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Neuropharmacology. 2015 Sep;96(Pt A):124-34. doi: 10.1016/j.neuropharm.2014.12.023. Epub 2015 Jan 10.

Obesity, adipokines and neuroinflammation.

Author information

1
Department of Neuroscience, Université de Montréal and Goodman Cancer Centre, Department of Biochemistry, McGill University, Montréal, Canada.
2
Robarts Research Institute, Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario N6A 5B7, Canada.
3
Department of Veterinary-Physiology and -Biochemistry, Justus-Liebig-University Giessen, Frankfurter Strasse 100, D-35392 Giessen, Germany.
4
Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Quebec H4H 1R3, Canada. Electronic address: giamal.luheshi@mcgill.ca.

Abstract

Global levels of obesity are reaching epidemic proportions, leading to a dramatic increase in incidence of secondary diseases and the significant economic burden associated with their treatment. These comorbidities include diabetes, cardiovascular disease, and some psychopathologies, which have been linked to a low-grade inflammatory state. Obese individuals exhibit an increase in circulating inflammatory mediators implicated as the underlying cause of these comorbidities. A number of these molecules are also manufactured and released by white adipose tissue (WAT), in direct proportion to tissue mass and are collectively known as adipokines. In the current review we focused on the role of two of the better-studied members of this family namely, leptin and adiponectin, with particular emphasis on their role in neuro-immune interactions, neuroinflammation and subsequent brain diseases. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.

KEYWORDS:

Adiponectin; Cytokines; Inflammation; Leptin; Neuroimmune-interactions; Neutrophil granulocytes; Psychiatric disorders

[Indexed for MEDLINE]

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