High-fat diet (HFD) may induce changes of metabolism and gut microbiota changes, and these changes are susceptible to diet adjustments such as tea treatment. However, the treatment effects may vary among different types of tea. In this study, we evaluated the effects of six types of tea on glucose and lipid metabolism and gut microbiota in HFD mice. We established HFD mouse model by 12 weeks feed with 60% fat diet, then treated with teas for six weeks. Here, we showed that treatment with different types of tea can inhibit weight gain and insulin resistance though different ways. Green tea regulated lipid metabolism by regulating the expression of adenosine 5 ′ -monophosphate-activated protein kinase (AMPK) and carnitine palmitoyltransferase-I (CPT-1). The effect of dark tea and white tea in reducing liver weight seemed to be related to activities of acetyl-CoA carboxylase (ACC). Yellow tea exhibited the best anti-inflammatory and antioxidant effects and effects of recovering the disorder of model mouse microbiota. The decrease in blood sugar and the upregulation of gluconeogenesis-related enzymes seemed to be related to the decrement of unclassified Lachnospiraceae. These different effects may result from the unique chemical compositions contained by different types of tea, which can regulate different lipid and glucose metabolism-related proteins. Despite variations in its compositions and metabolic reactions, tea is a potent antiobesity and hypoglycemic agent.
Background: Lifestyle and diet play a significant role in hyperuricaemia. Accumulating evidence indicates that tea consumption is associated with hyperuricaemia and gout. However, diverse compounds in different types of tea make it quite difficult to determine the relevant molecular mechanism. Here, we compared the effects of six types of tea on hyperuricaemia induced by potassium oxonate (PO) and hypoxanthine in rats and investigated the possible underlying mechanisms.Methods: Rats were randomly assigned to ten groups: the control, hyperuricaemia model, benzbromarone positive control, traditional Chinese medicine Simiao San positive control, green tea, yellow tea, black tea, white tea, red tea, and cyan tea treatment groups. After 21 days, uric acid (UA), xanthine oxidase (XOD), alanine aminotransferase (ALT),blood urea nitrogen (BUN), and creatinine (CRE) were assessed. Serum levels of interleukin-1β (IL-1β) were measured with an enzyme-linked immunosorbent assay. Haematoxylin-eosin staining and immunohistochemistry were used to assess liver and kidney injury. Results:The levels of UA, CRE, and BUN in the treatment group were decreased to varying degrees. There was a significant reduction in UA, CRE, and BUN levels for yellow tea compared to the positive control drugs. Yellow tea suppressed XOD activity and alleviated hepatic and kidney injury. Network pharmacology and untargeted metabolomics indicated that ten yellow tea bioactive ingredients and 35 targets were responsible for preventing hyperuricaemia, which was mediated by 94 signalling pathways, including IL-1β and TNF. Conclusion:These findings indicate that green tea cannot reduce the serum uric acid level of hyperuricaemic rats. Yellow tea can significantly improve hyperuricaemia by regulating the inflammatory response, autophagy, and apoptosis. This study provides a potential candidate for the treatment of hyperuricaemia and a basis for selecting therapeutic tea for patients with hyperuricaemia.
Background Lifestyle and diet play a significant role in hyperuricemia. Accumulating evidence indicates that tea consumption is associated with hyperuricemia and the risk of gout. However, diverse compounds in different types of tea make it quite difficult to find out the relevant molecular mechanism. Here, we compared the effects of six types of tea on hyperuricemia induced by potassium oxonate (PO) and hypoxanthine in rats and investigated possible underlying mechanisms. Methods Rats were randomly assigned into ten groups: control group, hyperuricemia model group, benzbromarone positive control group, traditional Chinese Medicine Simiao San positive control group, green tea, yellow tea, black tea, white tea, red tea, and cyan tea treatment groups. After 21 days, uric acid ( UA ), xanthine oxidase ( XOD ), blood urea nitrogen ( BUN ), and creatinine ( CRE ) were assessed. By enzyme-linked immunosorbent assay, serum levels of interleukin-1β. By hematoxylin-eosin staining and immunohistochemistry, liver and kidney injury were measured. Results The levels of UA, CRE, and BUN in the treatment group were decreased to extent degrees. There was a significant reduction of UA, CRE, BUN levels for yellow tea compared to the positive control drugs. Yellow tea suppressed the XOD activity to lessen hepatic and kidney injury. Network pharmacology and untargeted metabolomics indicated that ten yellow tea bioactive ingredients and 35 targets were responsible for preventing hyperuricemia mediated by 94 signaling pathways, such as IL-1β and TNF. Conclusion These findings indicate that green tea cannot reduce the serum uric acid level of hyperuricemic rats. Yellow tea can significantly improve hyperuricemia by regulating inflammatory response, autophagy, and apoptosis. This study provides a potential candidate for the treatment of hyperuricemia and a basis for selecting tea for patients with hyperuricemia.
PPARG (peroxisome proliferator-activated receptors gamma) is a nuclear receptor protein superfamily member, PPARG agonists have been proven to have broad anticancer properties in experimental studies. Associated clinical oncology investigations have been widely conducted, but no good relevant findings have been reported thus far. This might be caused by the limitations of a few cancer types of clinical studies. Simultaneously, screening natural products of PPARG agonists with minimal toxicity and side effects may aid in the clinical translation of PPARG agonists into the field of cancer. To that purpose, we investigated the association between PPARG gene expression and prognosis in 34 TCGA cancers and discovered that high PPARG gene expression was only a significant correlation (p < 0.05) with overall survival and progression-free survival in KIRP and UVM patients. An up-regulated PPARG expression with down-regulated ATP8B3 expression had the best prognosis in KIRP and UVM patients revealed by differential expression analysis, KEGG enrichment analysis, and tumor single-cell sequencing analysis. Flavonoids in yellow tea were demonstrated may both activate PPARG and inhibit the action of ATP8B3 using quantitative structure-activity relationships and molecular docking. As natural PPARG agonists, tea flavonoids are worth additional investigation in the field of clinical cancer research, especially in KIRP and UVM.
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