A group of Japanese scientists has found the answer to the puzzle, according to a study by researchers at Japanese universities in Tokyo and Saga, published by the online edition of the journal Human Reproduction.

The tests in mice indicate that paternal sperm is responsible for the shorter longevity of mammalian male versus females.

In their experiment, scientists have discovered that mice created using genetic material from two mothers and without the involvement of a parent living up to one third longer than normal mice with a mixture of maternal and paternal genes.

To explore this issue, researchers began to study the lifespan of mice produced no sperm. To this end, immature oocytes collected from mice one day old, manipulated the genetic material of these genes to behave like sperm and transplanted genes from this genetic material in unfertilized mature oocytes from adult mice that had eliminated the core.

These reconstructed oocytes became embryos which were transferred to a female mouse. The resulting pups had genetic material from two mothers but no father.

Furthermore, the authors created mice control through a natural pairing that were genetically identical mice from two mothers, irrespective of the fact that they were created in the normal way with genes of male and female mice. Both groups of mice were kept in the same environments without infections and with free access to food.

The study results were inconclusive. The mice created from two genomes women lived an average of 186 days longer than control mice created from the combination of a normal female and one male genome, whose life expectancy is between 600 and 700 days. These modified mice seemed to have a better immune system, with a significant increase in a type of white blood cell, eosinophils.

The study authors believe the reason for the difference in longevity may be related to a gene on chromosome 9, named Rasgrf1. “This gene is usually expressed from the chromosome inherited from the father and is a gene on chromosome 9 associated with postnatal growth,” said Tomohiro Kono of Tokyo University and co-author.

“Does not just genetics”

“This is very important genetic component in longevity of people,” agrees Mary Flora de Pablo, Professor, Biological Research Center of CSIC. The researchers say the study is “interesting model” which completes the analysis of the lifespan of mice on a type called “bimaternos” and on data that had already been published since 2004.

But longevity also “depends on environmental factors, modifiable,” explains De Paul. For example, “low-calorie diet, (without going to malnutrition) increases longevity and delays the onset of diseases associated with aging,” qualifies the teacher.

The end result of increased life expectancy in women than men in the developed world “is also a significant component derived from lower-risk behaviors in women than in men,” says the researcher, including appointment to a lower consumption of alcohol and drugs.

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Through an association study of the entire genome, the researchers found that a certain group of genes that reacts in response to viral infection was present in both rats and humans, and that these same genes were also associated with susceptibility to diabetes type 1.

“The diseases arising as a result of many genetic and environmental factors through networks of genes that cause tissue damage,” said Dr. Stuart Cook, author of the study, group director of molecular and cellular cardiology Science Center Clinical Medical Research Council and professor of clinical and molecular cardiology at Imperial College London.

“We use a method to identify the central command of the important control points of a network of genes of inflammation. This led us to discover hundreds of new genes that may cause diabetes, and a major control gene that controls the entire network” said Cook.
He added that one gene belongs to a class of genes that might be a good target for drug therapy in the future.

Each year in the U.S.. UU., More than 30,000 people are diagnosed with type 1 diabetes, formerly known as juvenile diabetes, according to the Juvenile Diabetes Research Foundation (JDRF). People suffering from type 1 diabetes do not produce enough hormone insulin to effectively utilize the sugars found in foods containing carbohydrates. To survive, people with type 1 diabetes must inject insulin or use an insulin pump for the rest of their lives.

Experts believe the disease is autoimmune, which means that the body’s immune system mistakenly attacks healthy cells, including cells of the pancreas that produce insulin, and destroys them. It is believed that people who develop type 1 diabetes have a genetic susceptibility to the disease, which is then triggered by something in the environment, perhaps a virus.

In the current study, researchers at first tried to find genes for type 1 diabetes. They began observing a certain set of genes in rats, in this case a network of genes controlled by a gene called interferon regulatory factor 7 (IRF7). The IRF7 is a master switch gene that controls your network. Overall, the network of genes controlled by IRF7 is known as a network of inflammation driven by IRF7 (IDINA). The researchers found that when there were differences in IRF7 also were differences in the way that other genes are expressed.

Then, Cook and colleagues looked for a network of genes in humans to behave in the same way. They found an area on chromosome 13q32 which is controlled by a gene called “induced gene 2 of Epstein-Barr virus (Ebi2). This gene seemed to be the human equivalent to the IRF7 gene in rats.
In this human version of Idina, the research found a gene called IFIH1, according to other research that is associated with the development of type 1 diabetes. “Generally, the investigation began in genetics and passed to the function. Here, starting with a function [a reaction of the immune system] and looking for a gene,” said Marie Nierras, director of research and scientific affairs at JDRF.

“The value of a result so if you can reach the same place using more than one way, this tends to support the hypothesis,” he said.

In this case, the hypothesis is supported the idea that Type 1 diabetes could be triggered by an immune system response to a virus. However, Nierras emphasized that this study does not prove conclusively that a virus is the trigger for type 1 diabetes.

“Today we know with more certainty that this network of genes has something to do, and a network, objectives may be obtained for evaluation. This research invites us to plan future experiments, and raises many more questions, as if to interrupt this branch of the network interrupt diabetes. Or, if you look at previous research with the knowledge of the results of this study, would help better explain why previous results? “Nierras raised.

Cook said that this type of association study of the entire genome can also be used for other diseases, and that this team hopes to eventually develop a new drug based on genetic target discovered.

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