral ossification
long bones formed this way
process of endochondral ossification
-mesenchymal cells lay down cartilage by differentiation
-bony cola formed by osteoblasts
chondrocytes enlarge n matrix calcifies
chond die bc lack of nutrients
matrix breaks down, cavity forms
artery enters and supplies cavity
osteoblasts lay down bone = primary oss centre
bone is REPLACING hyaline cartilage
osteoclasts form medullary cavity
secondary OC starts to develop
bone collar = periosteum so compact bone on outside and spongy on inside
what are growth plates
epiphyseal cartilage
what is bone age
degree of maturation of a childs bones
process of growth
HT secreted GH releasing hormone
somatotrophs on APG produce GH
GH acts on bones, adipose and liver tissue
liver produces IGF1
GH also stim IGF1 prod from bone
both IGF1 and GH promote growth in long bones, soft tissues and organs
GH
-gene on chr 17 pulsatile breakdown of adipose tissue stim aa transport into muscles stim liver to increase hepatic glucose output n decrease glucose uptake incr in plc circulation ENDOCRINE EFFECTS
how does the GH receptor help to produce a protein
enzymes coupled: when gH binds, receptor recruits enzyme
present in cell surface
induces conformational change
recruits enzyme JAK2
pplation of enzyme = activated
able to recruit stat 5, becomes pplated
pplated stat5 moves from cytoplasm = nucleus
binds to genes w response element for stat5
transcription of gene
IGF1
gene on chromosome 12 not pulsatile stim muslces to take up aa stim lipogenesis in liver; decreases plc output from liver, reduces circ glc levels ENDOCRINE in liver PARACRINE in bone
how does the IGF1 receptor work
enzyme coupled
enzyme built in, needs to be phosphorylated
cascade - PL3 kinase pathway = survival metabolism
how do the IGF binding proteins work
6
IGF carried mainly w IGFBP3
complex reaches cell, protease breaks down binding protein
exposes IGF to recept, or and binds
what are the two pathways the iGF and receptor can take
cell survival
proliferation MAP kinase
activation of enzyme kinase
when enzyme activated = enzyme adds pp mol to protein
activates it
phosphorylates next one
can also deactivate by removing
use of oestrogen in growth
resp for growth plates closing
acts on reserve zones
