Involvement of bone in systemic endocrine regulation

Title:

Involvement of bone in systemic endocrine regulation

Creator:

Ivana Žofková

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:f4163189-f81c-401e-9f46-fc601f9e6dcb
uuid:f4163189-f81c-401e-9f46-fc601f9e6dcb
issn:0862-8408

Subject:

osteocyty, mužské pohlavní ústrojí, osteocytes, male reproduction tract, sclerostin, phosphatonins, FGF23, Klotho α, phosphate homeostasis, 1,25(OH)2 vitamin D, chronic kidney disease, osteoblasts, osteocalcin, insulin secretion, insulin tissue sensitivity, testosterone expression, 14, and 612

Type:

model:article and TEXT

Format:

print, bez média, and svazek

Description:

The skeleton shows an unconventional role in the physiology and pathophysiology of the human organism, not only as the target tissue for a number of systemic hormones, but also as endocrine tissue modulating some skeletal and extraskeletal systems. From this point of view, the principal cells in the skeleton are osteocytes. These cells primarily work as mechano-sensors and modulate bone remodeling. Mechanically unloaded osteocytes synthetize sclerostin, the strong inhibitor of bone formation and RANKL, the strong activator of bone resorption. Osteocytes also express hormonally active vitamin D (1,25(OH)2D) and phosphatonins, such as FGF23. Both 1,25(OH)2D and FGF23 have been identified as powerful regulators of the phosphate metabolism, including in chronic kidney disease. Further endocrine cells of the skeleton involved in bone remodeling are osteoblasts. While FGF23 targets the kidney and parathyroid glands to control metabolism of vitamin D and phosphates, osteoblasts express osteocalcin, which through GPRC6A receptors modulates beta cells of the pancreatic islets, muscle, adipose tissue, brain and testes. This article reviews some knowledge concerning the interaction between the bone hormonal network and phosphate or energy homeostasis and/or male reproduction., I. Zofkova., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:5

Harvested from:

CDK

Metadata only:

false