Efecto de los polifenoles sobre la microbiota intestinal en el síndrome metabólico

Durante los últimos años, el estudio de la microbiota intestinal ha surgido como un campo de investigación emergente, ya que se ha demostrado que se ve involucrada en una infinidad de procesos metabólicos que repercuten en la salud del huésped. En concreto, se ha visto que las personas que padecen alguna de las patologías asociadas al síndrome metabólico poseen una microbiota intestinal alterada que provoca un estado patológico denominado “disbiosis intestinal”. Este estado, provocado en parte por el consumo actual de dietas altas en grasa y azúcares y pobres en fibra, se caracteriza por una disminución de la diversidad microbiana y una alteración en su composición, y parece estar fuertemente relacionado con la aparición y desarrollo de las patologías del síndrome metabólico. Entre las distintas estrategias descritas para modificar la microbiota intestinal alterada, se ha observado que la suplementación de la dieta con ciertos tipos de polifenoles, como el resveratrol o las antocianinas, pueden revertir la disbiosis intestinal, ayudando a la proliferación de bacterias beneficiosas para nuestro organismo, como Akkermansia muciniphila, a la vez que disminuyen la cantidad de bacterias nocivas, como las pertenecientes al filo Firmicutes y estimulando así una mayor producción de ácidos grasos de cadena corta, como el butirato. En este trabajo se ha llevado a cabo una revisión de la bibliografía disponible sobre la capacidad de diversos polifenoles (no flavonoides, flavonoles y flavanoles) de contrarrestar el efecto de una dieta occidental sobre la microbiota intestinal, revirtiendo los efectos del síndrome metabólico, así como un estudio de los principales mecanismos implicados en este proceso.In recent years, the study of the intestinal microbiota has emerged as a field of research. Since it has been shown that it is involved in an infinite number of metabolic processes that affect the health of the host. Specifically, people suffering from any of the pathologies associated with the metabolic syndrome have an altered intestinal microbiota that causes a medical state called "intestinal dysbiosis". This state is caused partially due to current consumption of diets high in fat and sugars, and poor in fiber. Consequently, decreasing microbial diversity and altering its composition. Strongly correlating with the appearance and development of metabolic syndrome pathologies. Among the different strategies described to modify the altered intestinal microbiota, it has been observed that dietary supplementation with certain types of polyphenols, such as resveratrol or anthocyanins can reverse intestinal dysbiosis. Therefore, promoting the proliferation of beneficial bacteria for our body, like Akkermansia muciniphila, while reducing the number of harmful bacteria such as those belonging to the Firmicutes phylum. As a result, stimulating a greater production of short chain fatty acids as butyrate. This paper reviews the available literature on various polyphenols (non-flavonoids, flavonols and flavanols) and their ability to counteract the effect of a western diet on the intestinal microbiota. Focusing on reversing the effects of the metabolic syndrome, as well as analyzing the main mechanism involved in this process

A new potential oncogenic mutation in the FERM domain of JAK2 in BCR-ABL1 negative and V617F negative chronic myeloproliferative neoplasms (CMPNs) revealed by a comprehensive screening of 17 tyrosine kinase coding genes

BCR/ABL1-negative chronic myeloproliferative neoplasms (CMPNs) are a heterogeneous group of clonal hematological malignancies. Over recent years, some genetic events in tyrosine kinase (TK) genes have been described as causal events of these diseases. To identify new genetic aberrations underlying these diseases, we used denaturing high performance liquid chromatography and fluorescence in situ hybridization (FISH) to analyze 17 genes from two receptor-TK families (III and IV) and from three cytoplasmic-TK families (Syk, Abl, and Jak) on samples from 44 BCR/ABL1-negative and JAK2(V617F)-negative CMPN patients with different clinical phenotypes. Although screening by FISH did not reveal novel chromosomal aberrations, several sequence changes were detected. None of them were frequent events, but we identified a new potential activating mutation in the FERM domain of JAK2(R340Q). None of the germline JAK2(V617F) single-nucleotide polymorphisms detected differed in distribution between patients and control subjects. In summary, data presented here show that these genes are not frequently mutated or rearranged in CMPNs, suggesting that molecular events causing these disorders must be located in other genes