Neuropsychiatric comorbidity in obesity: role of inflammatory processes.

Nathalie Castanon, Julie Lasselin, Lucile Capuron
Front. Endocrinol.. 2014-05-15; 5:
DOI: 10.3389/fendo.2014.00074

PubMed
Lire sur PubMed



1. Front Endocrinol (Lausanne). 2014 May 15;5:74. doi: 10.3389/fendo.2014.00074.
eCollection 2014.

Neuropsychiatric comorbidity in obesity: role of inflammatory processes.

Castanon N(1), Lasselin J(2), Capuron L(1).

Author information:
(1)UMR 1286, Laboratory of Nutrition and Integrative Neurobiology (NutriNeuro),
French National Institute for Agricultural Research (INRA) , Bordeaux , France ;
UMR 1286, Laboratory of Nutrition and Integrative Neurobiology (NutriNeuro),
University of Bordeaux , Bordeaux , France.
(2)UMR 1286, Laboratory of Nutrition and Integrative Neurobiology (NutriNeuro),
French National Institute for Agricultural Research (INRA) , Bordeaux , France ;
UMR 1286, Laboratory of Nutrition and Integrative Neurobiology (NutriNeuro),
University of Bordeaux , Bordeaux , France ; Stress Research Institute
(Stressforskningsinstitutet), Stockholm University , Stockholm , Sweden.

Neuropsychiatric symptoms are frequent in obesity. In addition to their
substantial economic and health impact, these symptoms significantly interfere
with the quality of life and social function of obese individuals. While the
pathophysiological mechanisms underlying obesity-related neuropsychiatric
symptoms are still under investigation and remain to be clearly identified, there
is increasing evidence for a role of inflammatory processes. Obesity is
characterized by a chronic low-grade inflammatory state that is likely to
influence neuropsychiatric status given the well-known and highly documented
effects of inflammation on brain activity/function and behavior. This hypothesis
is supported by recent findings emanating from clinical investigations in obese
subjects and from experimentations conducted in animal models of obesity. These
studies converge to show that obesity-related inflammatory processes, originating
either from the adipose tissue or gut microbiota environment, spread to the brain
where they lead to substantial changes in neurocircuitry, neuroendocrine
activity, neurotransmitter metabolism and activity, and neurogenesis. Together,
these alterations contribute to shape the propitious bases for the development of
obesity-related neuropsychiatric comorbidities.

DOI: 10.3389/fendo.2014.00074
PMCID: PMC4030152
PMID: 24860551

Auteurs Bordeaux Neurocampus