A paper just out a couple weeks ago on the effects on beta cell gene expression in daughter rats due to the high-fat diet of their fathers has turned some attention of those who are interested in epigenetics to contributions from males. This is apt as many genes are known or predicted to be imprinted in human males.
One gene shown by Ng, et al. to be 1.23-fold down-regulated in beta cells of daughters whose fathers were fed a high-fat diet is S1pr5. In humans, S1PR5 encodes a sphingosine-1-phosphate receptor. The ligand of this receptor, lysosphingolipid sphingosine 1-phosphate (S1P), regulates cell proliferation, apoptosis, motility, and neurite retraction and its actions may be both intracellular as a second messenger and extracellular as a receptor ligand [RefSeq].
It is highly relevant that Glessner, et al. (2010) identified a CNV (copy number variant) in S1PR5 that associates with childhood obesity. That CNV is a deletion but whether this leads to down-regulation of S1PR5 is not known. That is likely but not a sure bet until experimental data are taken. Nonetheless, this is an interesting gene and may steal some of the spotlight that Ng, et al. shine on IL13RA2, the human ortholog of the rat gene showing the greatest fold-change in expression between daughter rats whose fathers were fed different diets.