Steffensenmartinez0389

The relationship between gut microbiota and type 2 diabetes mellitus (T2DM) has drawn increasing attention, and the benefits of various treatment strategies, including nutrition, medication and physical exercise, maybe microbially-mediated. Metformin is a widely used hypoglycemic agent, while resistant starch (RS) is a novel dietary fiber that emerges as a nutritional strategy for metabolic disease. However, it remains unclear as to the potential degree and interactions among gut microbial communities, metabolic landscape, and the anti-diabetic effects of metformin and RS, especially for a novel type 3 resistant starch from Canna edulis (Ce-RS3). In the present study, T2DM rats were administered metformin or Ce-RS3, and the changes in gut microbiota and serum metabolic profiles were characterized using 16S-rRNA gene sequencing and metabolomics, respectively. After 11 weeks of treatment, Ce-RS3 exhibited similar anti-diabetic effects to those of metformin, including dramatically reducing blood glucose, ameliores, and possibly explaining the greater efficiency in improving metabolic control. The beneficial effects of Ce-RS3 and metformin might derive from changes in gut microbiota through altering host-microbiota interactions with impact on the host metabolome. Given the complementarity of Ce-RS3 and metformin in regulation of gut microbiota and metabolites, this study also prompted us to suggest possible "Drug-Dietary fiber" combinations for managing T2DM.A hallmark of diabetes mellitus is the inability of pancreatic β-cells to secrete sufficient amounts of insulin for maintaining normoglycemia. The formation of smaller islets may underlie the development of a diabetic phenotype, as a decreased β-cell mass will produce an insufficient amount of insulin. For a pharmacological intervention it is crucial to identify the proteins determining β-cell mass. Here, we identified the ternary complex factor (TCF) Elk-1 as a regulator of the size of pancreatic islets. Elk-1 mediates, together with a dimer of the serum-response factor (SRF), serum response element-regulated gene transcription. Elk-1 is activated in glucose-treated pancreatic β-cells but the biological functions of this protein in β-cells are so far unknown. Elk-1 and homologous TCF proteins are expressed in islets and insulinoma cells. Gene targeting experiments revealed that the TCF proteins show redundant activities. To solve the problem of functional redundancy of these homologous proteins, we generated conditional transgenic mice expressing a dominant-negative mutant of Elk-1 in pancreatic β-cells. The mutant competes with the wild-type TCFs for DNA and SRF-binding. Expression of the Elk-1 mutant in pancreatic β-cells resulted in the generation of significantly smaller islets and increased caspase-3 activity, indicating that apoptosis was responsible for the reduction of the pancreatic islet size. Glucose tolerance tests revealed that transgenic mice expressing the dominant-negative mutant of Elk-1 in pancreatic β-cells displayed impaired glucose tolerance. Thus, we show here for the first time that TCF controls important functions of pancreatic β-cells in vivo. Elk-1 may be considered as a new therapeutic target for the treatment of diabetes.Opioid drugs are widely used to treat chronic pain, but their misuse can lead to tolerance, dependence, and addiction and have created a significant public health problem. In addition, food-derived opioid peptides, known as exorphins, like gluten exorphins have been shown to have harmful effects in certain pathologies like celiac disease, for example. Several studies support the involvement of the opioid system in the development of disorders such as autism spectrum syndrome. Moreover, bidirectional communication between the intestine and brain has been shown to be altered in various neurodegenerative diseases including Alzheimer´s and Parkinson´s. The presence of opioid receptors in both the digestive tract and the central nervous system (CNS) suggests that opioid drugs and exorphins may modulate the gut-brain axis. Selleck JNJ-64619178 Morphine, for example, has shown a dysbiotic effect on the bacterial microbiota in addition to inducing an increase in intestinal permeability facilitating bacterial translocation. Furthermore, certain components of bacteria can modify the expression of opioid receptors at the central level increasing sensitivity to pain. Strategies based on use of probiotics have resulted in improvements in symptoms of autism and Parkinson´s disease. In this manuscript, we review the role of the opioid system in disorders and CNS pathologies and the involvement of the gut-brain axis.LSD1 (histone lysine specific demethylase 1) takes part in the physiological process of cell differentiation, EMT (epithelial-mesenchymal transition) and immune response. In this study, we found LSD1 expression in metastatic gastric cancer tissues was significantly higher than that in normal tissues. Furthermore, LSD1 deletion was found to suppress gastric cancer migration by decreasing intracellular miR-142-5p, which further led to the upregulation of migration suppressor CD9, a newly identified target of miR-142-5p. While LSD1 was reported as a demethylase of H3K4me1/2, H3K9me1/2 and several non-histone proteins, this is a new evidence for LSD1 as a functional regulator of miRNA. On the other hand, our data suggested that promoting the secretion of miR-142-5p using small extracellular vesicles as vehicles is a new mechanism for LSD1 abrogation to down-regulate intracellular miR-142-5p. Taken together, this study uncovered a new mechanism for LSD1 that can contribute to gastric cancer migration by facilitating miR-142-5p to target CD9.As traditional Chinese medicine, Bletilla striata has been widely applied to clinical treatment for its unique pharmacological profiles. This study aimed to investigate the beneficial role of Bletilla striata oligosaccharides (BO) in improving the metabolic syndrome by regulation of gut microbiota and intestinal metabolites. Treatment of HFD-fed mice with BO prevented weight gain, reversed the glucose intolerance and insulin resistance, and inhibited adipocyte hypertrophy. BO-treated mice also suppressed chronic inflammation and protected intestinal barrier from damage. These effects were linked to the reversal of gut microbiota dysbiosis, which contributed to the homeostasis of intestinal metabolites including bile acids, short-chain fatty acids and tryptophan catabolites. The depletion and reconstitution of intestinal flora from BO- or HFD-treated mice confirmed the significance of gut microbiota in regulation of HFD-induced metabolic disorders. We demonstrated for the first time that BO improved metabolic syndrome through the regulation of gut microbiota and intestinal metabolites.