Ask about this productRelated genes to: HSD3B7 antibody
- Gene:
- HSD3B7 NIH gene
- Name:
- hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 7
- Previous symbol:
- -
- Synonyms:
- C(27)-3BETA-HSD, SDR11E3
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-13
- Date modifiied:
- 2016-07-18
Related products to: HSD3B7 antibody
Related articles to: HSD3B7 antibody
- polysaccharide (EPP), a major bioactive sulfated polysaccharide derived from green algae, possesses potent hypoglycemic and hypolipidemic properties. This study aimed to evaluate the therapeutic efficacy of EPP in a murine model of type 2 diabetes mellitus (T2DM) and elucidate its underlying molecular mechanisms through an integrated multi-omics approach-comprising 16S rRNA microbiomics, untargeted metabolomics, and transcriptomics. Our findings demonstrate that EPP intervention significantly suppressed fasting blood glucose (FBG) levels, attenuated dyslipidemia, and enhanced systemic insulin sensitivity. At the microbiome level, EPP restored intestinal homeostasis by enriching beneficial taxa, specifically , , and , while depleting the T2DM-associated genus . These microbial shifts correlated with significantly elevated fecal concentrations of short-chain fatty acids (SCFAs), including acetate, propionate, and branched-chain fatty acids (isobutyrate and isovalerate). Integrated pathway analysis revealed that EPP significantly modulates steroid hormone biosynthesis; integrated pathway analysis suggested that EPP potentially modulates pathways related to steroid hormone biosynthesis, cholesterol metabolism, and primary bile acid synthesis. Quantitative RT-PCR validation confirmed that EPP treatment was accompanied by the upregulation of critical genes involved in bile acid and steroidogenesis (, , , and ) and the downregulation of and , the master transcriptional regulators of cholesterol biosynthesis and hepatic gluconeogenesis, respectively. Correlation analyses further indicated potential links between gut microbiota alterations, SCFA production, and glycemic control. Collectively, these results suggest that EPP may alleviate T2DM symptoms, which is associated with the modulation of the gut microbiota-hepatic cholesterol metabolism axis, positioning it as a promising functional food ingredient or therapeutic candidate for metabolic disorders. - Source: PubMed
Publication date: 2026/06/09
Zhu LiuyingWen XushengZhu WenrongHu XueqianXu YanqunPeng Xin - This study aimed to explore the regulatory effect and mechanism of 3β-hydroxy-Δ-C-steroid oxidoreductase (HSD3B7) on bovine follicular development. Bovine primary granulosa cells (GCs) with knockdown and overexpression were constructed, and the proliferation efficiency of GCs was examined by the cell counting kit-8 (CCK-8) method. Annexin V-EGFP/PI double staining was performed to detect the apoptosis level of GCs. The concentration of estradiol (E) in the culture medium and that of 2-methoxyestrone in GCs were determined by enzyme-linked immunosorbent assay (ELISA). The relative expression levels of the , , , and were determined by qRT-PCR. The protein levels of related genes were determined by Western blotting. The results showed that knockdown decreased the proliferation efficiency and CCND2 expression level of primary bovine follicular GCs, promoted the apoptosis, and increased Bim and Caspase-3 expression in GCs. Additionally, it decreased E secretion and CYP19A1 and STAR expression, and increased the concentration of 2-methoxyestrone, the main metabolite of E. The opposite results were obtained after overexpression. These results suggested that HSD3B7 positively regulated the development of bovine follicles by promoting the proliferation and E secretion and inhibiting the apoptosis of GCs. The results provide a new theoretical basis for further understanding the molecular regulatory network of bovine follicle development, and also lay a foundation for related research and practical application to improve bovine reproductive efficiency. - Source: PubMed
Cheng JunliHan JunYan JunrongZhu ZhiweiLi Pengfei - Congenital bile acid synthesis defect type 1 (CBASD1) is an extremely rare autosomal recessive metabolic disorder caused by mutations in the HSD3B7 gene, resulting in defective bile acid synthesis and accumulation of hepatotoxic intermediates. We report a seven-month-old female infant born to consanguineous parents who presented with progressive jaundice since one month of age, severe pruritus, failure to thrive, and abdominal distension with hepatosplenomegaly. Biochemical evaluation revealed marked conjugated hyperbilirubinemia, elevated cholestatic enzymes, coagulopathy, and mild hypoalbuminemia, with low-normal gamma-glutamyl transferase levels. Elastography