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
- Neonatal jaundice (NJ) affects 60-80% of neonates, yet the underlying microbial mechanisms remain elucidated, despite known links between gut dysbiosis and bilirubin and bile acid (BA) metabolism. Through two-stage shotgun metagenomic-metabolomic analysis of 150 fecal samples from 120 neonates, we identified key taxa linked to bile acid (BA) metabolism in moderate-to-severe NJ. Furthermore, multi-omics integration revealed significant interkingdom correlations among gut phages, bacteria, and BAs. Dysbiosis featured enriched Streptococcus and Escherichia, depleted Bifidobacterium animalis, and group-specific phage signatures. In the independent clinical validation cohort, jaundice intervention normalized the dysbiotic profile, demonstrating significant suppression of pathogenic taxa concomitant with restoration of B. animalis abundance. In vitro, B. animalis subsp. lactis Y103-OTU5 remodeled BA via deconjugation. In a phenylhydrazine hydrochloride (PHZ)-induced murine model of hemolytic jaundice, oral administration of isolated B. animalis subsp. lactis Y103-OTU5 significantly attenuated hyperbilirubinemia and hepatic inflammation, likely via Cyp7a1/Cyp7b1-dependent modulation of BA synthesis and detoxification pathways. Structural equation modeling revealed a tripartite regulatory network: phages indirectly modulated BA through bacterial remodeling, while B. animalis directly regulated BA pathways, positioning it as a potential therapeutic candidate for hemolysis-associated neonatal jaundice. Collectively, these findings reveal a gut phage-bacteria-BA network in NJ, highlighting B. animalis as a therapeutic candidate with dual modulation of BA metabolism and phage-bacteria interactions. - Source: PubMed
Publication date: 2026/06/29
Chen XianhongChen ChengZhang PengOuYang XiaohongMa HaiyanChen WanlingLi TingtingHan JingWang YanliWang HuijuanZhou QiujingCheng GuoqiangZhou WeiYu ZhangbinZhou WenhaoWang MingbangZeng Shujuan - Knee osteoarthritis (KOA) is a global public health crisis and a leading cause of disability among middle-aged and elderly populations. Historically characterized as a passive "wear-and-tear" process, the understanding of KOA has undergone a fundamental paradigm shift. While aberrant biomechanical loading remains a primary initiator of joint damage, it is increasingly recognized that systemic metabolic dysfunction and chronic low-grade inflammation act as the critical forces driving sustained disease progression. - Source: PubMed
Publication date: 2026/05/18
Yan ManliZhang XinLiu HaoKang QingyangLi JianjiangZhang BaoqingLin DingkunLi Xiang - Fatty liver is a common metabolic disease in dairy cows during early postpartum period, which is characterized by excessive hepatic triacylglycerol (TAG) accumulation. However, the mechanisms of bile acid (BA) metabolism in dairy cows experiencing fatty liver remain poorly elucidated. The farnesoid X receptor () plays a critical role in the regulation of BA homeostasis. Consequently, the aim of this study was to investigate the effect of -mediated BA metabolism following stimulation with high concentrations of free fatty acids (FFA). - Source: PubMed
Publication date: 2026/04/30
Jia BinTian YanGao ChanghongChang YaqiZhang ZexinSong YuxiXia ChengQu YongliYang Wei - Age-related hepatic metabolic dysfunction significantly impairs the health and productivity of laying hens. Puerarin (Pue), a natural isoflavone, exhibits diverse pharmacological activities relevant to liver and gut health. Our previous work demonstrated that dietary supplementation with Pue improved laying performance and egg quality, while reducing the feed conversion ratio in aged laying hens. Building on these findings, we employed an integrated multi-omics approach to investigate whether Pue exerts hepatoprotective effects by restoring gut-liver axis homeostasis, thereby supporting liver function and potentially extending the production performance of aged laying hens. - Source: PubMed
Publication date: 2026/05/15
Du XubinZhao DongZhang YuchenWu XinyueHe JiawenLiu FeiYu Debing - : Based on previous findings on the Lingguizhugan (LGZG)-mediated gut-liver axis, this study clarifies the therapeutic mechanisms of LGZG in metabolic dysfunction-associated steatotic liver disease (MASLD), with a focus on the gut microbiota-bile acid-TGR5 (GPBAR1) axis. : C57BL/6J mice were fed a high-fat diet (HFD) for 8 weeks to induce MASLD, followed by 4-week LGZG intervention (21.57 g/kg/day, oral gavage). Metabolic phenotypes, gut microbiota (16S rRNA sequencing), serum/hepatic bile acids (targeted metabolomics), and molecular targets (qPCR/Western blot) were analyzed. : LGZG significantly alleviated HFD-induced obesity, insulin resistance, and hepatic steatosis, while enhancing whole-body energy expenditure (increased oxygen consumption (VO), and heat production ( < 0.05). It also reduced serum ALT ( < 0.001) and AST levels ( < 0.01). Mechanistically, LGZG remodeled the gut microbiota, specifically increasing , and _NK4A236_group while decreasing . This shift inhibited the intestinal FXR-Fgf15 axis, concurrently activating the hepatic alternative bile acid synthesis pathway (upregulating CYP27A1 and CYP7B1 protein expression; < 0.001 and < 0.01, respectively). Consequently, systemic accumulation of non-12α-hydroxylated bile acids (non-12-OH BAs) such as hyocholic acid (HCA) and 7-ketolithocholic acid (7-ketoLCA) occurred-known TGR5 agonists and intestinal FXR antagonists. These changes elevated serum GLP-1 levels ( < 0.05) and activated adipose TGR5-cAMP/PKA/CREB signaling. The metabolic benefits primarily originated from non-12-OH BAs enrichment and TGR5-mediated adipose browning, not hepatic FXR activation. : Our findings show that LGZG ameliorates MASLD by remodeling bile acid profiles via intestinal FXR-Fgf15 axis inhibition and hepatic alternative synthesis pathway activation. This study highlights the TGR5-targeting properties of LGZG, providing a mechanistic basis for its therapeutic use in metabolic disorders. - Source: PubMed
Publication date: 2026/03/24
Sun Yun-HongDing Pei-LunWang XueWang Yi-RongZhu Ming-ZheWang KaiDai LiangDang Yan-QiJi GuangLi MengZhou Wen-Jun