Adipokines and inflammation: is it a question of weight?

Abstract

Obesity has reached epidemic proportions in the Western society and is increasing in the developing world. It is considered as one of the major contributors to the global burden of disability and chronic diseases, including autoimmune, inflammatory and degenerative diseases. Research conducted on obesity and its complications over the last two decades has transformed the outdated concept of white adipose tissue (WAT) merely serving as an energy depot. WAT is now recognized as an active and inflammatory organ capable of producing a wide variety of factors known as adipokines. These molecules participate through endocrine, paracrine, autocrine or juxtacrine crosstalk mechanisms in a great variety of physiological or pathophysiological processes, regulating food intake, insulin sensitivity, immunity and inflammation. Although initially restricted to metabolic activities (regulation of glucose and lipid metabolism), adipokines currently represent a new family of proteins that can be considered key players in the complex network of soluble mediators involved in the pathophysiology of immune/inflammatory diseases. However, the complexity of the adipokine network in the pathogenesis and progression of inflammatory diseases has posed, since the beginning, the important question of whether it may be possible to target the mechanism(s) by which adipokines contribute to disease selectively without suppressing their physiological functions. Here, we explore in depth the most recent findings concerning the involvement of adipokines in inflammation and immune responses, in particular in rheumatic, inflammatory and degenerative diseases. We also highlight several possible strategies for therapeutic development and propose that adipokines and their signalling pathways may represent innovative therapeutic strategies for inflammatory disorders.

Plasma Adipokines Profile in Prepubertal Children with a History of Prematurity or Extrauterine Growth Restriction

“…Adipokines are bioactive molecules similar to cytokines in structure, mainly secreted by pre-and mature cells derived from AT in response to changes in adipocyte glycerol storage and inflammation [29]. These biological mediators have pro-and anti-inflammatory properties and modulate several physiological functions, such as energy balance, insulin sensibility, inflammatory and immune responses, appetite, and vascular homeostasis [30].…”

CITED2 mediates the mechanical loading–induced suppression of adipokines in the infrapatellar fat pad

“…53,54 While mechanical overloading of joints contributes to obesity-associated OA, 55 chronic low-grade inflammation and metabolic dysfunction may also play a role. 56 The IPFP, a white fat tissue located in the knee joint, secretes several proinflammatory mediators, growth factors, and adipokines, 14,17,57 and is recognized as an active participant in OA pathogenesis. 15 In the present study, we found that IPFP expression of adipsin and adiponectin, two adipokines that have been implicated in playing a role in joint tissue homeostasis and OA, 14,17,57 is suppressed by moderate exercise, an action likely mediated by the transcriptional regulator CITED2.…”

The Roles of the NLRP3 Inflammasome in Neurodegenerative and Metabolic Diseases and in Relevant Advanced Therapeutic Interventions

“…Obesity-induced alterations in adipocytes and macrophages cause insulin resistance (IR) with subsequent induction of AT fibrosis [67]. Besides energy conservation, ATs secrete adipokines, molecules that contribute (via endocrine, autocrine, and paracrine signaling mechanisms) to various physiological and pathophysiological conditions, thereby regulating inflammation and immunity, insulin sensitivity, and food intake [68]. Furthermore, a reduction in the secretion of insulin-sensitive adipokines accompanied by oversecretion of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) is closely related to the etiology of various metabolic conditions.…”