Inflammatory processes in obesity: focus on endothelial dysfunction and the role of adipokines as inflammatory mediators

Abstract

Obesity predisposes the affected individuals to several metabolic, inflammatory, cardiovascular and malignant pathologies and is a top risk factor for premature mortality. It is now well known that inflammation has a major causative role in obesity-associated disease development and that obesity favors the establishment of a pro-inflammatory milieu at the level of adipose microenvironment. These inflammatory signals result in a disruption of normal cellular-crosstalk between adipose and non-adipose components leading to an altered metabolic and immunological status and a dysfunctional phenotype. Abnormal secretion of adipokines – small adipose-derived signaling molecules – can further assist in the inflammatory processes to offset the adipose tissue towards a dysfunctional state. Although adipokines have been recognized as the link between obesity and pathogenesis, studies are needed to fully understand their mechanism of action and underscore their therapeutic value. Here, we have reviewed obesity-induced metabolic and immunological changes at the level of vasculature and emphasize on the importance of adipokines, particularly leptin, vaspin and visfatin, for their therapeutic relevance.

Keywords:

• Inflammation
• obesity
• vaspin leptin
• visfatin

Additional information

Funding

This work was supported by grants from Ohio University-HCOM (RP1206) and Ohio University-Baker Funds Award (FN1006078). MS was supported by the MCB program, a SEA grant and a Kopchick Fellowship, all from Ohio University.