Gut microbiota and obesity: an overview of microbiota to microbial-based therapies.

The increasing prevalence of obesity and overweight is a significant public concern throughout the world. Obesity is a complex disorder involving an excessive amount of body fat. It is not just a cosmetic concern. It is a medical challenge that increases the risk of other diseases and health circumstances, such as diabetes, heart disease, high blood pressure and certain cancers. Environmental and genetic factors are involved in obesity as a significant metabolic disorder along with diabetes. Gut microbiota (GM) has a high potential for energy harvesting from the diet. In the current review, we aim to consider the role of GM, gut dysbiosis and significant therapies to treat obesity. Dietary modifications, probiotics, prebiotics, synbiotics compounds, using faecal microbiota transplant, and other microbial-based therapies are the strategies to intervene in obesity reducing improvement. Each of these factors serves through various mechanisms including a variety of receptors and compounds to control body weight. Trial and animal investigations have indicated that GM can affect both sides of the energy-balancing equation; first, as an influencing factor for energy utilisation from the diet and also as an influencing factor that regulates the host genes and energy storage and expenditure. All the investigated articles declare the clear and inevitable role of GM in obesity. Overall, obesity and obesity-relevant metabolic disorders are characterised by specific modifications in the human microbiota's composition and functions. The emerging therapeutic methods display positive and promising effects; however, further research must be done to update and complete existing knowledge.

Gut Microbiota and Colorectal Cancer Risk Factors.

Colorectal cancer is a type of gut cancer originating either from the rectum or colon. Genetic and environmental factors, such as the gut microbiome, play pivotal roles in colorectal cancer incidence rates. Therefore, we aimed to review the risk factors of CRC comprising gut bacteriomes and their intra-interactions with each other in the context of CRC development. Gut microbiota alteration, especially bacteriome alteration as the dominant player, seems to be the common feature amongst all risk factors. Although it is not quite obvious whether these alterations are the causes or the consequences of the tumorigenesis risk factors, they are common and almost universal among CRC-affected individuals. In addition, bacterial genotoxicity, biofilm formation, oxidative stress, bacterial metabolome, and dysbiosis are assessed in CRC development. The present study suggests that gut microbial alterations could be the key intermediate, as a cause or a consequence, between most risk factors of CRC and the way they promote or contribute to CRC development.

Postbiotics versus probiotics in early-onset colorectal cancer.

Probiotics and postbiotics mechanisms of action and applications in early-onset colorectal cancer (EOCRC) prevention and treatment have significant importance but are a matter of debate and controversy. Therefore, in this review, we aimed to define the probiotics concept, advantages and limitations in comparison to postbiotics, and proposed mechanisms of anti-tumor action in EOCRC prevention and treatment of postbiotics. Biotics (probiotics, prebiotics, and postbiotics) could confer the health benefit by affecting the host gut microbiota directly and indirectly. The main mechanisms of action of probiotics in exerting anticancer features include immune system regulation, inhibition of cancer cell propagation, gut dysbiosis restoration, anticancer agents' production, gut barrier function renovation, and cancer-promoting agents' reduction. Postbiotics are suggested to have different mechanisms of action to restore eubiosis against EOCRC, including modulation of gut microbiota composition, gut microbial metabolites regulation, and intestinal barrier function improvement via different features such as immunomodulatory, anti-inflammatory, antioxidant, and anti-proliferative properties. A better understanding of postbiotics challenges and mechanism of action in therapeutic applications will allow us to sketch accurate trials in order to use postbiotics as bio-therapeutics in EOCRC.

Homeobox B4 gene expression is upregulated by ghrelin through PI3-kinase signaling pathway in rat's bone marrow stromal cells.

