Project description:The mechanisms of chronic kidney disease-associated secondary hyperparathyroidism are partially understood. In this project we aimed to gain new information and propose research hypotheses by proteome and phosphoproteome profiling of normal and hyperplastic rat parathyroid glands. Glands were microdissected from rats on normal control diet or CKD-inducing high adenine diet enriched with phosphorus to produce secondary hyperparathyroidism. Protein extracts were pooled from 4 glands (2 rats) for proteome profiling (3 normal and 3 CKD pools), and from 12 glands (6 rats) for phosphoproteome profiling (2 normal and 2 CKD pools).
Project description:The mechanisms of chronic kidney disease-associated secondary hyperparathyroidism are partially understood. In this project we aimed to gain new information and propose research hypotheses by proteome and phosphoproteome profiling of normal and hyperplastic rat parathyroid glands. Glands were microdissected from rats on normal control diet or CKD-inducing high adenine diet enriched with phosphorus to produce secondary hyperparathyroidism. Protein extracts were pooled from 12 glands (6 rats) for phosphoproteome profiling (3 normal and 3 CKD pools).
Project description:Investigation of the effect of chow diet integration with standard baker's yeast leavened carasau bread (SB) or with functional sourdough-leavened carasau bread (FB) on the gut microbiota of young rats.
Project description:Several studies have established a link between high-salt diet, inflammation, and hypertension. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut–kidney axis. We aimed to confirm the effects of high salt and calcitriol on the gut–kidney immune system and the composition of the intestinal flora. We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Calcitriol can reduce colon and kidney inflammation, and there are gene expression changes consistent with restored intestinal barrier function. The protective effect of calcitriol may be mediated indirectly by immunological properties. Additionally, the molecular pathways of the gut microbiota-mediated BP regulation may be related to circadian rhythm signals, which needs to be further investigated. An innovative association analysis of the microbiota may be a key strategy to understanding the association between gene patterns and host.
Project description:High protein diet alter gut microbiota composition and activity. The objective of this study is to determine the consequences of a high protein diet for the colonic epithelium in rats.
Project description:This study was performed to investigate the effect of aging and high fat diet on gut microbiota in F344 rats by the pyrosequencing method.
Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
Project description:Obesity is a leading cause of primary hypertension in children, and a high-fat intake and the gut microbiota may be involved in the pathogenesis of obesity-related hypertension (OrHTN), but the underlying mechanisms are not fully understood. Here, we show that high-fat diet (HFD) feeding alters the gut microbiota composition in OrHTN rats, resulting in a reduced abundance of the butyrate-producing bacteria Ruminococcus and a subsequent decrease in plasma butyrate levels. Histone 3 lysine 9 butyrylation (H3K9bu) levels decreased in the kidneys of OrHTN rats, which downregulates the expression of the hypertension-related MAS1 gene. Furthermore, sodium butyrate affected H3K9bu modification levels in a concentration-dependent manner, with decreased H3K9bu and downregulated MAS1 expression at low concentrations in human proximal tubular epithelial cells. Our results suggest that a HFD contributes to the development of OrHTN by altering the gut microbiota and its metabolites, leading to the downregulation of H3K9bu and hypertension-related gene expression.
Project description:A high-sugar diet induces lifestyle-associated metabolic diseases, such as obesity and diabetes, which may underlie the pro-tumor effects of a high-sugar diet. We supplied GL261 syngeneic glioblastoma (GBM) model mice with a short-term high-glucose diet (HGD) and found an increased survival rate with no evidence of metabolic disease. Modulation of the gut microbiota by an HGD was critical for enhancing the anti-tumor immune response. Single-cell RNA sequencing showed that modulation of the gut microbiota by an HGD increased the T cell-mediated anti-tumor immune response in GBM mice. We found that the cytotoxic CD4+ T cell population in GBM mice increased due to synergy with anti-PD-1 immune checkpoint inhibitors, but this depended on an HGD. Thus, we determined that an HGD enhanced anti-tumor immune responses in GBM mice through changes in the gut microbiota and suggest that the role of an HGD in GBM should be re-examined.