Barrera-Esparza María, Carreón-Torres Elizabeth, Jiménez-Osorio Angélica Saraí, Angel-García Julieta, Jiménez-Garza Octavio, Flores-Chávez Olga Rocío, Mendoza-Catalán Geu S, Estrada-Luna Diego
Coordinación de Unidades de Segundo Nivel, Oficina Central, Servicios de Salud del Instituto Mexicano del Seguro Social para el Bienestar (IMSS-BIENESTAR), Mexico City, Mexico.
Physics Institute, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico.
Front Endocrinol (Lausanne). 2025 May 13;16:1578552. doi: 10.3389/fendo.2025.1578552. eCollection 2025.
Fatty acids disorders may lead to insulin resistance, resulting in long-term oxidative stress and inflammatory processes, both mediated by adipose tissue. Either in normal condition or obesogenic status, adipose cells components play an important role in several physiological and metabolic conditions. It has been shown that bioactive compounds can influence the development of obesity and its pathological complications such as insulin resistance. In this study, we performed a network between bioactive compounds and adipose tissue vis-a-vis insulin resistance. We constructed a regulatory network of 62 adipocyte cell components that incorporates current evidence of cellular and molecular interactions involved in healthy and obesity states. The network incorporated information about inflammation pathways and inhibition of insulin signaling; insulin signaling and GLUT 4 translocation; triglycerides production; ATP production; M2 macrophages recruitment; adipogenesis and lipolysis as well as mitochondrial biogenesis. Our mathematical model showed a discernment between the impact of various bioactive substances on the transitions from health to obesity and vice versa. We found that anthocyanins, punicalagin, oleanolic acid, and NRG4 proved to be critical nodes in the transition from obesity to the healthy state, due to their switch-on potential to up-regulate the complex network resulting in a beneficial transition.
脂肪酸紊乱可能导致胰岛素抵抗，引发长期氧化应激和炎症过程，这两者均由脂肪组织介导。无论是在正常状态还是致肥胖状态下，脂肪细胞成分在多种生理和代谢状况中都发挥着重要作用。研究表明，生物活性化合物可影响肥胖症的发展及其病理并发症，如胰岛素抵抗。在本研究中，我们构建了生物活性化合物与脂肪组织相对于胰岛素抵抗的网络。我们构建了一个由62种脂肪细胞成分组成的调控网络，该网络纳入了健康状态和肥胖状态下细胞与分子相互作用的现有证据。该网络纳入了有关炎症途径和胰岛素信号传导抑制、胰岛素信号传导和葡萄糖转运蛋白4易位、甘油三酯生成、ATP生成、M2巨噬细胞募集、脂肪生成和脂肪分解以及线粒体生物发生的信息。我们的数学模型显示了各种生物活性物质对从健康状态转变为肥胖状态以及反之亦然的影响之间的差异。我们发现，花青素、石榴皮素、齐墩果酸和NRG4被证明是从肥胖状态转变为健康状态的关键节点，因为它们具有开启上调复杂网络从而实现有益转变的潜力。