demonstrated advanced fibrosis (F4), and abdominal computed tomography showed cirrhotic liver changes with splenomegaly. Due to progressive liver failure despite medical therapy, the patient underwent living donor liver transplantation. The explanted liver demonstrated cholestatic hepatitis and cirrhosis, with ductular proliferation and giant-cell transformation, and no evidence of malignancy. Subsequent genetic testing identified a homozygous pathogenic mutation in the HSD3B7 gene, confirming the diagnosis of CBASD1. This case highlights the importance of early biochemical evaluation, urine bile acid profiling, and genetic testing in infants with low gamma-glutamyl transferase (GGT) cholestasis to enable timely diagnosis, continue medical optimization, and proceed with liver transplant in the future. - Source: PubMed
Publication date: 2026/02/05
Khan MahnoorShehzad Muhammad UmairKhattak Umaima MZeeshan NidaSeerat Iqtadar - Lipid metabolic reprogramming represents a fundamental oncogenic mechanism. However, clinical relevance of lipid metabolism (LM) alterations in gliomas remain to be fully elucidated. LM-based classification and subsequent correlative analyses were performed using glioma bulk RNA-seq datasets retrieved from The Cancer Genome Atlas (TCGA). Radiomic models were constructed and validated using magnetic resonance imaging (MRI) datasets from The Cancer Imaging Archive (TCIA) and our in-house glioma cohort. Immunohistochemical (IHC) staining was employed to detect the protein expression of the key gene in glioma tissue samples. Single cell RNA-seq datasets from the GBMap database were used to characterize the distribution and functional roles of the key gene in the tumor microenvironment (TME) of gliomas. Consensus clustering based on LM pathways identified three distinct subtypes, respectively dominated by steroid metabolism (ST-type), triglyceride metabolism (TC-type), and sphingolipid metabolism (SP-type). The SP-type was independently associated with poorer prognosis and displayed enhanced activity in pathways linked to aggressive tumor phenotypes and radiotherapy resistance. Radiomic features enabled accurate identification of SP-type gliomas, thereby offering a non-invasive strategy for predicting this subtype. Genes GLA, GBL1, and HSD3B7 were identified as signature genes of the SP-type. Higher expression of HSD3B7 was associated with poor prognosis and exerted functional effects on multiple signaling pathways across various cellular components of the TME, which may contribute to glioma progression. Gliomas exhibited marked heterogeneity in LM and can be classified into three subtypes, with the SP-type exhibiting the most aggressive clinical behavior. - Source: PubMed
Publication date: 2026/02/11
Tu ShaohuaZhang PengChi XiaohanZhang YangJi Nan - The hepatotoxic compound 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) has been widely utilized to establish various liver disease models. However, the molecular networks and metabolic regulatory mechanisms underlying DDC-induced liver injury remain to be fully elucidated. In this study, an integrated transcriptomic and metabolomic approach was employed to investigate the mechanisms of DDC-induced hepatotoxicity. C57BL/6 J mice were administered a 0.1 % DDC-supplemented diet for two weeks to induce liver injury, followed by collection of serum and liver tissue samples for analysis. The results demonstrated that DDC treatment significantly elevated markers of liver injury, cholestasis, and fibrosis. Histopathological examination revealed hepatocyte damage, inflammatory cell infiltration, and increased collagen deposition in DDC-treated mice. Liver transcriptomic analysis identified 814 differentially expressed genes, while serum metabolomic profiling detected 958 differentially expressed metabolites. Integrated pathway analysis revealed co-enrichment of 14 pathways in both transcriptomic and metabolomic datasets, including steroid hormone biosynthesis, glycerophospholipid metabolism, retrograde endocannabinoid signaling, and primary bile acid biosynthesis. Validation experiments using qRT-PCR and UPLC-MS/MS demonstrated that DDC treatment upregulated hepatic mRNA levels of Cyp27a1, Mrp2, and Mrp3, while downregulating Cyp8b1, Hsd3b7, Scp2, and Hsd17b4. Serum analysis showed significant increases in the concentrations of CA, TCA, GCA, TCDCA, α-MCA, β-MCA, Tβ-MCA, TUDCA, CDCA, UDCA, ω-MCA, and HDCA, along with decreased LCA levels. These findings indicate that DDC-induced liver injury involves multiple pathways and mechanisms, with disruption of bile acid homeostasis representing a central pathological feature. - Source: PubMed
Publication date: 2025/12/02
Zhang ZijunJi RongKu AhuaA RuhanSong Binbin