44 research outputs found
Efecto de los polifenoles sobre la microbiota intestinal en el siÌndrome metaboÌlico
Durante los uÌltimos anÌos, el estudio de la microbiota intestinal ha surgido como un campo de investigacioÌn emergente, ya que se ha demostrado que se ve involucrada en una infinidad de procesos metaboÌlicos que repercuten en la salud del hueÌsped. En concreto, se ha visto que las personas que padecen alguna de las patologiÌas asociadas al siÌndrome metaboÌlico poseen una microbiota intestinal alterada que provoca un estado patoloÌgico denominado âdisbiosis intestinalâ. Este estado, provocado en parte por el consumo actual de dietas altas en grasa y azuÌcares y pobres en fibra, se caracteriza por una disminucioÌn de la diversidad microbiana y una alteracioÌn en su composicioÌn, y parece estar fuertemente relacionado con la aparicioÌn y desarrollo de las patologiÌas del siÌndrome metaboÌlico.
Entre las distintas estrategias descritas para modificar la microbiota intestinal alterada, se ha observado que la suplementacioÌn de la dieta con ciertos tipos de polifenoles, como el resveratrol o las antocianinas, pueden revertir la disbiosis intestinal, ayudando a la proliferacioÌn 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 asiÌ una mayor produccioÌn de aÌcidos grasos de cadena corta, como el butirato. En este trabajo se ha llevado a cabo una revisioÌn de la bibliografiÌa 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 siÌndrome metaboÌlico, asiÌ 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
FISH and mutational screening of the ABL, SYK and JAK tirosine kinase family genes in BCR-ABL1 negative and V617FJAK2 negative chronic myeloproliferative neoplasms (CMPNs)
ÂżExisten mĂĄs mutaciones en JAK2 en pacientes con SĂndromes Mieloproliferativos CrĂłnicos BCR-ABL negativos?
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