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Sepsis is a life-threatening condition with high hospital mortality. Elevated mortality has also been observed in patients after hospital discharge due to post-sepsis syndrome (PSS). The etiology of PSS is still not entirely known, but it involves inflammation. Plasma extracellular vesicles (EVs) are recognized as a unique mechanism of intercellular communication in inflammatory processes. It has been reported that EV microRNA (miRNA) production during the acute sepsis phase may persist until after disease resolution and is associated with PSS. We employed mass spectrometry and qPCR analysis to determine the protein and miRNA composition of plasma-derived EVs of 36 patients during sepsis-related hospitalization, immediately after ICU discharge (post-sepsis), and three, six, twelve, and up to 36 months post-sepsis. We determined that patients’ immune system cells were the primary EV source. Fifteen differentially expressed EV miRNAs (DEmiRs) were identified in samples from septic patients compared to the control group. Predictive analyses revealed that these DEmiRs could influence inflammation by modulating pathways mediated by NF-κB, STAT3, and TLR4 signaling activation. Thirteen miRNAs (-15b-5p,-16-5p,-20a-5p,-25-3p,-27a-3p,-29a-3p,-30d-5p,-93-5p,-146a-5p,-148a-3p,-191-5p,-195-5p,-223-3p) were downregulated in the death group compared to the survivor group, making them candidate prognostic markers of ICU survival. One year after ICU discharge, the expression of miR-21-5p and miR-195-5p were decreased in the survivor group. The miRNAs identified in the present study represent potential biomarkers for the survival prognosis of post-sepsis patients.

Proton pump inhibitors (PPIs) are one of the most prescribed drugs around the world. PPIs induce microbiota modulation such as obesity both in humans and in animal models. However, since PPIs can induce microbiota modulation despite the absence of a high-fat diet or weight gain, it is an interesting model to correlate microbiota modulation with the establishment of non-alcoholic fatty liver disease (NAFLD). We investigated the effect of pantoprazole treatment on TLR4 signaling and liver histology in C57BL/6J mice for 60 days, trying to correlate microbiota modulation with some aspects of liver injury. We performed glucose (GTT) and insulin (ITT) tolerance tests, serum lipopolysaccharide (LPS) dosage, liver histology, liver and intestine extraction for Western blot and qPCR. Fecal microbiota were investigated via metagenomics. Chronic treatment with pantoprazole induced microbiota modulation and impaired ileum barrier integrity, without an association with insulin resistance. Furthermore, increased circulating LPS and increased Toll-like receptor 4 (TLR4) and TGFβ downstream signaling may have an important role in the development of the observed liver microvesicular steatosis and fibrosis. Finally, this model of PPI-induced changes in microbiota might be useful to investigate liver microvesicular steatosis and fibrosis.

Maternal energy metabolism undergoes a singular adaptation during lactation that allows for the caloric enrichment of milk. Changes in the mammary gland, changes in the white adipose tissue, brown adipose tissue, liver, skeletal muscles and endocrine pancreas are pivotal for this adaptation. The present review details the landmark studies describing the enzymatic modulation and the endocrine signals behind these metabolic changes. We will also update this perspective with data from recent studies showing transcriptional and post-transcriptional mechanisms that mediate the adaptation of the maternal metabolism to lactation. The present text will also bring experimental and observational data that describe the long-term consequences that short periods of lactation impose to maternal metabolism.

Some studies have demonstrated the participation of leptin in magnesium metabolism. On the other hand, there is evidence of the role of magnesium in the leptin intracellular signaling pathway. Therefore, the aim of this study was to investigate the existence of a relationship between serum leptin concentrations and magnesium biomarkers in women with obesity. Case-control study involving 108 women aged between 20 and 50 years, divided into two groups: obese (n = 52) and control (n = 56). Body weight, height and waist circumference, body mass index, dietary magnesium intake, magnesium biomarkers and serum leptin concentrations were measured. Serum leptin concentrations showed a statistically significant difference between groups (p 0.001). Mean values of magnesium intake were lower than intake recommended, and with no statistically significant difference between two groups (p 0.05). Women with obesity had lower plasma and erythrocyte magnesium concentrations than control group did (p 0.001). Magnesium concentrations found in the urine of women with obesity were higher than the control group was, with a statistically significant difference (p 0.001). There was a correlation between serum leptin and magnesium biomarkers (p 0.001). Women with obesity show an inadequate magnesium nutritional status characterized by low plasma and erythrocyte concentrations and high concentrations in urine, and they also have high serum leptin concentrations. Thus, it was possible to observe a correlation between hyperleptinemia and magnesium biomarkers, requiring further studies to determine whether the dysfunction of this hormone can influence the compartmentalization of the mineral in obese organisms.