Experimental, clinical, and epidemiological evidence has clearly demonstrated that local, systemic, and vascular inflammation are involved not only in the pathogenesis of metabolic diseases, including type 2 diabetes and obesity, but also in their associated renal, cardiovascular, gastrointestinal, lung, and muscle and bone manifestations. Complementarily, various nutritional factors and metabolites have been recognized as regulators of inflammation, jointly suggesting a tight crosstalk between the metabolic and the immune systems, inspiring the term “metabolic inflammation.”

Within the pathogenesis of obesity-associated morbidities, it is now widely appreciated that multiple modalities of interorgan communication exist. Identifying mediators of interorgan communication in these settings is therefore essential for gaining a clear mechanistic understanding on how dysfunction of one organ can lead to distant organ failure. Moreover, it may lay critical grounds for identifying and developing novel effective therapies to decrease the health consequences of metabolic inflammation.

To promote discussion and further development in this exciting area of research, we invite investigators to contribute with original research articles, as well as review articles, that seek to elucidate the role of mediators of interorgan communication within the context of metabolic inflammation. We are interested in articles that explore the physiological manifestations, mechanisms, and potential advance towards pharmacological modulation aimed at the prevention/management of the various consequences of one of the key drivers of human morbidity in modern sedentary times. Potential topics include, but are not limited to:

• Adipose tissue-derived factors mediating interorgan crosstalk
• Skeletal muscle-derived secretory factors (myokines) and skeletal muscle adiposity in metabolic inflammation
• Liver-derived inflammatory mediators
• Renal-derived inflammatory mediators
• Intestinal inflammation and metabolic dysfunction
• Dietary components and production of mediators of metabolic inflammation
• Nonprotein factors as contributors to metabolic disease

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