Osteoporosis and the Growth Hormone-Insulin-Like Growth Factor Axis

Geusens, Piet; Boonen, Steven

doi:10.1159/000066483

Cited by 40 publications

(32 citation statements)

References 46 publications

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“…IGFs play also an important role in bone remodeling. Low-serum IGF levels decrease osteoblast proliferation and bone matrix formation and reduce the activation of osteoclasts (29). Several studies have demonstrated a positive correlation between the BMD of the lumbar spine and the IGF-I concentration (30).…”

Section: Acquired Factorsmentioning

confidence: 99%

Bone Disease in Haemoglobin Disorders

Voskaridou

Terpos

2013

Thalassemia Reports

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Bone disease represents a prominent cause of morbidity in patients with thalassaemia and other haemoglobin disorders. The delay in sexual maturation, the presence of diabetes and hypothyroidism, the parathyroid gland dysfunction, the haemolytic anaemia, the progressive marrow expansion, the iron toxicity on osteoblasts, the iron chelators, and the deficiency of growth hormone or insulin growth factors have been identified as major causes of osteoporosis in thalassaemia. Adequate hormonal replacement, effective iron chelation, improvement of hemoglobin levels, calcium and vitamin D administration, physical activity, and smoking cessation are the main to-date measures for the management of the disease. During the last decade, novel pathogenetic data suggest that the reduced osteoblastic activity, which is believed to be the basic mechanism of bone loss in thalassemia, is accompanied by a comparable or even greater increase in bone resorption. Therefore, potent inhibitors of osteoclast activation, such as the aminobisphosphonates, arise as key drugs for the management of osteoporosis in thalassaemia patients and other haemoglobin disorders.

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Section: Acquired Factorsmentioning

confidence: 99%

Bone Disease in Haemoglobin Disorders

Voskaridou

Terpos

2013

Thalassemia Reports

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“…Normal mammalian aging is characterized by reduced potency in the GH/IGF-1 axis. Reduction in IGF-1 levels with age is directly linked to atrophy of bone, skeletal muscle, cardiac muscle, and other tissues displaying pathological aging (Adamo and Farrar, 2006;Anversa, 2005;Ceda et al, 2005;Geusens and Boonen, 2002). Exogenous administration of GH to aged individuals improves body composition, fitness, bone density, and other biological markers, albeit with some side effects .…”

Section: Introductionmentioning

confidence: 99%

How does suppression of IGF-1 signaling by DNA damage affect aging and longevity?

Hinkal

Donehower

2008

Mechanisms of Ageing and Development

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Long-lived animals have evolved a robust set of defenses to maintain genomic integrity over their entire lifespan. The DNA damage response and DNA repair pathways are critical pillars of organismal defenses, minimizing somatic mutations in both post-mitotic and mitotic cells. These genomic maintenance systems not only prevent the premature emergence of cancers, but may also maintain normal tissue function and organismal longevity. Genetic defects in a number of DNA repair and DNA damage response genes often leads to a dramatic increase in cancer incidence; in other cases, premature aging or progeroid syndromes may be induced. In this review, we discuss two recent reports of two nucleotide excision repair deficient models that exhibit dramatic premature aging and shortened longevity. The DNA repair defects were also associated with a significant inhibition of the growth hormone/insulin-like growth factor 1 (GH/IGF-1) axis, an endocrine signaling pathway shown to influence aging and longevity in both vertebrates and invertebrates. Potential mechanisms of how DNA damage might affect IGF-1 signaling and aging are discussed, with a particular emphasis on the role of such signaling alterations in the adult tissue stem cell compartments.

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“…IGF-1 plays an important role in bone remodelling. Low serum IGF levels decrease osteoblast proliferation and bone matrix formation and reduce the activation of osteoclasts (64). A positive correlation between BMD at the lumbar spine and IGF-1 concentration has been detected (48,65).…”

Section: Gh-igf-1 Axismentioning

confidence: 88%

Pathogenesis of Thalassemia Major–Associated Osteoporosis: Review of the Literature and Our Experience

Gaudio¹,

Morabito²,

Catalano³

et al. 2018

Jcrpe

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Due to increasing life expectancy in thalassemia major (TM), osteoporosis is emerging as a significant problem. Its aetiology is multifactorial, culminating in increased bone resorption and remodelling. Hypogonadism and marrow expansion seem to play an important role, but iron overload, deferoxamine toxicity, a defective GH-IGF-1 axis and multiple endocrinopathies may represent additional causes of bone damage. Many of these patients, though under appropriate treatment programs, do not achieve normal peak bone mass. The RANK/RANKL/OPG and the Wnt/βCatenin systems work as major mediators of imbalanced bone turnover and bone loss. Additional genetic factors, such as collagen type I alpha 1 and vitamin D receptor gene polymorphisms, may exert some influence on the enhanced fracture risk observed in TM. To date, in spite of adequate hormone replacement, chelating therapy, and acceptable haemoglobin levels, subjects with TM display impaired bone density and imbalanced bone turnover, so the puzzle of the pathogenesis of thalassemia major-induced osteoporosis remains far from being solved.

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Osteoporosis and the Growth Hormone-Insulin-Like Growth Factor Axis

Cited by 40 publications

References 46 publications

Bone Disease in Haemoglobin Disorders

Bone Disease in Haemoglobin Disorders

How does suppression of IGF-1 signaling by DNA damage affect aging and longevity?

Pathogenesis of Thalassemia Major–Associated Osteoporosis: Review of the Literature and Our Experience

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