High-fat diet during pregnancy overrides genes in children, say researchers

By Eliot Beer

- Last updated on GMT

'We conclude that the protection from diet induced obesity in Gipr-/- mice is ‘overruled’ by deleterious and persistent foetal programming effects of a high-fat diet,' wrote the authors. © iStock
'We conclude that the protection from diet induced obesity in Gipr-/- mice is ‘overruled’ by deleterious and persistent foetal programming effects of a high-fat diet,' wrote the authors. © iStock

Related tags: Obesity

A mother’s high-fat diet during pregnancy can override offspring’s genes and cause weight gain and insulin resistance, according to a new animal study in the journal Diabetes.

The study by a German team used “Gipr-/-​“ mice – animals bred without the gene to create receptors for the gut hormone gastric inhibitory polypeptide (GIP), the absence of which stops mice from becoming obese. Using pregnant mice, the researchers fed one group of Gipr-/- animals with a high-fat diet, another Gipr-/- group with a regular diet, and one group of wild-type, unaltered mice with a regular diet – the diets were maintained during the animals pregnancies and lactation periods.

The team then fed the weaned offspring from all three groups a regular diet for 22 weeks, followed by a high-fat diet for 20 weeks. Their results from this showed the parental high-fat diet had overridden the absence of the GIP receptor genes.

High-fat diet’s delayed effect

Our results demonstrate that Gipr-/- mice exposed to a high-fat diet during IU/L [pregnancy and lactation], weaned onto a regular chow for 22 weeks and then re-exposed to the HFD lose their metabolic protection​,” wrote the study’s authors.

This phenotype was similar to wild type mice which were exposed to a control chow during IU/L, but also challenged with a high-fat diet later in life. We therefore conclude that the protection from diet induced obesity in Gipr-/- mice is ‘overruled’ by deleterious and persistent foetal programming effects of a high-fat diet​,” they added.

The researchers described the effects of a high-fat diet as a “first hit” during pregnancy, which then made the mice overreact to the “second hit” of their own high-fat diet as adults. The Gipr-/- mice exposed to a high-fat diet during pregnancy and lactation also had larger fat storage cells (adipocytes), which are correlated with adipose tissue dysfunction and insulin resistance.

The GIP signalling pathway is necessary for adipocyte development. This might explain why lacking the GIPR protects Gipr-/- mice from diet induced obesity. However, if the HFD appears as a ‘second hit’ later in life, this protection disappears and the foetal programming effect of a HFD overrules the Gipr-/- phenotype​,” wrote the authors.

Some protection remains

They did note that the Gipr-/- mice exposed to a high-fat diet as foetuses still gained less weight than wild-type mice, when exposed to a high-fat diet as adults. This may mean there is some residual protection from the absence of GIP receptors, they suggested.

Andreas Pfeiffer, professor at the German Institute of Human Nutrition and co-author of the paper, said: “Our results indicate that the GIP also plays a role in energy consumption, which is controlled by the brain, probably indirectly by reducing the insulin sensitivity of the hypothalamus​.”

The study’s authors said that while it could not be ruled out that these findings were applicable to humans, more study in this area is needed. 

Source: Diabetes

Published online ahead of print, doi: 10.2337/db15-047

A High Fat Diet during Mouse Pregnancy and Lactation targets GIP-regulated Metabolic Pathways in Adult Male Offspring​”

Authors: Kruse, M; Keyhani-Nejad, F; Isken, F; Nitz, B; Kretschmer, A; Reischl, E; de las Heras Gala, T; Osterhoff, M A; Grallert, H; Pfiffer, A F H

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