This 2018 US baboon study was on fetal effects from maternal obesity before and during pregnancy:
“Approximately 64% of women of childbearing age in the USA [are] overweight or obese..The baboon is a well-characterized animal model sharing many physiological, metabolic, and genetic characteristics with humans allowing direct translation of findings to human pregnancy.
Our study shows that fetal exposure to the MO [maternal obesity] intrauterine environment results in dysregulation of fetal hepatic genes central to metabolism.
These findings were further supported by identification of miRNAs that were inversely expressed with key genes in these pathways..suggest important early molecular mechanisms by which MO programs fetal hepatic lipid metabolism.
Future studies are required in MO post-natal offspring to determine the extent to which the fetal phenotype persists, and the degree to which this increases offspring risk of cardiometabolic disorders in later life.”
The study provided many measurements that may be relevant to humans. Other consequential measurements were missing that may have made the study’s findings even more applicable to humans:
- No placental measurements other than weight. The organ through which the fetus received its nutrients, signaled its needs, modulated its growth rate, developed its organs, was only measured by weight?
- No other epigenetic analyses such as DNA methylation and histone modifications.
Were these omitted due to limited resources?
http://onlinelibrary.wiley.com/doi/10.1113/JP275422/pdf “Primate fetal hepatic responses to maternal obesity: epigenetic signalling pathways and lipid accumulation”