Effect of Maccog Tcm Tea On Improving Glucolipid Metabolism and Gut Microbiota in Patients With Type 2 Diabetes in Community

OBJECTIVES: This work aimed to observe the effect of consuming Chinese herb tea on glucolipid metabolism and gut microbiota in patients with type 2 diabetes mellitus (T2DM). METHODS: Ninety patients with T2DM were recruited from a community and randomly divided into the control group (CG) and intervention group (IG). CG maintained conventional treatment and lifestyle, and IG accepted additional maccog traditional Chinese medicine (TCM) tea (mulberry leaf, radix astragali, corn stigma, cortex lycii, radix ophiopogonis, and gynostemma) for 12 weeks. Glucolipid metabolism, hepatorenal function, and gut microbiota were then measured. RESULTS: After the intervention, the decreases in fasting plasma glucose (FPG) and total cholesterol (TC) were greater (P CONCLUSIONS: Administration of maccog TCM tea for 12 weeks slightly improved glucolipid metabolism and significantly increased the abundance of beneficial gut microbiota in community patients with T2DM. The increase in beneficial bacteria abundance may be involved in the improvement of glucose metabolism indicators. In addition, this intervention is safe and feasible. CLINICAL TRIAL REGISTRATION: https://www.chictr.org.cn/showproj.aspx?proj=31281, identifier ChiCTR1800018566

OTUB1 promotes osteoblastic bone formation through stabilizing FGFR2

Abstract Bone homeostasis is maintained by the balance between osteoblastic bone formation and osteoclastic bone resorption. Dysregulation of this process leads to multiple diseases, including osteoporosis. However, the underlying molecular mechanisms are not fully understood. Here, we show that the global and conditional osteoblast knockout of a deubiquitinase Otub1 result in low bone mass and poor bone strength due to defects in osteogenic differentiation and mineralization. Mechanistically, the stability of FGFR2, a crucial regulator of osteogenesis, is maintained by OTUB1. OTUB1 attenuates the E3 ligase SMURF1-mediated FGFR2 ubiquitination by inhibiting SMURF1’s E2 binding. In the absence of OTUB1, FGFR2 is ubiquitinated excessively by SMURF1, followed by lysosomal degradation. Consistently, adeno-associated virus serotype 9 (AAV9)-delivered FGFR2 in knee joints rescued the bone mass loss in osteoblast-specific Otub1-deleted mice. Moreover, Otub1 mRNA level was significantly downregulated in bones from osteoporotic mice, and restoring OTUB1 levels through an AAV9-delivered system in ovariectomy-induced osteoporotic mice attenuated osteopenia. Taken together, our results suggest that OTUB1 positively regulates osteogenic differentiation and mineralization in bone homeostasis by controlling FGFR2 stability, which provides an optical therapeutic strategy to alleviate osteoporosis