2 research outputs found
Epigenetic and Molecular Alterations in Obesity: Linking CRP and DNA Methylation to Systemic Inflammation
No full textObesity is marked by excessive fat accumulation in the adipose tissue, which disrupts metabolic processes and causes chronic systemic inflammation. Commonly, body mass index (BMI) is used to assess obesity-related risks, predicting potential metabolic disorders. However, for a better clustering of obese patients, we must consider molecular and epigenetic changes which may be responsible for inflammation and metabolic changes. Our study involved two groups of patients, obese and healthy donors, on which routine analysis were performed, focused on BMI, leukocytes count, and C-reactive protein (CRP) and completed with global DNA methylation and gene expression analysis for genes involved in inflammation and adipogenesis. Our results indicate that obese patients exhibited elevated leukocytes levels, along with increased BMI and CRP. The obese group revealed a global hypomethylation and upregulation of proinflammatory genes, with adipogenesis genes following the same trend of being overexpressed. The study confirms that obesity is linked to systematic inflammation and metabolic dysfunction through epigenetic and molecular alterations. The CRP was correlated with the hypomethylation status in obese patients, and this fact may contribute to a better understanding of the roles of specific genes in adipogenesis and inflammation, leading to a better personalized therapy
The Relationship between Proinflammatory Molecules and PD-L1 in Patients with Obesity Who Underwent Gastric Sleeve Surgery—A Pilot Study
No full textIn the last few decades, obesity played a pivotal role by having a high impact on global economic and health systems due to its associated diseases, with cardiovascular, respiratory, musculoskeletal, oncological, mental, and social implications. One of the most incriminated physiopathological mechanisms in obesity is chronic inflammation. The primary goal of this pilot study was to determine the molecular aspects of inflammation among patients with obesity compared to participants with a normal BMI (≤25 kg/m2), as well as within a smaller subset of obese individuals who have been evaluated three months following sleeve gastrectomy. The research employs conventional blood tests and plasma measurements of particular molecules, such as proinflammatory cytokines and proteins that play critical roles in immune and inflammatory regulation. The results revealed a promising kinetic effect after bariatric surgery on IL-18, MCP-1, and PD-L1 molecules. The proinflammatory makers IL-18 (p = 0.006) and MCP-1 (p = 0.035) were elevated in the obese group compared to the control, while the follow-up group displayed lower levels of these molecules. Commonly investigated in oncology related studies, PD-L1 was recently linked to adipose tissue gain and its associated inflammatory effect. Until now, there is no clinical evidence for the relationship between circulating PD-L1 and proinflammatory markers derived from low-grade inflammation of the adipose tissue. The circulating PD-L1 levels were significantly lowered in the obese group compared to the control (p = 0.049), and after sleeve gastrectomy, the PD-L1 level increased. The present study is the first investigating this type of crosstalk and its potential involvement in bariatric patient management
