Endocrine Abstracts

JOINT1247

Introduction: Obesity affects bone metabolism through various mechanisms. Adipocytes and osteoblasts originate from a common progenitor, mesenchymal stem cells. Obesity itself by promoting adipocytes differentiation can lead to osteoporosis. Whereas chronic inflammation also shown associated with obesity and can also increase osteoclast activity, resulting in bone resorption. We tried to identify more common factors for development of obesity and osteoporosis.

Material and Methods: We gathered available data from internet Published data from the past two decades from sources such as MEDLINE, PubMed, Scopus, and Web of Science were systematically analyzed to evaluate to common factors development of obesity and osteoporosis.

Results: Literature search showed range of factors. Major factor is hormonal Influences. Adipose tissue is an active endocrine organ that secretes various hormones and cytokines, increasing fat mass leads to their higher production and can significantly affects bone metabolism. The interplay between energy metabolism and bone health is complex, with bone cells actively participating in metabolic regulation. Osteocalcin: This bone-derived hormone influences glucose metabolism and fat mass. Dysregulation of osteocalcin in obesity can affect both metabolic health and bone quality. Bone Marrow Adiposity: Increased adiposity within the bone marrow can interfere with bone remodeling by altering the balance between osteoblast and adipocyte differentiation. Dietary factors, high fat intake can interfere with calcium absorption, affecting bone health. Weight loss interventions, including bariatric surgery, have been shown to have mixed effects on bone health, sometimes leading to decreased BMD and increased fracture risk. Mechanical factor Increased body weight in obese individuals leads to greater mechanical loading on the skeleton, which stimulates bone formation through mechanotransduction. This process involves the conversion of mechanical stimuli into biochemical signals that promote osteoblast activity and bone mineralization. However, the distribution of this loading and its effects on different bone sites can vary, potentially leading to uneven bone strength. TNF-α and IL-6: These cytokines increase osteoclast activity, leading to enhanced bone resorption. The chronic inflammatory state associated with obesity can thus predispose individuals to bone loss and increased fracture risk despite higher bone mineral density.

Conclusion: The relationship between bone and adipocytes is multifaceted, involving shared origins, hormonal influences, mechanical loading, cell signaling, and metabolic factors. Understanding these connections is crucial for developing strategies to improve bone health and manage obesity-related bone issues.