Evolução da colonização da microbiota fecal de recém-nascidos prematuros submetidos à colostroterapia / Evolution of fecal microbiota colonization in preterm infants submitted to colostrum therapy

A amamentação tem um papel importante no desenvolvimento neonatal e no estabelecimento da microbiota intestinal. Neste contexto, a administração orofaríngea de colostro, ou colostroterapia, torna-se uma prática importante para o desenvolvimento do recém-nascido prematuro, auxiliando na maturação do trato gastrintestinal, na introdução precoce do leite materno e pode ser capaz de proteger o bebê contra bactérias patogênicas. Desta maneira, o objetivo do presente estudo foi avaliar o estabelecimento da microbiota intestinal em recém-nascidos prematuros submetidos à colostroterapia. O estudo contou com a inclusão de 33 recém-nascidos prematuros internados na unidade de terapia intensiva neonatal do Hospital Maternidade Leonor Mendes de Barros, em São Paulo. Os recém-nascidos foram divididos em quatro grupos, de acordo com o regime de colostroterapia e dieta, a saber: colostroterapia exclusiva com colostro cru (CCE, n=7), colostroterapia exclusiva com colostro pasteurizado (CPE, n=9), colostroterapia com colostro pasteurizado e dieta prevalente de colostro pasteurizado (CPC, n=10) e colostroterapia com colostro pasteurizado e dieta prevalente de leite humano pasteurizado (CPP, n=7). Foram coletadas amostras de fezes semanalmente durante os primeiros 22 dias de vida do bebê, e a microbiota intestinal foi caracterizada por sequenciamento da região V4 do gene 16S rRNA e análises de PCR em tempo real. Entre os grupos de CCE e CPE nota-se que existe diferença na comunidade bacteriana através das análises de abundância relativa da microbiota. Porém, a abundância de gêneros potencialmente patogênicos está aumentada nos grupos CPC e CPP. A presença de bifidobactérias e aumento contínuo ao longo dos primeiros dias de vida no grupo CPE e CPP, é um resultado que pode ser utilizado para reforçar o uso do leite pasteurizado na ausência do leite fresco, mostrando que o mesmo pode favorecer a prevalência de gêneros benéficos para a microbiota intestinal. Neste estudo, além de compararmos a modulação do colostro cru e pasteurizado na microbiota intestinal do bebê a partir da colostroterapia exclusiva, pudemos mostrar que o colostro pasteurizado desempenha um papel diferente que o leite humano pasteurizado na microbiota intestinal

Breastfeeding plays an important role in neonatal development and establishment of the intestinal microbiota. In this context, oropharyngeal administration of colostrum, or colostrum therapy, becomes an important practice for the development of preterm infant, assisting in maturation of the gastrointestinal tract, early introduction of breast milk and may be able to protect the baby against pathogenic bacteria. Thus, the aim of the present study was to evaluate the establishment of the intestinal microbiota in preterm infants submitted to colostrum therapy. The study included 33 preterm infants admitted to the neonatal intensive care unit of the Hospital Maternidade Leonor Mendes de Barros, in São Paulo. The newborns were divided into four groups according to the colostrum therapy and diet regimen: exclusive colostrum therapy with raw colostrum (CCE, n = 7), exclusive colostrum therapy with pasteurized colostrum (CPE, n = 9), colostrum therapy with pasteurized colostrum and pasteurized colostrum diet (CPC, n = 10) and colostrum therapy with pasteurized colostrum and pasteurized human milk diet (CPP, n = 7). Stool samples were collected weekly during the first 22 days of the baby's life, and the intestinal microbiota was characterized by sequencing the V4 region of the 16S rRNA gene and realtime PCR analysis. Between the CCE and CPE groups, there is a difference in the bacterial community through the microbiota relative abundance analysis. However, the abundance of potentially pathogenic genera is increased in the CPC and CPP groups. The presence of bifidobacteria and continuous increase throughout the first days of life in the CPE and CPP group is a result that can be used to reinforce the use of pasteurized milk in the absence of fresh milk, showing that it may favor the prevalence of beneficial bacteria genera to the intestinal microbiota. In this study, in addition to comparing the modulation of raw and pasteurized colostrum in the baby's intestinal microbiota from exclusive colostrum therapy, we were able to show that pasteurized colostrum plays a different role than pasteurized human milk in the intestinal microbiota of preterm infant

MicroRNA Expression Signature Is Altered in the Cardiac Remodeling Induced by High Fat Diets.

