The association between tea consumption and non-malignant digestive system diseases: A Mendelian randomized study.

BACKGROUND: Tea consumption might be closely related to non-malignant digestive diseases. Nevertheless, this correlation remains inadequately comprehended. Therefore, our objective was to elucidate the essence of these connections. METHODS: This study employed a Mendelian randomization approach to investigate the impact of tea consumption on specific digestive disorders. Genetic data associated with tea consumption were obtained from the UK Biobank (UKB), encompassing 447,485 participants. We chose a gene-wide association study with no sample overlap and UKB as our data source for all outcomes. The primary analytical method utilized was inverse variance weighting, and multiple analytical models were employed to enhance the analysis's reliability and ensure robust results. RESULT: Our investigation revealed that tea consumption was linked to an elevated susceptibility to gastroesophageal reflux disease (GERD). However, there was a lack of substantial evidence suggesting an association between tea intake and Crohn's disease (CD), ulcerative colitis (UC), or non-alcoholic fatty liver disease (NAFLD). CONCLUSIONS: Our study suggests that the excessive consumption of tea may heighten the likelihood of GERD. These results hold potential significance in guiding dietary pattern modifications for individuals with GERD. Furthermore, there may be value in implementing GERD monitoring and preventive measures in populations with elevated tea consumption.

Modulating host gene expression via gut microbiome-microRNA interplay to treat human diseases.

The human gastrointestinal (GI) tract hosts trillions of microbial inhabitants involved in maintaining intestinal homeostasis, dysbiosis of which provokes a motley of pathogenic and autoimmune disorders. While the mechanisms by which the microbiota modulates human health are manifold, their liberated metabolites from ingested dietary supplements play a crucial role by bidirectionally regulating the expression of micro-ribonucleic acids (miRNAs). miRNAs are small endogenous non-coding RNAs (ncRNAs) that have been confirmed to be involved in an interplay with microbiota to regulate host gene expression. This comprehensive review focuses on key principles of miRNAs, their regulation, and crosstalk with gut microbiota to influence host gene expression in various human disorders, by bringing together important recent findings centric around miRNA-microbiota interactions in diseases along various axis of the gut with other organs. We also attempt to lay emphasis on exploiting the avenues of gut-directed miRNA therapeutics using rudimentary dietary supplements to regulate abnormal host gene expression in diseases, opening doors to an accessible and economical therapeutic strategy.

Genomic medicine in gastroenterology: A new approach or a new specialty?

Throughout history, many medical milestones have been achieved to prevent and treat human diseases. Man's early conception of illness was naturally holistic or integrative. However, scientific knowledge was atomized into quantitative and qualitative research. In the field of medicine, the main trade-off was the creation of many medical specialties that commonly treat patients in advanced stages of disease. However, now that we are immersed in the post-genomic era, how should we reevaluate medicine? Genomic medicine has evoked a medical paradigm shift based on the plausibility to predict the genetic susceptibility to disease. Additionally, the development of chronic diseases should be viewed as a continuum of interactions between the individual's genetic make-up and environmental factors such as diet, physical activity, and emotions. Thus, personalized medicine is aimed at preventing or reversing clinical symptoms, and providing a better quality of life by integrating the genetic, environmental and cultural factors of diseases. Whether using genomic medicine in the field of gastroenterology is a new approach or a new medical specialty remains an open question. To address this issue, it will require the mutual work of educational and governmental authorities with public health professionals, with the goal of translating genomic medicine into better health policies.

Study on relationship between the thickness of tongue fur and the expressions of apoptosis-related genes of the tongue epithelial cells in patients with diseases of the digestive system.

To investigate the relationship between the thickness of tongue fur, apoptosis of the tongue fur epithelial cells and expressions of apoptosis-related genes in diseases of the digestive system, apoptosis-related genes TGF-beta3, fas mRNA and protein products were detected with terminal deoxynucleotidyl transferase-mediated deoxyurine triphosphate (d-UTP) nick-end labeling (TUNEL) technique, in situ hybridization, immunohistochemical methods, and image analysis technique, respectively. Results indicated that compared with the normal tongue fur, over-expression of fas gene was found in the peeling fur with an increase in cell apoptosis, while a low-expression of TGF-beta3 in the thick fur with a decrease in cell apoptosis. The changes in expression levels of fas and TGF-beta3 genes, apoptosis-promoting genes in the tongue fur epithelial cells, had a similar tendency of cell apoptosis level. It is concluded that the changes in expression levels of fas and TGF-beta3 are possibly important reasons influencing apoptosis of epithelial cells of tongue fur and leading to changes in thickness of the tongue fur.

Defective dietary fat processing in transgenic mice lacking aquaporin-1 water channels.

Immunocytochemistry showed expression of aquaporin-1 (AQP1) water channels at sites involved in dietary fat processing, including intrahepatic cholangiocytes, gallbladder, pancreatic microvascular endothelium, and intestinal lacteals. To determine whether AQP1 has a role in dietary fat digestion and/or absorption, mice were placed on a diet that contained 50% fat. Whereas wild-type mice (3-3.5 wk of age, 10-12 g) gained 49 +/- 5% (SE, n = 50) body weight in 8 days, and heterozygous mice gained 46 +/- 4%, AQP1 null mice gained only 4 +/- 3%; weights became similar after return to a 6% fat diet after 6 days. The null mice on a high-fat diet acquired an oily appearance, developed steatorrhea with increased stool triglyceride content, and manifested serum hypotriglyceridemia. Supplementation of the high-fat diet with pancreatic enzymes partially corrected the decreased weight gain in null mice. Absorption of [(14)C]oleic acid from small intestine was not affected by AQP1 deletion, as determined by blood radioactivity after duodenal infusion. Lipase activity in feces and small intestine was remarkably greater in AQP1 null than wild-type mice on low- and high-fat diets. Fluid collections done in older mice (that are less sensitive to a high-fat diet) by ductal cannulation showed threefold increased pancreatic fluid flow in response to secretin/cholecystokinin, but volumes, pH, and amylase activities were affected little by AQP1 deletion, nor were bile flow rates and bile salt concentrations. Together, these results establish a dietary fat misprocessing defect in AQP1 null mice.