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Hormonal regulation of longitudinal bone growth.

Nilsson, Anders, 1958 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för ortopedi,Institute of Surgical Sciences, Department of Orthopaedics
Ohlsson, Claes, 1965 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för internmedicin,Institute of Internal Medicine, Dept of Medicine
Isaksson, Olle, 1943 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
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Lindahl, Anders, 1954 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin,Institute of Laboratory Medicine, Dept of Clinical Chemistry/Transfusion Medicine
Isgaard, Jörgen, 1959 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
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 (creator_code:org_t)
1994
1994
Engelska.
Ingår i: European journal of clinical nutrition. - 0954-3007. ; 48 Suppl 1
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • The regulation of postnatal somatic growth is complex. Genetic, nutritional factors and hormones exert regulatory functions. Hormones that have an established role in the regulation include growth hormone (GH), thyroid hormone and sex steroids. GH promotes mainly the growth of the long bones in terms of final height, while the action of the sex steroids and thyroid hormone is less well known. Longitudinal bone growth is the result of chondrocyte proliferation and subsequent endochondral ossification in the epiphyseal growth-plates. The growth-plate is a cartilaginous template that is located between the epiphysis and the metaphysis of the long bones. GH and insulin-like growth factor-I (IGF-I) have different target cells in the epiphyseal growth-plate. GH stimulates the slowly dividing prechondrocytes in the germinative cell layer while IGF-I promotes the clonal expansion in the proliferative cell layer of a GH primed cell. Thyroid hormone blocks the clonal expansion and stimulates chondrocyte maturation. IGF-I mRNA is primarily regulated by GH, and IGF-I is produced in several tissues such as the liver, muscle, fat and epiphyseal growth plates. However, IGF-I mRNA is also increased during compensatory growth of heart and kidneys and by estrogen in the Fallopian tube in the rat. Nutrition, i.e. energy from fat and carbohydrates and proteins, also influences the final height, but the cellular mechanism of action is not known. The aim of this article is to review hormonal action on longitudinal bone growth.

Nyckelord

Animals
Bone Development
physiology
Cell Division
Epiphyses
cytology
metabolism
physiology
Gonadal Steroid Hormones
physiology
Growth Hormone
physiology
Growth Plate
physiology
Humans
Insulin-Like Growth Factor I
genetics
metabolism
Nutritional Physiological Phenomena
Osteocytes
cytology
metabolism
physiology
RNA
Messenger
Thyroid Hormones
physiology

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