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Osteosarcopenic adiposity (OSA) phenotype and its connection with cardiometabolic disorders: Is there a cause-and-effect?

表型 内科学 医学 内分泌学 生物 遗传学 基因
作者
Jasminka Z. Ilich,Biljana Pokimica,Danijela Ristić-Medić,Snježana Petrović,Aleksandra Arsić,Nadja Vasiljević,Vesna Vučić,Owen Kelly
出处
期刊:Ageing Research Reviews [Elsevier BV]
卷期号:98: 102326-102326 被引量:3
标识
DOI:10.1016/j.arr.2024.102326
摘要

The objectives were to examine if there is a causal relationship between osteosarcopenic adiposity (OSA) syndrome (coexistence of osteopenia/osteoporosis, sarcopenia, and excess adiposity) and cardiometabolic disorders or if these disorders initiate the development of OSA and its worsening. The search was conducted in PubMed, Scopus, and Web of Science to include articles up to the end of 2023. Of n=539 articles retrieved, n=15 met the eligibility criteria. Only studies conducted in adults and with all three body composition compartments (bone, muscle/lean, adipose) measured were considered. The results revealed that several cardiometabolic disorders, namely, hypertension, dyslipidemia (elevated total and LDL-cholesterol, lower HDL-cholesterol), insulin resistance, hyperglycemia, lower serum vitamin D, and some inflammatory markers were accompanied by OSA. In most cases, the OSA phenotype was associated with worse outcomes than cases with healthy or less impaired body composition. Our initial questions about the reciprocal cause-and-effect relationships could be surmised with more certainty for the OSA and some cardiovascular risks (hypertension, dyslipidemia) and some metabolic abnormalities (several inflammatory markers). The results of this review underscore the importance of body composition in health and from a clinical perspective, all three body composition compartments should be measured by standardized technologies using regulated diagnostic criteria to identify OSA. Randomized trials and prospective studies in diverse groups of older and younger individuals are necessary to determine if the relationships between OSA and clinical endpoints are causal and reversible through intervention and to uncover the mechanisms.
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