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Background  Obesity is a growing global concern with strong associations with cardiovascular disease, cancer and type-2 diabetes. Although various genome-wide association studies have identified more than 40 genes associated with obesity, these genes cannot fully explain the heritability of obesity, suggesting there may be other contributing factors, including epigenetic effects.    Results  We performed genome wide DNA methylation profiling comparing normal-weight and obese 9–13 year old children to investigate possible epigenetic changes correlated with obesity. Of note, obese children had significantly lower methylation levels at a CpG site located near  coronin 7  ( CORO7 ), which encodes a tryptophan-aspartic acid dipeptide (WD)-repeat containing protein most likely involved in Golgi complex morphology and function. Anatomical profiling of  coronin 7  ( Coro7 ) mRNA expression in mice revealed that it is highly expressed in appetite and energy balance regulating regions, including the hypothalamus, striatum and locus coeruleus, the main noradrenergic brain site. Interestingly, we found that food deprivation in mice downregulates hypothalamic  Coro7  mRNA levels, and injecting ethanol, an appetite stimulant, increased the number of  Coro7  expressing cells in the locus coeruleus. Finally, by employing the genetically-tractable  Drosophila melanogaster  model we were able to demonstrate an evolutionarily conserved metabolic function for the  CORO7  homologue  pod1 . Knocking down the  pod1  in the  Drosophila  adult nervous system increased their resistance to starvation. Furthermore, feeding flies a high-calorie diet significantly increased  pod1  expression.    Conclusion  We conclude that coronin 7 is involved in the regulation of energy homeostasis and this role stems, to some degree, from the effect on feeding for calories and reward.

Implication of coronin 7 in body weight regulation in humans, mice and flies