Abstract

group compared with their metabolically healthy counterparts. However, the difference between MHO subjects and their metabolically unhealthy counterparts was not significant. The authors also showed that the levels of these adipokines were significantly correlated with several parameters that are usually used to define metabolic health [10]. Because insulin resistance and excess adiposity are considered core pathophysiologies of metabolic unhealthiness, it could be easily assumed that adipokines might have a role in the pathogenic mechanism or could be influenced by metabolic health status. Although prospective studies to define the cause-and-effect relationship are lacking, previous studies have also investigated the crosssectional relationship between various adipokines and metabolic health. Similar to the results of Lee et al. [10], individuals with the MUHNO phenotype were known to have higher circulating levels of leptin, TNF-α, and interleukin 6 (IL-6) and lower levels of adiponectin compared with the MHNW group [11-13]. Several reports also demonstrated lower levels of TNF-α, IL-6, plasminogen activator inhibitor-1, progranulin, retinol-binding protein-4, and chemerin and higher levels of adiponectin in individuals with the MHO phenotype compared with metabolically unhealthy obese subjects [13-15]. Because there is no consensus on how to define metabolic health status, the clinical characteristics, metabolic profiles and outcomes can be largely affected by the diagnostic criteria used [8,16]. Although some conflicting results for adipokine levels also exist, current data support a close relationship to

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