Inflammation and metabolic dysfunction: links to cardiovascular diseases

Abstract

Abdominal obesity is a major risk factor for cardiovascular disease, and recent studies highlight a key role of adipose tissue dysfunction, inflammation, and aberrant adipokine release in this process. An increased demand for lipid storage results in both hyperplasia and hypertrophy, finally leading to chronic inflammation, hypoxia, and a phenotypic change of the cellular components of adipose tissue, collectively leading to a substantially altered secretory output of adipose tissue. In this review we have assessed the adipo-vascular axis, and an overview of adipokines associated with cardiovascular disease is provided. This resulted in a first list of more than 30 adipokines. A deeper analysis only considered adipokines that have been reported to impact on inflammation and NF-κB activation in the vasculature. Out of these, the most prominent link to cardiovascular disease was found for leptin, TNF-α, adipocyte fatty acid-binding protein, interleukins, and several novel adipokines such as lipocalin-2 and pigment epithelium-derived factor. Future work will need to address the potential role of these molecules as biomarkers and/or drug targets.

Insulin-independent reversal of type 1 diabetes in nonobese diabetic mice with brown adipose tissue transplant

“…Inflammation is an innate characteristic of T1D, as it is with other metabolic disease such as obesity, insulin resistance, and T2D (2,5,11,13,40,43,60,64). Recovery from metabolic disease is associated with decreased inflammation, both systemic and in adipose tissue (17,37,52,55,57,58,67,78).…”

Visceral obesity, but not metabolic syndrome, is associated with the presence of post-thrombotic syndrome

“…Moreover, visceral adipose tissue (VAT) is now considered an important source of inflammatory molecules that can be implicated in the progression of vascular damage [15,16]. All these factors might represent a possible explanation for the association between abdominal obesity and the development of PTS.…”

Direct, inflammation-mediated and blood-pressure-mediated effects of total and abdominal adiposity on diastolic function: EPIPorto study

“…Adipose tissue is an important source of proinflammatory cytokines [17]. Previous studies have linked inflammation with diastolic dysfunction in patients with hypertension [40] and coronary artery disease [41] and, in experimental studies, the inhibition of inflammatory pathways prevented diastolic dysfunction development [42].…”

“…Obesity can induce DD by several potential mechanisms [14,12]. The effect can be direct by adipokine secretion [15,16], by inducing a systemic pro-inflammatory state [17,18] and changes in LV hemodynamics [19,20], or indirect through its association with other cardiovascular risk factors, such as hypertension, insulin resistance and diabetes [10]. The role of central versus total adiposity on diastolic function is less well characterized.…”