Recent studies have revealed the involvement of microRNAs (miRNAs) in the control of cardiac hypertrophy and myocardial function. In addition, several reports have demonstrated that high fat (HF) diet induces cardiac hypertrophy and remodeling. In the current study, we investigated the effect of diets containing different percentages of fat on the cardiac miRNA expression signature. To address this question, male C57Bl/6 mice were fed with a low fat (LF) diet or two HF diets, containing 45 kcal% fat (HF45%) and 60 kcal% fat (HF60%) for 10 and 20 weeks. HF60% diet promoted an increase on body weight, fasting glycemia, insulin, leptin, total cholesterol, triglycerides, and induced glucose intolerance. HF feeding promoted cardiac remodeling, as evidenced by increased cardiomyocyte transverse diameter and interstitial fibrosis. RNA sequencing analysis demonstrated that HF feeding induced distinct miRNA expression patterns in the heart. HF45% diet for 10 and 20 weeks changed the abundance of 64 and 26 miRNAs in the heart, respectively. On the other hand, HF60% diet for 10 and 20 weeks altered the abundance of 27 and 88 miRNAs in the heart, respectively. Bioinformatics analysis indicated that insulin signaling pathway was overrepresented in response to HF diet. An inverse correlation was observed between cardiac levels of GLUT4 and miRNA-29c. Similarly, we found an inverse correlation between expression of GSK3ß and the expression of miRNA-21a-3p, miRNA-29c-3p, miRNA-144-3p, and miRNA-195a-3p. In addition, miRNA-1 overexpression prevented cardiomyocyte hypertrophy. Taken together, our results revealed differentially expressed miRNA signatures in the heart in response to different HF diets. J. Cell. Physiol. 231: 1771-1783, 2016. © 2015 Wiley Periodicals, Inc.

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor.

Elevated thyroid hormone (TH) levels induce cardiac hypertrophy partially via type 1 Angiotensin II receptor (AT1R). MicroRNAs (miRNAs) are key regulators of cardiac homeostasis, and miR-133 has been shown to be involved in cardiac hypertrophy. However, the potential role of miR-133 in cardiac growth induced by TH is unknown. Thus, we aimed to investigate the miR-133 expression, as well as its potential role in cardiac hypertrophy in response to TH. Wistar rats were subjected to hyperthyroidism combined or not with the AT1R blocker. T3 serum levels were assessed to confirm the hyperthyroid status. TH induced cardiac hypertrophy, as evidenced by higher cardiac weight/tibia length ratio and α-actin mRNA levels, which was prevented by AT1R blocker. miR-133 expression was decreased in TH-induced cardiac hypertrophy in part through the AT1R. Additionally, the cardiac mRNA levels of miR-133 targets, SERCA2a and calcineurin were increased in hyperthyroidism partially via AT1R, as evaluated by real-time RT-PCR. Interestingly, miR-133 levels were unchanged in T3-induced cardiomyocyte hypertrophy in vitro. However, a gain-of-function study revealed that miR-133 mimic blunted the T3-induced cardiomyocyte hypertrophy in vitro. Together, our data indicate that miR-133 expression is reduced in TH-induced cardiac hypertrophy partially by the AT1R and that miR-133 mimic prevents the cardiomyocyte hypertrophy in response to T3 in vitro. These findings provide new insights regarding the mechanisms involved in the cardiac growth mediated by TH, suggesting that miR-133 plays a key role in TH-induced cardiomyocyte hypertrophy.