Dwaib Haneen S, AlZaim Ibrahim, Eid Ali H, Obeid Omar, El-Yazbi Ahmed F
Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Department of Nutrition and Food Sciences, Faculty of Agricultural and Food Sciences, American University of Beirut, Beirut, Lebanon.
Front Pharmacol. 2021 Apr 9;12:626313. doi: 10.3389/fphar.2021.626313. eCollection 2021.
Cardiometabolic syndrome (CMS) is a cluster of maladaptive cardiovascular, renal, thrombotic, inflammatory, and metabolic disorders. It confers a high risk of cardiovascular mortality and morbidity. CMS is triggered by major shifts in lifestyle and dietary habits with increased consumption of refined, calorie-dense diets. Evidence indicates that diet-induced CMS is linked to Adipose tissue (AT) inflammation. This led to the proposal that adipose inflammation may be involved in metabolic derangements, such as insulin resistance and poor glycemic control, as well as the contribution to the inflammatory process predisposing patients to increased cardiovascular risk. Therefore, in the absence of direct pharmacological interventions for the subclinical phase of CMS, time restricted feeding regimens were anticipated to alleviate early metabolic damage and subsequent comorbidities. These regimens, referred to as intermittent fasting (IF), showed a strong positive impact on the metabolic state of obese and non-obese human subjects and animal models, positive AT remodeling in face of overnutrition and high fat diet (HFD) consumption, and improved CV outcomes. Here, we summarize the available evidence on the role of adipose inflammation in triggering cardiovascular impairment in the context of diet induced CMS with an emphasis on the involvement of perivascular adipose tissue. As well, we propose some possible molecular pathways linking intermittent fasting to the ameliorative effect on adipose inflammation and cardiovascular dysfunction under such circumstances. We highlight a number of targets, whose function changes in perivascular adipose tissue inflammation and could be modified by intermittent fasting acting as a novel approach to ameliorate the inflammatory status.
心脏代谢综合征（CMS）是一组适应性不良的心血管、肾脏、血栓形成、炎症和代谢紊乱。它赋予心血管疾病高死亡率和发病率的风险。CMS是由生活方式和饮食习惯的重大转变引发的，其中精制、高热量饮食的摄入量增加。有证据表明，饮食诱导的CMS与脂肪组织（AT）炎症有关。这导致了一种观点，即脂肪炎症可能参与代谢紊乱，如胰岛素抵抗和血糖控制不佳，以及对炎症过程的影响，使患者心血管风险增加。因此，在缺乏针对CMS亚临床阶段的直接药物干预措施的情况下，限时进食方案有望减轻早期代谢损伤和随后的合并症。这些方案被称为间歇性禁食（IF），对肥胖和非肥胖人类受试者以及动物模型的代谢状态产生了强烈的积极影响，面对营养过剩和高脂饮食（HFD）摄入时脂肪组织出现积极重塑，并改善了心血管结局。在此，我们总结了关于脂肪炎症在饮食诱导的CMS背景下引发心血管损伤作用的现有证据，重点是血管周围脂肪组织的参与。此外，我们提出了一些可能的分子途径，将间歇性禁食与此种情况下对脂肪炎症和心血管功能障碍的改善作用联系起来。我们强调了一些靶点，其在血管周围脂肪组织炎症中的功能发生变化，并且可以通过间歇性禁食作为改善炎症状态的新方法来加以改变。
