Date post: | 18-Nov-2014 |
Category: |
Health & Medicine |
Upload: | yapa |
View: | 2,910 times |
Download: | 4 times |
HORMONES INVOLVED IN BONE
METABOLISM
by Yapa Wijeratne
Faculty of MedicineUniversity of Peradeniya Sri Lanka
1. PTH
2. Calcitriol
3. Calcitonin
4. Oestrogen
5. Cortisol ( glucocorticoids)
6. Thyroid hormones
7. Insulin
8. GH
9. IGF
1.PTH
Secreted by Chief cells of the parathyroid gland 84 amino acid(AA) ↓ [Ca+2]ECF (+) secretion ↑ [PO4
-3]serum
PTH active PTH(amino terminal fragment)
1-84 1-34
carboxy terminal fragment
35-84
PTH
Act directly on bones –
1. ↑osteoclast (OC) activity to ↑bone resorption → ↑mobilize [Ca+2] → ↑[Ca+2]serum
2. ↓Reabsorption of [PO4-3]in PCT
3. ↑Reabsorption of [Ca+2] in DCT
4. ↑ formation of 1,25 DHCC & this ↑ [Ca+2] absorption from the intestine.
2.Calcitriol
1. ↑Transcription of calbinding D protein in the intestine.
2. ↑Intestinal Ca+2 absorption by facilitating Ca+2
transport.
3. Facilitates Ca+2 reabsorption in the kidney.
4. ↑The synthetic activity of osteoblast (OB) & is necessary for normal calcification of matrix
3.Calcitonin
By Parafollicular cells of thyroid gland. 32 AA Secretion is regulated by serum[Ca+2].
1. Inhibit OC bone resorption
2. ↑Ca+2 Excretion in the urine
4.Estrogen
1. ↑OB functions
2. ↓OC functions
3. ↓Renal excretion of Ca+2 & PO4-3
4. ↓intestinal excretion of Ca+2 & PTH function
5. Cortisol ( glucocorticoids)
lower plasma Ca2+ levels by inhibiting osteoclast formation and activity.
Over long periods they cause osteoporosis by ↓bone formation & ↑bone resorption.
1. ↓bone formation by inhibiting protein synthesis in OB.
2. ↓Absorption of Ca+2 & PO4-3 from the intestine
3. ↑Renal excretion of Ca+2 & PO4-3
6. Thyroid hormones
Promote normal growth and skeletal development. May cause hypercalcemia, hypercalciuria, and, in
some instances, osteoporosis.
7. Insulin
↑Bone formation (via OB activity) DM → ↓insulin → Significant bone loss in
untreated DM.
8.GH Anabolic effect on bone Promotes the growth of the skeleton These effects in are believed to be mediated by IGF I & II
acting on cells of the OB.
↑urinary excretion of Ca+2 & hydroxyproline ↑Intestinal absorption of Ca+2
NET EFFECT (+) Ca+2 balance
↓urinary excretion of PO4-3
9.IGF -I
Long arm of chromosome 12 & produces a 70 AA polypeptide.
Receptor (®) IGF-I = insulin ® → stimulates Tyr kinase activity &
autophosporylation of the Tyr residue in ® → cell differentiation & division
IGF-I
1. Stimulate Growth without GH
2. Stimulate Protein synthesis in bone
3. Has stimulatory effect on1. Hematopoiesis
2. Ovarian steroidogenesis
3. Myoblast proliferation
4. Differentiation of lens
IGF-II
67 AA peptide Short arm of chromosome 11 [IGF II]plasma vary with
Age Physiological condition (peak during puberty)
Neonates children puberty adult
IGF-BPS
IGF molecules in the circulation are mostly bound to variety.
IGF-BPS I (-) action of IGF I It is present in ↑ [ ] in fetal serum & amniotic fluid.