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Epigenetics. © INRA, INRA

Livestock epigenetics: laying the foundation for future benefits

Epigenetics and foie gras

Work carried out at the INRA research center in Toulouse (in collaboration with two other experimental research units) has shown that if female ducks consume a methionine-deficient diet, the liver mass of their offspring is affected. Researchers have hypothesized that this effect is the result of epigenetic mechanisms, namely DNA or histone hypomethylation.

By Pascale Mollier, translated by Jessica Pearce
Updated on 07/10/2014
Published on 05/22/2014

Five mulard ducklings clustered together on their litter.. © INRA, SLAGMULDER Christian
Five mulard ducklings clustered together on their litter. © INRA, SLAGMULDER Christian

Foie gras is often produced using mulard ducks. The mulard is a hybrid breed created by mating a “common” (Pekin) duck with a Muscovy drake; it is particularly well suited to foie gras production. Researchers at the INRA research center in Toulouse are studying how the amount of dietary methionine consumed by a Pekin female can affect her mulard offspring. Methionine is an essential amino acid and acts as a donor of activated methyl groups, which can then be added to various molecules in the cell (see box below).

The amount of methionine available to females affects the liver mass of their offspring

The Toulouse group conducted an experiment in which they fed Pekin ducks a methionine-deficient diet and then bred them with Muscovy drakes to obtain mulard offspring, which were raised to produce foie gras. Liver mass was then compared for the 17 male and 18 female mulards in the treatment group and an equivalent number of male and female mulards born to mothers fed a normal diet.

There was a significant difference between the two groups: compared to the control, liver mass in the treatment group increased by 70 g for males and decreased by 100 g for females. When the eggs of ducks in the treatment group were examined, they were found to contain lower levels of nutrient reserves.

In light of other research results (see below), the researchers have come up with a hypothesis that remains to be tested: when a female consumes a methionine-deficient diet, it affects liver mass in her offspring because of epigenetic mechanisms, namely DNA or histone hypomethylation resulting from a scarcity of methyl groups.

Other work suggests that dietary methionine availability affects liver metabolism as well

Another study examined the effects of methionine deficiency in sheep (1). Female sheep were fed a methionine-deficient diet, starting eight weeks before they conceived and ending six days after conception. At that point, their embryos were transferred to surrogate females that had not been fed a methionine-deficient diet. When the lambs carried to term were 22 months old, they weighed significantly more than average. When the methylation patterns of genes found in the liver cells of 90-day-old fetuses were examined, it was found that hypomethylation was omnipresent in the lambs conceived by the females fed the methionine-deficit diet, a pattern that was more pronounced in males. These results show that epigenetic modifications tied to dietary deficiencies in methionine can take place shortly after conception.  

A separate study in rats (2) has found that lipids build up in the livers of animals born to mothers with low levels of methyl group donors (such as methionine). This phenomenon, referred to as hepatic steatosis, is tied to the hypomethylation of a transcriptional activator involved in fatty acid metabolism.

(1) Sinclair KD, Allegrucci C, Singh R, Gardner DS, Sebastian S, Bispham J, Thurston A, Huntley JF, Rees WD, Maloney CA, Lea RG, Craigon J, McEvoy TG, Young LE. 2007. DNA methylation, insulin resistance, and blood pressure in offspring determined by maternal periconceptional B vitamin and methionine status. Proc Natl Acad Sci U S ADec; 104 (49):19351-6.

(2) Pooya S, Blaise S, Moreno Garcia M, Giudicelli J, Alberto JM, Guéant-Rodriguez RM, Jeannesson E, Gueguen N, Bressenot A, Nicolas B, Malthiery Y, Daval JL, Peyrin-Biroulet L, Bronowicki JP, Guéant JL. 2012. Methyl donor deficiency impairs fatty acid oxidation through PGC-1α hypomethylation and decreased ER-α, ERR-α, and HNF-4α in the rat liver. J HepatolAug; 57 (2):344-51.

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Associated Division(s):
Animal Genetics , Animal Physiology and Livestock Systems
Associated Centre(s):
Occitanie-Toulouse

METHIONINE: AN ESSENTIAL AMINO ACID

Methionine is a nonpolar sulfur-containing alpha-amino acid. Its sulfur atom is part of a thioether functional group (-S-CH3). It is one of the eight essential amino acids in humans, and it plays a crucial role in reproduction, cell survival, protein methylation, and DNA methylation. Methionine is a precursor of S-adenosylmethionine, or SAM, a molecule that acts as a methyl (CH3) donor: the sulfur atom in the thioether group readily releases the methyl group. This makes methionine an essential metabolite in transmethylation reactions in cells (e.g., methylation of DNA, RNA, or proteins).