Ask about this productRelated genes to: CYP7B1 Blocking Peptide
- Gene:
- CYP7B1 NIH gene
- Name:
- cytochrome P450 family 7 subfamily B member 1
- Previous symbol:
- SPG5A
- Synonyms:
- -
- Chromosome:
- 8q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-02
- Date modifiied:
- 2018-02-28
Related products to: CYP7B1 Blocking Peptide
Related articles to: CYP7B1 Blocking Peptide
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disorder and progresses through distinct pathological stages whose specific drivers remain unclear. Here we show that cytosolic prostaglandin E synthase (cPGES) drives MASLD progression in a cell-type-specific, prostaglandin E-independent manner by controlling glucocorticoid receptor (GR) function. In hepatocytes, cPGES sequesters GR in the cytosol through HSP90 binding, impairing direct GR-driven transcription of the cholesterol-handling enzymes CYP7B1 and SERPINA1E and promoting cholesterol accumulation and simple steatosis. In macrophages, cPGES suppresses GR nuclear translocation, downregulating metallothioneins (MT1/2), skewing macrophage polarization, and aggravating steatohepatitis. We identified a cPGES inhibitor, SQ-030, that ameliorated steatosis and inflammation in preclinical models. Thus, cPGES is a dual-functioning therapeutic target: its hepatocyte inhibition restores cholesterol homeostasis in early disease, whereas its macrophage blockade resolves inflammation in advanced disease, supporting stage-specific intervention strategies. - Source: PubMed
Publication date: 2026/08/27
Zhong DandanQiao RanranQuan GuoguiSong ChangFu KequanZou YingyingQi XiaolongSu WenLiu YingLi FeiYang BaoxueAbulizi AbudumijitiCai BenzhiSun Ying - Hepatic sexual dimorphism is critical for maintaining sex-specific metabolic pathways and xenobiotic clearance. We have demonstrated that in fibroblast growth factor 15 (Fgf15) transgenic (Tg) mice, FGF15 overexpression significantly reduced bile acid (BA) levels and induced hepatic feminization in males, marked by a male-to-female shift in expression of the drug metabolizing enzymes. This feminization is linked to the disruption of pulsatile growth hormone (GH) secretion pattern and signaling. However, it remained unclear whether FGF15 overexpression broadly disrupts hepatic sexual dimorphism or specifically drives a directional feminization program independent of biological sex. In this study, we profiled the hepatic transcriptome of female Fgf15 Tg mice and replenished male Fgf15 Tg mice with exogenous, pulsatile GH to test to what degree changes in the GH axis maintain liver dimorphism under low BA conditions. Beyond suppressing BA synthesis and altering steroid metabolism, female Tg mice altered expression of genes in xenobiotic metabolism and detoxification pathways, suggesting that the FGF15/BA axis regulates xenobiotic processing in females as well. Notably, FGF15 overexpression further amplified the baseline female expression profile of drug-metabolizing enzymes, characterized by the upregulation of female-predominant genes (Cyp2b9, Cyp3a41, Sult1e1, and Ugt1a1) and the suppression of male-predominant genes (Cyp7b1, Cyp2d9, Hsd3b5, and Igf1). Furthermore, pulsatile GH replenishment in male Tg mice partially restored male-predominant gene expression patterns. Taken together, these findings demonstrate that overexpression of intestine-derived FGF15 drives the feminization of sexually dimorphic hepatic gene expression independent of biological sex, a process that is at least partially mediated by impaired GH signaling. SIGNIFICANCE STATEMENT: Fibroblast growth factor 15 (Fgf15) overexpression intensified hepatic feminization of drug-metabolizing enzyme expression in female Fgf15 transgenic mice, similar to male Fgf15 transgenic mice. Restoring growth hormone signaling partially rescued the male-predominant gene expression pattern in male Fgf15 transgenic mice. This indicates that disruptions to growth hormone pulsatility, alongside sustained hepatic signal transducer and activator of transcription 5 activation, contribute to FGF15-induced hepatic gene feminization. - Source: PubMed
Publication date: 2026/07/15
Dai ManyunShi HongBasaly VeroniaMeadows VikKong BoGuo Grace L - Eggs serve as an indispensable global nutritional resource, sustaining the economic foundation of the commercial poultry industry. To meet this continuous demand, egg formation involves an exceptionally energy-intensive biological process requiring continuous yolk precursor synthesis, which imposes a massive metabolic burden on laying hens. However, the comprehensive metabolic differences across the gut-liver-adipose axis between peak laying hens with high or low egg production remain incompletely characterized. A total of 180 healthy Hy-Line Brown laying hens (45-week-old) were continuously fed and monitored for production performance over a 6-week period. Following the exclusion of individuals with extremely low egg production (≤10 eggs during the 6-week monitoring period; n = 5) and candidate hens that repeatedly produced unqualified eggs over multiple weeks (n = 20), the remaining hens were ranked by 6-week average laying rate and allocated into FH (high-production hens at 50 weeks of age, n = 15) and FL (low-production hens at 50 weeks of age, n = 14) groups. Initial body weight did not differ significantly between groups (FH: 1936 ± 29.0 g; FL: 1894 ± 48.2 g; P-value = 0.446). We integrated transcriptomic, untargeted metabolomic, targeted bile acid metabolomics, and microbiome (16S rRNA and metagenomic) profiles to characterize comprehensive metabolic changes across the gut-liver-adipose axis associated with divergent egg-production phenotypes. The results showed that: (1) FH