Parental diet induced obesity programs the offspring’s epigenetic susceptibility to an obesogenic environment
2Gonda Brain Research Center, Bar-Ilan University, Israel
3Faculty of Life Sciences, Bar-Ilan University, Israel
4Institute of Animal Sci, ARO, The Volcani Center, Israel
Parental obesity is a risk factor for future generations. Proopiomelanocortin (POMC) is an anorexigenic precursor neuropeptide regulating food intake and body weight (BW) in the hypothalamic arcuate nucleus (ARC). We have found that maternal high fat diet (HFD) resulted in obese offspring with associated malprogramming of Pomc gene expression. To examine the possibility of epigenetic heredity while minimizing (maternal) environmental effects, we examined the effect of paternal HFD on the offspring.
Method: Male Wistar rats received from postnatal day (PND)21 to PND90 either HFD or chow (control) and were mated with chow fed dams. After conception the males were removed. Dams and offspring ate chow. Half of the offspring from both paternal diets were challenged with HFD from PND40-60.
Results: Male offspring to HFD fathers (OtHFDf) weighed less than offspring to control fathers during the 1st two postnatal weeks, but not later. At PND21 (weaning) they showed higher methylation in site 3 and 4 on the Pomc promoter, NF-KB potential binding sites, compared to offspring of control fathers. OtHFDf gained significantly more weight and tended to have higher plasma leptin levels than controls in HFD challenge, at PND60. OtHFDf presented significantly higher Pomc and AgRP mRNA levels, compared to chow fed offspring of chow-fed fathers. Pomc promoter of adult HFD-fed males’ spermatozoon was relatively hypermethylated in CpG sites 1-4 and they showed higher percentage of total methylation compared to chow-fed controls.
Conclusions: These results support paternal epigenetic heredity of obesity-related traits.
Support: Israel Science Foundation.
Powered by Eventact EMS