What is an epigenetic effect

Epigenetics: Eating habits are reflected in the genome

Genes or the environment - which one has more power over our health? There is no simple answer, this is also and particularly evident in complex metabolic diseases such as obesity and diabetes. Due to their genetic makeup, some people are at a higher risk of disease than others. However, whether they actually become obese or diabetic in the course of their lives depends to a large extent on their eating habits and sporting activities. A new discipline called epigenetics is researching the extent to which the body's own and external influences overlap and influence one another (see info box). According to this, we not only inherit a large number of health-relevant genes from our parents, but also their epigenetic programming - and thus the probability of whether and how severely certain diseases break out.

It has long been known that expectant parents set the course for the development of their children through their lifestyle. That is why women are well advised to avoid tobacco and alcohol as much as possible during or some time before pregnancy. But future fathers also have an impact on the later health of their children: Smoking and an unhealthy diet change the epigenetic code - and thereby determine which genes in the genome are activated and which are not. Such changes can occur, for example, in intestinal, fat or liver cells, but also in sperm and egg cells and are then passed on to the offspring during conception.


A team of scientists from the German Center for Diabetes Research (DZD) at the Helmholtz Center in Munich and the Technical University of Munich has now examined the type and extent of the inheritance of epigenetic information in more detail. The studies were carried out on a strain of mice, the animals of which are genetically largely identical. If these mice are fed a particularly high-fat food, they become overweight and develop type 2 diabetes. Earlier studies had shown that the offspring of diseased mice, compared to offspring of healthy conspecifics, accumulate more fat faster and more fat when they eat fatty food.

The DZD researchers investigated the question of what causes these serious differences in the development of the mouse pups. To do this, they fed a group of rodents with high-fat food until the animals were fat and diabetic. A group of control animals, on the other hand, received normal food and accordingly remained slim and healthy. Afterwards, fat and slender mice should be paired specifically in such a way that four groups of offspring result: those with two fat parents or two slender parents and those with only one fat parent. A difficulty had to be overcome that had made the interpretation of earlier studies difficult: How can epigenetic influences be separated from other effects of the parental organism? Fat and slender dams could in fact shape the health development of their young in different ways due to their deviating metabolism, either during pregnancy or later when suckling - regardless of possible epigenetic influences. The research team around study director Prof. Dr. Johannes Beckers found a way out of this dilemma. It brought egg cells and sperm from fat or slender test animals together in a test tube and then had the artificially created embryos carried to term by healthy mice of the same strain. This enabled the epigenetic effects of the maternal and paternal germ cells to be broken down; In addition, it was impossible for them to be superimposed by physiological signals from the maternal organism.

The research, which was carried out with funding from the Federal Ministry of Education and Research (BMBF), recently appeared in the renowned journal "Nature Genetics". DZD board member Prof. Dr. Martin Hrabě de Angelis summarizes the most important results of the study he initiated: "We were able to show for the first time that the inheritance of acquired traits - in this case obesity, i.e. a derailed metabolism - is actually passed on through epigenetic mechanisms." Both the paternal and the maternal path, says the scientist: “We see two different effects in the daughter generation: on the one hand, an increase in weight and, on the other hand, a metabolic derailment in the form of insulin resistance. Fathers and mothers contribute roughly the same amount to weight gain, although the underlying mechanisms are different. In the case of insulin resistance, the maternal influence seems to be stronger. ”A detailed analysis revealed that male and female offspring are affected differently by the epigenetic inheritance: the daughters of fat mice put on even more weight than their brothers; those, on the other hand, had bigger problems with blood sugar.


Martin Hrabě de Angelis sees the results of the study as a possible explanation for why more and more people have been suffering from obesity and diabetes since the 1960s: “Changes in the genes themselves cannot explain this increase; it is progressing too quickly. Now we have found another important cause: the epigenetic inheritance of a metabolic disorder acquired through malnutrition. ”Molecular biological studies should now provide information about the chemical changes in the genome of the germ cells. In addition to various RNA transcripts in the cell body, chemical changes at certain points in the DNA, so-called methylations, are also possible.

Another research team at the DZD under the leadership of the German Institute for Nutritional Research (DIfE) in Potsdam-Rehbrücke discovered that diet-related changes in methylation patterns can drastically influence the state of health of mice. The scientists around Prof. Dr. Annette Schürmann had fed genetically identical mice on a high-fat diet and then documented the health development of the animals. It turned out that some mice gained much more weight than the other animals and that they also developed fatty liver in adulthood. How did these clear differences come about in genetically identical mice? A thorough analysis showed that a gene involved in lipid metabolism in the sick animals was epigenetically modified by increased methylation as early as six weeks. As a result, the gene product was produced in significantly smaller quantities in the liver of the affected mice, until the sugar metabolism finally derailed. The phenomenon is not limited to mice: the DIfE researchers also found the same epigenetic changes in the blood cells of people who suffered from abnormal obesity and impaired sugar metabolism.

Presumably there are certain time windows in which epigenetic information can be established permanently or can be withdrawn again. “Finding this time window is our great hope,” emphasizes Hrabě de Angelis, referring to a promising experiment: “If you have a metabolic imbalance in mice at a very early stage and later change their diet so that these animals become normally slim again, then the problem is not carried over to the next generation. ”This opens up new possibilities for influencing the development of obesity and diabetes, believes the Munich scientist and emphasizes:“ A good lifestyle not only promotes one's own health, it also pays off for generations later out."

Epigenetics is a new discipline within genetics. She researches the properties of genes that appear not through the DNA itself, but through its readiness for reading. Epigenetic information is conveyed by various biomolecules, which, like chemical locks, deny or enable access to certain DNA sequences and thus control whether they can be activated. In addition to the genes themselves, the epigenetic code also determines our fate. It can cause a person to develop a hereditary disease while sparing their genetically identical twin. Some epigenetic markings change in a day-night rhythm, others remain permanent, and still others are passed on to subsequent generations via the germ cells. Which epigenetic code is established in a person and whether it changes in the course of life is determined not only by the body's own signaling substances, but also by eating habits and other aspects of lifestyle. The DZD examines the importance of epigenetic factors in the development of diabetes and obesity.

Contact Person:
Prof. Dr. Johannes Beckers
Institute for Experimental Genetics
Helmholtz Centre Munich
German Research Center for Health
and environment (GmbH)
Ingolstädter Landstrasse 1
85764 Neuherberg
089 3187-3513
089 3187-4084
[email protected]

Prof. Dr. Dr. h.c. Martin Hrabě de Angelis
Institute for Experimental Genetics
Helmholtz Centre Munich
German Research Center for Health
and environment (GmbH)
Ingolstädter Landstrasse 1
85764 Neuherberg
089 3187-3302
089 3187-3500
[email protected]

Press contact:
Dr. Astrid Glaser
Press and public relations
German Center for Diabetes Research V.
Office at the Helmholtz Center Munich
Ingolstädter Landstrasse 1
85764 Neuherberg
089 3187-1619
089 3187-2223
[email protected]