Maternal diet and obesity can cause “fatty liver” in fetus, study finds
08 Mar 2018 --- Obesity and a high-fat, high-sugar diet during pregnancy may predispose children to obesity, study finds. The study, published in The Journal of Physiology, found that such conditions create a “fatty liver” in the fetus. The observations may explain why children of obese mothers live shorter lives than the offspring of normal weight mothers. "Fatty Livers" can lead to very troubling issues including later life obesity, cancers, and metabolic and cardiovascular problems.
“This research is important as throughout the world over fifty percent of women of reproductive age are overweight or obese. Maternal obesity, combined with high fat, high sugar diets, makes it more likely that children will suffer from liver disease and face health problems such as obesity and heart disease later in life,” commented Peter Nathanielz, one of the lead researchers.
The primate study aimed to shed light on the poorly understood mechanism of “developmental programming.” In this context, this means the link between obese pregnant mothers and the obesity in their child. It found that as the fetus develops in an obese woman, fat accumulates in its liver and many metabolic pathways are disturbed.
Although there is always some fat in the liver, levels that are considered above normal lead to a “fatty liver.” Importantly, if dealt with early, this can be reversed and the negative implications potentially avoided.
In fact, this study is a first in reporting the critical discovery of microRNAs (a DNA product which modifies protein synthesis) and their role in this increased deposition of liver fat. The discovery was made in non-human primates.
In order to determine which genes were changed in the liver of the fetuses of obese pregnant monkeys, and to identify which microRNAs regulate these genes, genomic and epigenomic methods were used.
The altered cellular signaling pathways were identified using bioinformatics approaches, and microscopic studies were conducted to quantify the amount of stored fat and sugar present in the liver cells. Their shape was also assessed, as this is also an indicator of liver cell health.
“It wasn’t until we saw the microscope slides for the staining of liver sections showing very high amounts of lipid in fetuses of obese mothers that we realized the dramatic impact of maternal obesity at such an early developmental time point. Histological analyses of these livers showing the condition steatosis, underlined the detrimental impact of maternal obesity on the developing fetus,” Nathanielz adds.
Although the researchers were able to see significant changes, there are still limitations with generalizing the findings. For example, a significant principle of developmental programming is that substantial changes may lie dormant in subjects, only to emerge under stress of when hormones kick in around puberty or aging.
The researchers now plan to investigate now the metabolic and cardiovascular health of the offspring of obese monkey mothers, including liver function at regular intervals across the life course to follow the progress of these fetal changes.
This will allow them to assess whether unwanted consequences of maternal obesity can pass across generations from mother to daughter to grandchildren. They also plan to identify interventions that can reverse these adverse changes using the same technologies employed in this study.
These findings could have immensely important implications for a society that is struggling under the weight of childhood obesity. About one in three children is overweight in the USA today.
