The antidepressant fluoxetine acts on energy balance and leptin sensitivity via BDNF View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Gaia Scabia, Ilaria Barone, Marco Mainardi, Giovanni Ceccarini, Manuela Scali, Emma Buzzigoli, Alessia Dattilo, Paolo Vitti, Amalia Gastaldelli, Ferruccio Santini, Tommaso Pizzorusso, Lamberto Maffei, Margherita Maffei

ABSTRACT

Leptin and Brain Derived Neurotrophic Factor (BDNF) pathways are critical players in body weight homeostasis. Noninvasive treatments like environmental stimulation are able to increase response to leptin and induce BDNF expression in the brain. Emerging evidences point to the antidepressant selective serotonin reuptake inhibitor Fluoxetine (FLX) as a drug with effects similar to environmental stimulation. FLX is known to impact on body weight, with mechanisms yet to be elucidated. We herein asked whether FLX affects energy balance, the leptin system and BDNF function. Adult lean male mice chronically treated with FLX showed reduced weight gain, higher energy expenditure, increased sensitivity to acute leptin, increased hypothalamic BDNF expression, associated to changes in white adipose tissue expression typical of "brownization". In the Ntrk2tm1Ddg/J model, carrying a mutation in the BDNF receptor Tyrosine kinase B (TrkB), these effects are partially or totally reversed. Wild type obese mice treated with FLX showed reduced weight gain, increased energy output, and differently from untreated obese mice, a preserved acute response to leptin in terms of activation of the intracellular leptin transducer STAT3. In conclusion, FLX impacts on energy balance and induces leptin sensitivity and an intact TrkB function is required for these effects to take place. More... »

PAGES

1781

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-018-19886-x

DOI

http://dx.doi.org/10.1038/s41598-018-19886-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1100592843

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29379096


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