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International audience; Background/objectives: While excessive food consumption represents a key factor in the development of obesity, the underlying mechanisms are still unclear. Ghrelin, a gut-brain hormone involved in the regulation of appetite, is impaired in obesity. In addition to its role in eating behavior, this hormone was shown to affect brain regions controlling reward, including the striatum and prefrontal cortex, and there is strong evidence of impaired reward processing in obesity. The present study investigated the possibility that disrupted reward-related brain activity in obesity relates to ghrelin deficiency.Subjects/methods: Fifteen severely obese subjects (BMI > 35 kg/m(2)) and fifteen healthy non-obese control subjects (BMI < 30 kg/m(2)) were recruited. A guessing-task paradigm, previously shown to activate the ventral striatum, was used to assess reward-related brain neural activity by functional magnetic resonance imaging (fMRI). Fasting blood samples were collected for the measurement of circulating ghrelin.Results: Significant activations in the ventral striatum, ventromedial prefrontal cortex and extrastriate visual cortex were elicited by the fMRI task in both obese and control subjects. In addition, greater reward-related activations were present in the dorsolateral prefrontal cortex, and precuneus/posterior cingulate of obese subjects compared to controls. Obese subjects exhibited longer choice times after repeated reward and lower circulating ghrelin levels than lean controls. Reduced ghrelin levels significantly predicted slower post-reward choices and reward-related hyperactivity in dorsolateral prefrontal cortices in obese subjects.Conclusion: This study provides evidence of association between circulating ghrelin and reward-related brain activity in obesity and encourages further exploration of the role of ghrelin system in altered eating behavior in obesity.

Chapitre 16; International audience; There is mounting evidence for a close relationship between obesity and depression. Depression is frequent in obese subjects and, in turn, obesity is associated with a greater risk of depression. Moreover, recent data suggest a role for obesity in treatment-resistant depression. While the association is bidirectional, the paths and mechanisms by which obesity can lead to depression appear to be particularly relevant to biological psychiatry, as they can provide new information on the pathophysiology and treatment of mood disorders. This chapter will review those pathophysiological pathways and processes that are shared by obesity and depression and that are likely to underlie the intricate relationship between the two disorders. Their potential translational implications and relevance to the development of personalized strategies for the treatment and management of depression will be further discussed.

International audience; Background Recent reports suggest that the risk of depressive symptoms in obesity is potentiated in subjects presenting a metabolically unhealthy phenotype. Inflammation is often considered a defining criteria of metabolic health. However, this factor may drive the association of metabolic health with depressive symptoms given its well-known role in the pathophysiology of depression. This study aimed at determining the relative contribution of inflammation and metabolic abnormalities to depressive symptoms in obesity. Methods One-hundred severely obese adults (BMI ≥ 35–40 kg/m2) and 25 non-obese control individuals (BMI Results Total MADRS scores were significantly higher in obese subjects with significant inflammation (hs-CRP ≥ 5 mg/L) compared to those with low inflammation (hs-CRP Conclusions These results indicate that systemic inflammation represents a stronger contributor of obesity-related depressive symptoms than metabolic health per se. This supports the notion that inclusion of inflammation in the definition of metabolically unhealthy obesity drives the association found between poor metabolic health and depressive symptoms.