You are what your mother ate
Poor diet during pregnancy increases an offspring's vulnerability to the effects of aging, according to research by scientists at the University of Cambridge (Cambridge, UK). Their findings, published online on March 8 in the Proceedings of the National Academy of Sciences, provide insight into why children born to mothers who consumed an unhealthful diet during pregnancy have an increased risk of type 2 diabetes (a significant contributing factor to heart disease and cancer) later in life.
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"What is most exciting about these findings is that we are now starting to really understand how nutrition during the first nine months of life spent in the womb shapes our long-term health by influencing how the cells in our body age," said Susan Ozanne, the senior author on the paper.
It is well established that environmental factors interact with genes throughout life, affecting the expression of those genes and, consequently, tissue function and disease risk. Diet during critical periods of development, such as during the nine months in the womb, has been cited as one such environmental factor. Epigenetics, which refers to modifications to DNA that regulate how much of a gene is produced, has been suggested to underlie these effects.
However, until now, very little was understood about the underlying mechanisms that control the interaction between diet during gestation and gene expression in offspring throughout their adult life. Research, funded by the Biotechnology and Biological Sciences Research Council and the British Heart Foundation, has now shown that the gene Hnf4a, which has been linked to type 2 diabetes, is regulated by maternal diet through epigenetic modifications to our DNA. Additionally, they found that poor diet exacerbates the rate at which these key epigenetic modifications accumulate during the aging process.
Previous research has shown that the gene Hnf4a plays an important role both during development of the pancreas and later in the production of insulin. The researchers hypothesized that diet during pregnancy influences the expression of this gene later in life, thereby influencing the risk of diabetes.
To test their theory, the researchers used a well-established rat model where, by altering the protein content of the mother's diet during pregnancy, the offspring develop type 2 diabetes in old age.
First, they studied the RNA from insulin-secreting cells in the pancreas from offspring of normally fed as well as malnourished mothers in young adult life and in old age. When they compared the two, they found that there was a significant decrease in the expression of the Hnf4a gene in the offspring prone to type 2 diabetes. The expression of Hnf4a also decreased with age in both groups.
Second, they studied the DNA and found that the decrease of Hnf4a was caused by epigenetic changes. The age-associated epigenetic silencing was more pronounced in rats exposed to poor maternal diet. They concluded that the epigenetic changes resulting from maternal diet and aging lead to the reduced expression of the Hnf4a gene, decreasing the function of the pancreas and therefore its ability to make insulin (and thereby increasing the risk of diabetes).
The scientists then studied the DNA from insulin-secreting cells from human pancreases to show that expression of this important gene was controlled in the same way in humans.
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