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You Are What Your Father Ate

January 4, 2011

(Ivanhoe Newswire) — We’re all familiar with the saying, “Ëœyou are what you eat.’  That is true, however, it was recently reported that we are also what our parents ate too.

Researchers shed light on an emerging idea showing mice sired by fathers fed on a low-protein diet demonstrate various and reproducible changes in the activity of chief metabolic genes in their livers.  Those changes ““ despite the fact that the fathers never saw their offspring and spent minimal time with their mothers ““ occurred and suggest that the nutritional information is passed on to the next generation via the sperm and not through some sort of social influence.

Epigenetic reprogramming ““ heritable chemical modifications to DNA that can modify the way genes are expressed without altering the fundamental sequence of their As, Gs, Ts and Cs ““ of genes may be a significant mechanism for passing information about the environment, and in this case the nutritional environment, from one generation to the next. “The take away is that we are more than just our genes,” which Oliver Rando of University of Massachusetts Medical School was quoted as saying, “and there are many ways our parents can ‘tell’ us things.”

The concept that what our fathers and grandfathers ate can influence our metabolism isn’t one that is recent.  Perhaps the paramount evidence in humans comes from epidemiological studies demonstrating that if your paternal grandfather went hungry, then you will be at a larger risk of developing both obesity and cardiovascular disease.  Earlier this year, a study in rats found that fathers on a high-fat diet can pass health problems on to their daughters.

The researchers of the latest study nonetheless wanted to investigate whether environmental conditions have transgenerational effects by screening the movement of genes in mice whose fathers were fed on a low-protein diet from the time they were weaned until they reached sexual maturity.  It was reported that hundreds of genes altered in the offspring of those protein-starved males.  Epigenomic profiling of the young mouse livers illustrated abundant differences depending on paternal diet, including but not limited to chemical modification of a sequence of DNA that is thought to serve as an enhancer for the key lipid transcription factor known as Ppara.  Those alterations were linked with lower activity of the Ppara gene.  “It’s consistent with the idea that when parents go hungry, it’s best for offspring to hoard calories,” Rando added, noting the transcription factor’s role in controlling cholesterol and lipid synthesis in the liver.

It isn’t yet apparent whether the changes in cholesterol metabolism will substantiate favorable in the circumstance of a low-protein diet, although it’s an alluring idea.

They aren’t sure yet how the information is encoded and passed from father to offspring either.  It isn’t evident in that the sperm don’t show identical epigenetic pattern seen in the livers of the offspring.

One thing is clear however; these most recent findings in combination with additional proof have essential implications for future studies and their mice now present a practical model for working out the mechanisms accountable for transgenerational reprogramming of metabolism.

“Together, these results suggest rethinking basic practices in epidemiological studies of complex diseases such as diabetes, heart disease, or alcoholism,” researchers concluded. “We believe that future environmental exposure histories will need to include parental exposure histories as well as those of the patients to disentangle induced epigenetic effects from the currently sought genetic and environmental factors underlying complex diseases.  Our observations provide an inbred mammalian model for transgenerational reprogramming of metabolic phenotype that will enable dissection of the exposure history necessary for reprogramming and genetic analysis of the machinery involved in reprogramming, and they suggest a number of specific pathways likely to be the direct targets of epigenetic reprogramming.”

Rando is interested to see what exactly occurs in the next generation of mice.  “The human studies suggest that it is grandchildren who are most affected by their grandparents’ exposure histories,” he adds.

SOURCE: Cell, January 2011




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