hens exhibited higher serum APOB and lower conjugated bile acids (TCDCA, TCA, and THDCA), with hepatic upregulation of FASN, PPARA, CPT1A, and VTG1 along with downregulation of CYP7A1, CYP7B1, CYP8B1, and CYP27A1; (2) intersecting module hub genes (MHGs) with differentially expressed genes (DEGs) identified 354 upregulated and 299 downregulated core genes, with EEF2 identified as the primary hepatic downregulated hub gene; (3) in abdominal fat, GSEA revealed significant enrichment in fatty acid transport (NES = 1.54), long-chain fatty acid metabolic process (NES = 1.39), and steroid hormone biosynthesis (NES = 1.85), accompanied by significant downregulation of ANGPTL4 and upregulation of HSD3B1, VTG1, VTG2, and VTG3; (4) ileal mucosal transcriptomics identified 619 DEGs (502 upregulated), with GSEA highlighting enrichment in cell junction organization (NES = 1.52) and tube morphogenesis (NES = 1.39), which were further categorized into functional modules including enteric synaptic signaling, epithelial adhesion, mucosal vascularization, and tissue renewal; (5) the functional profile of the ileal microbiota in FH hens showed enrichment of functions related to complex carbohydrate degradation and carbohydrate-binding modules, with keystone taxa including Blautia and Bifidobacterium associated with production and lipid markers. Collectively, these findings suggest that high egg production during the peak laying period is associated with coordinated metabolic differences across the liver, abdominal fat tissue, and intestine. The observed profiles included reduced hepatic translation-related and primary bile acid synthesis-related signatures, adipose endocrine-related changes and microbial functional potential related to carbohydrate utilization and antioxidant-related functional potential. These findings provide candidate multi-omics features for precision nutritional strategies and genetic improvement in commercial poultry. - Source: PubMed
Publication date: 2026/07/27
Ma JunjieQin KailongQiao ZhihaoRen ZhouzhengYang XiaojunLiu Yanli - Immunosuppressant tacrolimus (TAC) induces glucose metabolism disorder and diabetes mellitus (DM) closely associated with intestinal microbiota dysbiosis and reduced bile acid levels, and this study aimed to explore the ameliorative effect and underlying mechanism of hyodeoxycholic acid (HDCA) on TAC-induced DM in rat models. - Source: PubMed
Publication date: 2026/07/28
Hu NanQian MinyanLiu YanruJiang ZhenweiXu CaomeiZhang WentingJiang Jingting - This study explored the mechanism by which Tougu Xiaotong Capsules(TGXTC) improve osteoarthritis(OA) degeneration, focusing on the regulation of cholesterol metabolism in OA chondrocytes via microRNA-16-5p(miR-16-5p). In vivo experiments were performed. A total of fifty 8-week-old C57BL/6 mice were acclimated for one week and then randomly divided into a blank group(10 mice) and a modeling group(40 mice). The OA model was established in the modeling group using the modified Hulth method. These mice were then randomly subdivided into four groups(n=10 per group): model, TGXTC, miR-16-5p antagomir, and TGXTC+miR-16-5p antagomir. Mice in the antagomir groups received intra-articular injections of miR-16-5p antagomir. After four weeks of intervention, cartilage structure was observed using Masson's trichrome, hematoxylin-eosin(HE), safranin O-fast green, and toluidine blue staining. The mRNA levels of miR-16-5p and cholesterol metabolism-related factors-ATP-binding cassette transporter A1(ABCA1), apolipoprotein A1(ApoA1), liver X receptor beta(LXRβ), sterol regulatory element-binding protein(SREBP), cholesterol-25-hydroxylase(CH25H), 25-hydroxycholesterol-7-alpha-hydroxylase(CYP7B1), and endoplasmic reticulum stress-associated factors C/EBP homologous protein(CHOP) and caspase-3, were detected by quantitative real-time PCR(RT-qPCR). The protein expression levels of ABCA1, ApoA1, LXRβ, SREBP, CH25H, CYP7B1, CHOP, and caspase-3 were analyzed by Western blot. In vitro experiments were also conducted. A chondrocyte degeneration model was established by stimulating mouse chondrocytes with thapsigargin(TG). RT-PCR was used to examine the levels of ABCA1, ApoA1, LXRβ, SREBP, CH25H, CYP7B1, CHOP and caspase-3 under miR-16-5p inhibition conditions. Flow cytometry was employed to assess the effect of TGXTC on the apoptosis rate of TG-induced chondrocytes following miR-16-5p inhibition. Histological staining results showed that, compared to the model group, the TGXTC group exhibited relatively clear and intact cartilage layer structure. Furthermore, compared to the miR-16-5p antagomir group, the TGXTC+miR-16-5p antagomir group showed improved cartilage surface damage. RT-PCR results indicated that, compared to the model group, the TGXTC group had significantly increased mRNA levels of miR-16-5p and ABCA1, ApoA1, and LXRβ, while the mRNA levels of SREBP, CH25H, CYP7B1, CHOP, and caspase-3 decreased. Western blot results showed that, compared to the model group, the TGXTC group showed upregulated protein expression of ABCA1, ApoA1, and LXRβ, and downregulated protein expression of SREBP, CH25H, CYP7B1, CHOP, and caspase-3. The RT-qPCR results for the in vitro experiments showed that in miR-16-5p-inhibited chondrocytes, TGXTC intervention increased the mRNA levels of ABCA1, ApoA1, and LXRβ, and decreased those of SREBP, CH25H, CYP7B1, CHOP, and caspase-3. Flow cytometry results confirmed that TGXTC mitigated the apoptosis of TG-induced chondrocytes. In conclusion, TGXTC can alleviate cholesterol metabolism disorders in osteoarthritic chondrocytes by regulating miR-16-5p. - Source: PubMed
Fu Chang-LongChen Dan-LingGuo Jing-YiLan Shu-JieChen Jia-NanYe Xiao-Qian