Irisin and Secondary Osteoporosis in Humans.

Roberta Zerlotin,Giorgio Mori,Filippo Maselli,Maria Grano,Graziana Colaianni,Angela Oranger,Silvia Concetta Colucci,Patrizia Pignataro,Manuela Dicarlo

doi:10.3390/ijms23020690

Abstract

Irisin is a peptide secreted by skeletal muscle following exercise that plays an important role in bone metabolism. Numerous experiments in vitro and in mouse models have shown that the administration of recombinant irisin promotes osteogenesis, protects osteocytes from dexamethasone-induced apoptosis, prevents disuse-induced loss of bone and muscle mass, and accelerates fracture healing. Although some aspects still need to be elucidated, such as the dose- and frequency-dependent effects of irisin in cell cultures and mouse models, ample clinical evidence is emerging to support its physiological relevance on bone in humans. A reduction in serum irisin levels, associated with an increased risk of osteoporosis and bone fractures, was observed in postmenopausal women and in both men and women during aging, Recently, cohort studies of subjects with secondary osteoporosis showed that these patients have lower circulating levels of irisin, suggesting that this myokine could be a novel marker to monitor bone quality in this disease. Although there are still few studies, this review discusses the emerging data that are highlighting the involvement of irisin in some diseases that cause secondary osteoporosis.

Highlights

Osteoporosis is a progressive multifactorial skeletal disorder characterized by the deterioration of bone microarchitecture and increased susceptibility to fracture risk [1].The increase in life expectancy, causing a higher average age of the population, as the main achievement of modern science, leads to an increase in the incidence of chronic diseases typical of the elderly, such as osteoporosis [1]
We provided in vitro evidence demonstrating that treatment with rec-irisin in osteoblasts reduces the expression of p21, one of the effectors of the senescence process [20]
The results showed that growth hormone deficiency (GHD) is associated with lower irisin levels, in turn associated with changes in body composition and metabolic endpoints [65]

Summary

Introduction

Osteoporosis is a progressive multifactorial skeletal disorder characterized by the deterioration of bone microarchitecture and increased susceptibility to fracture risk [1]. Rec-irisin activated the MAP kinases, Erk and Erk, and increased the expression of the transcription factor Atf through an Erk-dependent pathway in osteocytes [16] These results revealed the basic mechanisms of irisin’s action on osteocytes; to increase their functions and exert antiapoptotic effects, confirming that mechanosensory cells in bone are sensitive to the exercise-mimetic myokine irisin [16]. We provided in vitro evidence demonstrating that treatment with rec-irisin in osteoblasts reduces the expression of p21, one of the effectors of the senescence process [20] These results suggest that this molecule could represent a viable therapeutic option to delay osteoporosis caused by senescence [21].

Irisin in Primary Hyperparathyroidism

Irisin in Primary

Findings

Conclusions