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Several reports suggest obesity and bipolar disorder (BD) share some physiological and behavioural similarities. For instance, obese individuals are more impulsive and have heightened reward responsiveness, phenotypes associated with BD, while bipolar patients become obese at a higher rate and earlier age than people without BD; however, the molecular mechanisms of such an association remain obscure. Here we demonstrate, using whole transcriptome analysis, that  Drosophila Ets96B , homologue of obesity-linked gene  ETV5 , regulates cellular systems associated with obesity and BD. Consistent with a role in obesity and BD, loss of nervous system  Ets96B  during development increases triacylglyceride concentration, while inducing a heightened startle-response, as well as increasing hyperactivity and reducing sleep. Of notable interest, mouse  Etv5  and  Drosophila Ets96B  are expressed in dopaminergic-rich regions, and loss of  Ets96B  specifically in dopaminergic neurons recapitulates the metabolic and behavioural phenotypes. Moreover, our data indicate Ets96B inhibits dopaminergic-specific neuroprotective systems. Additionally, we reveal that multiple SNPs in human  ETV5  link to body mass index (BMI) and BD, providing further evidence for  ETV5  as an important and novel molecular intermediate between obesity and BD. We identify a novel molecular link between obesity and bipolar disorder. The  Drosophila ETV5  homologue  Ets96B  regulates the expression of cellular systems with links to obesity and behaviour, including the expression of a conserved endoplasmic reticulum molecular chaperone complex known to be neuroprotective. Finally, a connection between the obesity-linked gene  ETV5  and bipolar disorder emphasizes a functional relationship between obesity and BD at the molecular level.

The Drosophila ETV5 Homologue Ets96B: Molecular Link between Obesity and Bipolar Disorder