This review examines how adiposopathy affects cardiometabolic diseases and implies a connection to physical activity.
An excess of calories impairs visceral adipose tissue functioning, including heart adipose and perivascular-adipose-tissue (PAT). The secretory activity of adipose tissue (AT), which encompasses both pro-inflammatory and endocrine mediators, plays a pivotal role in inter-organ communication and contributes significantly to the pathogenesis of obesity. Excessive fat in visceral adipocytes hinders the endocrine and immunological response, resulting in pathological alterations and presenting significant threats to human health risk. Previous research has established that increased pro-inflammatory cytokines and decreased immune-modulatory disrupt the communication between vasculature, liver, and myocyte. Adiposopathy or dysfunctional AT contributes to the development of cardio-metabolic-risk factors (CMRF). These risk factors include metabolic resistance, hypertension, dyslipidemia, atherosclerosis, and a hypercoagulable state. These risk factors consecutively, unswervingly, and circuitously contribute to the growth of cardiometabolic disorders. The perivascular adipose tissue envelops most blood arteries throughout the body. Functional PAT has anticontractile and immune-modulatory properties. However, it has been proposed that impaired PAT activity may contribute to the association between CMRF and vascular dysfunction. Vascular oxidative stress is a critical contributor to the progression of cardiometabolic disorders associated with obesity, type 2 diabetes, and hypertension. Increasing evidence from both human and animal studies suggests that physical exercise supports the normalization of adipocyte size and promotes the browning of white adipose tissue (WAT). This review covers the existing studies concerning the impact of adiposopathy on cardiometabolic disorders and the significance of physical activity in reinstating adipocyte function. Additionally, it explores the processes that connect PAT to age-related vascular pathologies.
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Nadendla et al. (2025) studied this question.
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