Objective: To explore the correlation between BMI and gut microbiota of college students in Inner Mongolia,and to provide a reference basis for revealing the relationship between intestinal flora and obesity. Methods: Totally 88 college students from Inner Mongolia Medical University were enrolled, Height and weight were measured,and the feces samples were collected. The bacterial metagenome was extracted from dry feces samples for the concentration detection in per gram of dry feces,expressed as μg/μL. Correlation between BMI and metagenomics concentration of gut microbiota was statistically analyzed. Meanwhile,the metagenomics concentration of gut microbiota in different BMI groups was compared with each other. Results: There was a negative correlation between BMI and the metagenomics concentration of gut microbiota(r=-0.27,P<0.05). Significant difference in the concentration of gut microflora was observed between the normal group and the obesity group,the normal group and the overweight/obesity group(F=3.62,P<0.05). Among the female volunteers,there were significant differences between normal group and overweight group,between normal group and obesity group(F=1.87,P<0.05). No significant differences in metagenomics concentration of gut microbiota were found in different BMI groups(F=0.60, P>0.05). Conclusion There is a correlation between BMI and gut microbiota of college students in Inner Mongolia，the concentration of gut microflora metagenome in overweight and obese people decreased significantly.

OBJECTIVE: To explore the interaction between Tubulin beta 4B class IVb (TUBB4B) and Agtpbp1/cytosolic carboxypeptidase- like1 (CCP1) in mouse primary spermatocytes (GC-2 cells) and the role of TUBB4B in regulating the development of GC-2 cells. METHODS: Lentiviral vectors were used to infect GC-2 cells to construct TUBB4B knockdown and negative control (NC-KD) cells. The stable cell lines with TUBB4B overexpression (Tubb4b-OE) and the negative control (NC-OE) cells were screened using purinomycin. RT-qPCR and Western blotting were used to verify successful cell modeling and explore the relationship between TUBB4B and CCP1 expressions in GC-2 cells. The effects of TUBB4B silencing and overexpression on the proliferation and cell cycle of GC-2 cells were evaluated using CCK8 assay and flow cytometry. The signaling pathway proteins showing significant changes in response to TUBB4B silencing or overexpression were identified using Western blotting and immunofluorescence assay and then labeled for verification at the cellular level. RESULTS: Both TUBB4B silencing and overexpression in GC-2 cells caused consistent changes in the mRNA and protein expressions of CCP1 (P < 0.05). Similarly, TUBB4B expression also showed consistent changes at the mRNA and protein after CCP1 knockdown and restoration (P < 0.05). TUBB4B knockdown and overexpression had no significant effect on proliferation rate or cell cycle of GC-2 cells, but caused significant changes in the key proteins of the nuclear factor kappa-B (NF-κB) signaling pathway (p65 and p-p65) and the mitogen-activated protein kinase (MAPK) signaling pathway (ErK1/2 and p-Erk1/2) (P < 0.05); CCP1 knockdown induced significant changes in PolyE expression in GC-2 cells (P < 0.05). CONCLUSIONS TUBB4B and CCP1 interact via a mutual positive regulation mechanism in GC-2 cells. CCP-1 can deglutamize TUBB4B, and the latter is involved in the regulation of NF-κB and MAPK signaling pathways in primary spermatocytes.
Animals ; Male ; Mice ; GTP-Binding Proteins/metabolism* ; Mitogen-Activated Protein Kinases/metabolism* ; NF-kappa B/metabolism* ; RNA, Messenger ; Serine-Type D-Ala-D-Ala Carboxypeptidase/metabolism* ; Signal Transduction ; Spermatocytes ; Tubulin/genetics*