Abstract
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.
Highlights
Cardiometabolic syndrome (CMS) has long been recognized as a cluster of maladaptive cardiovascular, renal, thrombotic, inflammatory, and metabolic disorders by several global health authorities (Castro et al, 2003)
In the present review, we summarize the available evidence on the role of negative adipose remodeling in triggering cardiovascular impairment in the context of CMS with an emphasis on the involvement of perivascular adipose tissue (PVAT)
Adipose tissue deleterious remodeling and CMS are tightly linked to positive energy balance and high fat diet (HFD) intake (Bays et al, 2007)
Summary
Cardiometabolic syndrome (CMS) has long been recognized as a cluster of maladaptive cardiovascular, renal, thrombotic, inflammatory, and metabolic disorders by several global health authorities (Castro et al, 2003). Metabolic disorders that could be considered a culmination of CMS, including diet-induced obesity (DIO) (WHO, 2019) and type 2 diabetes (International Diabetes Federation, 2019), have increased in prevalence over the past few decades together with their associated cardiovascular morbidities. The different regimens of IF have been shown to improve the metabolic state of obese and non-obese animal models and human subjects (Patterson et al, 2015; StOnge et al, 2017) In this context, it becomes necessary to understand the potential impact of such an intervention on the pathogenetic pathways linking early metabolic dysfunction to cardiovascular impairment. The possible molecular pathways linking IF to the ameliorative effect on adipose inflammation and cardiovascular dysfunction under such circumstances are examined
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