OBJECTIVE: Ghrelin, a 28 amino acid peptide, has diverse physiological roles. Phosphatidylino-sitol-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) are involved in some of the recognized actions of ghrelin. It has been shown that ghrelin upregulates HOXB4 gene expression but the real mechanism of this effect is not clear. METHODS: Rat bone marrow stromal cells (BMSCs) were cultured in DMEM. BMSCs were treated with ghrelin (100 µM) for 48 h. Real-time PCR for HOXB4 was performed from Control (untreated BMSCs), BG (BMSCs treated with 100 µM ghrelin), PD (BMSCs treated with 10 µM PD98059, a potent inhibitor of mitogen-activated protein kinase, and 100 µM ghrelin), LY (BM-SCs treated with 10 µM LY294002, a strong inhibitor of phosphoinositide 3-kinase, and 100 µM ghrelin) and SY (BMSCs treated with 10 µM LY294002 plus 10 µM PD98059, and 100 µM ghrelin) groups. Relative gene expression changes were determined using Relative expression software tool 9 (REST 9). RESULTS: HOXB4 gene has been overexpressed in ghrelin-treated BMSCs (p<0.05). PI3K inhi-bition by LY294002 significantly downregulated the ghrelin-induced overexpression of HOXB4 (p<0.05). CONCLUSION: We can conclude that ghrelin, through PI3K/Akt pathway, may improve BMSC transplantation potency by reducing its apoptosis. Moreover, upregulating HOXB4 in BMSC and its possible differentiation to HSCs might in the future open the doors to new treatment for hematologic disorders. Therefore, activating the PI3K/Akt pathway, instead of using a non-specific inducer, could be the principal point to increase the efficiency of BMSC-based cell therapies in the future.

A nickel(ii) complex under water-oxidation reaction: what is the true catalyst?

In the present study, the water-oxidizing activity of nickel(ii) phthalocyanine-tetrasulfonate tetrasodium (1), which is a stable Ni(ii) complex under moderate conditions, was investigated. The role of Ni oxide in water oxidation as a true catalyst was investigated. The electrodes after water oxidation by both the complex and Ni salt were analyzed and a relation was proposed between the decomposition of the Ni complex and water oxidation. On the surface of the electrode, there are some areas without any detectable nanoparticles; thus, the detection of such Ni oxides on the surface of the electrode is not easy in the first seconds of the reaction, even using some of the usual methods such as Scanning Electron Microscopy or electrochemical analysis. Such experiments indicated that a precise analysis is necessary to reject the role of nanoparticles in the presence of Ni phthalocyanine under water oxidation. The findings also showed that under water-oxidation conditions and in the presence of the complex, Ni oxide is a good candidate for a true catalyst.

Ghrelin Upregulates Hoxb4 Gene Expression in Rat Bone Marrow Stromal Cells.

OBJECTIVES: Ghrelin is a peptide which has a proliferative and antiapoptotic effect in many cells including bone marrow stromal cells (BMSCs). Homeobox protein B4 (HOXB4) is a transcription factor involved in stem cell regeneration and survival. The aim of the study was to find out the efect of ghrelin on Hoxb4 expression in BMSCs. MATERIALS AND METHODS: In this experimental study, rat BMSCs were cultivated in Dulbecco's Modified Eagle Medium (DMEM). Passage three BMSCs were treated with ghrelin 100 µM for 48 hours. Real-time polymerase chain reaction (PCR) was carried out from the untreated BMSCs (B), BMSCs treated with 125 µM H2O2 (BH), BMSCs treated with 100 µM ghrelin then 125 µM H2O2 (BGH) and BMSCs treated with 100 µM ghrelin (BG) groups. For immunofluorescence, cells were incubated with an anti-HOXB4 monoclonal antibody. Primary antibodies were visualized using the Fluorescein isothiocyanate (FITC) method. All data are presented as mean ± SEM and P<0.05 was considered as statistical significant. RESULTS: Hoxb4 expression significantly increased in the BG compared with BH and BGH groups. Furthermore, 100 µM ghrelin, increased the mean of HOXB4 positive immunoreactive cells compared to the BH group. CONCLUSIONS: Ghrelin probably enhances proliferation and viability of BMSCs through Hoxb4 upregulation. However, the signaling pathway and other biological outcomes of this effect should be elucidated in different stem cells.