Obesity triggers a low-grade chronic inflammation, known as metaflammation, which has been causally linked to obesity-related metabolic complications. However, 10-15% of obese individuals exhibit a healthy obesity phenotype without these complications.In this research project, we investigate the role of primary cilia in determining whether obesity leads to metabolic complications (unhealthy obesity) or remains metabolically benign (healthy obesity). Our work focuses on patients with Bardet-Biedl Syndrome (BBS), a ciliopathy linked to obesity, revealing distinct outcomes based on genetic mutations. Using mouse models, we found that primary cilia influence immune cell activity and adipocyte development in WAT. Building on these findings, we will investigate how cilia regulate immune cell differentiation and function, comparing BBS mouse models and BBS patients. We will also study BBS patients undergoing appetite-modulating treatment to identify mechanisms that may apply to broader populations, including participants from large-scale obesity studies. Ultimately, our goal is to uncover pathways that control metaflammation versus healthy obesity, laying the groundwork for new therapeutic strategies.

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