Aurora magazine

Short chain fatty acids from the microbiota suppress insulin signals, reducing fat deposits. According to a study published in Science, the phenomenon could also affect fetal development. Indeed, some experiments show that acids can cross the placenta, passing from the maternal microbiota to the fetal environment. They could therefore regulate insulin levels and also affect the development of the baby's metabolism.

In recent years, the intestinal microbiota has been undergoing attacks both from the massive use of antibiotics and from the low-fiber diet. The lack of a healthy and functional microbiota exposes to various diseases, most of which are metabolic. The authors of the study then analyzed the effects in pregnancy, to verify whether they involved only the mother or even the fetus.

The researchers divided pregnant guinea pigs into two groups: half spent gestation in an environment free of a specific pathogen, half in a germ-free environment. The small ones in the second group were much more prone to develop metabolic problems. Later, they repeated the experiment; this time, the guinea pigs of the second group ate few fibers throughout the gestation. Again, the little ones experienced the same problem.

According to the researchers, the short chain fatty acids of the gut microbiota pass from the mother to the fetus. When the microbiota is deficient, the embryo receives less fatty acids. The deficit affects the development of the baby's metabolic system, thus making it more vulnerable to future obesity problems.

Source: sciencemag.org

An IDIBELL Neurometabolic Diseases team has identified a new model for X-linked adrenoleukodystrophy, also called X-ALD. The models in question are the Caenorhabditis elegans or C. elegans, worms about 1 millimeter long with a very simple organism. This will facilitate the study of the disease, for which there are no treatments at the moment.

X-ALD is a rare genetic disorder that affects the nervous system. Until now, the study of the disease has been complicated: there were no effective models that would allow the study of possible pharmacological targets. The job in question could change things.

Researchers believe that C. elegans is a perfect model for the disease. The worms in question may indeed suffer from a similar version of human disease, characterized by the deficit of the ALDP protein. This makes it possible to study the effects of this deficit in a controlled environment and, above all, to find a way to counter them.

The first results are encouraging: Dr. Esther Dalfó reports the discoveries made to date. The tests done on C elegans suggest that the neurological alterations typical of the disease are caused by the cells of the glia. The oxidative stress caused by the mitochondria would damage the cells in question, leaving the nerve tissues exposed. This would lead to the damage found in those suffering from the disease. The next step will be to understand how to stop the process.

There are several branches of medical research that make use of C. elegans. These worms are small and simple, despite having characteristics similar to those of much more complex animals. In addition, 40% of their genome is homologous to ours.

Source: idibell.cat

For years they have told us the same story: whoever wakes up late is a lazy person, does not have enough willpower. Reality is much more complex. Research conducted by the University of San Francisco shows that genes decide - at least in part - what time we wake up. The habit of getting up at 5 in the morning could therefore depend on our DNA.

The study authors analyzed the data and DNA of 2,422 volunteers. The participants are all under 30 years old and usually wake up between 3 and 5 in the morning. Among their relatives, there is at least one with similar habits. This last detail confirms the idea that it is behavior dictated by genes, rather than habit.

According to the study, the time we get up depends largely on our membership chronotype. About one in 300 people have what causes them to wake up very early, while others are prone to get up later. Each chronotype is determined by different genetic variants, which determine the relationship between sleep and wakefulness. In some cases, the chronotype is similar in all family members. Much more often, it also changes within the same family.

The most interesting discovery, however, does not concern the times of our alarm clock. Genetically morning people could be at an advantage, at least on a social level. Those who wake up early are better off in the studio, more successful at work and more proactive. According to the researchers, it could be due to early exposure to sunlight, which stimulates the metabolism and improves mood.

Source: d.repubblica.it

Antenatal oxygen deficiency could favor the appearance of schizophrenia. The deficit is in fact linked to preeclampsia, which in turn could affect astrocytes. The effects of hypoxia on these brain cells could favor the appearance of the disease. This was stated in a study published in Scientific Reports, conducted by the Santa Casa de São Paulo Medical School (FCM-SCSP) in Brazil.

The researchers observed the effects of hypoxia on astrocyte mitochondria. Indeed, astrocytes are the most numerous cells within the brain, as well as the most important. Their job is to metabolize neurotransmitters such as glutamate, a key factor in schizophrenia. Their malfunction could therefore change the way neurons communicate, even leading to brain damage.

The author of the study, Dr. Luiz Felipe Souza and Silva, analyzed the effects of hypoxia in guinea pigs affected by hypertension. Babies born from guinea pigs exhibited schizophrenia-like symptoms in humans. Treatment with antipsychotic drugs has alleviated the symptoms, just like in humans. From what has been observed, cells subjected to hypoxia have altered mitochondrial calcium levels.

This hinders the production of energy for astrocytes, which therefore are unable to combat oxidative stress. Still, some types of hypoxia do not have this effect, on the contrary: cells produce a greater number of mitochondria, to balance their malfunction. The researchers are therefore looking for a way to trigger this process in case of hypoxia, so as to reduce the risk of permanent consequences.

Source: fapesp.br/en