DHEA_S
- Known as:
- DHEA_S
- Catalog number:
- BQ 079S
- Product Quantity:
- 96/kit
- Category:
- -
- Supplier:
- Bioquant
- Gene target:
- DHEA_S
Related products to: DHEA_S
5-Androsten-3beta-OL-7, 17-Dione (DHEA) Antibody7a_Hydroxy DHEA 7a_Hydroxy DHEA7_Keto dehydroepi androsterone Keto DHEAAcP_ DHEAAnti- Dehydroepiandrosterone (DHEA) Sulfate-3 AntibodyAnti- Dehydroepiandrosterone (DHEA) Sulfate-7 AntibodyAntibody to Dehydroepiandrosterone (DHEA) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to Dehydroepiandrosterone (DHEA) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntimicrobial Drugs: Natural Steroids: DEHYDROEPIANDROSTERONE SULPHATE (DHEA-S), Host animal: Sheep, Format: Purified monoclonal antibodyAntimicrobial Drugs: Natural Steroids: DEHYDROEPIANDROSTERONE SULPHATE (DHEA-S), Host animal: Sheep, Format: Purified monoclonal antibodyBile salt sulfotransferase,Dehydroepiandrosterone sulfotransferase,DHEA-ST,Homo sapiens,HST,HST,Human,Hydroxysteroid Sulfotransferase,ST2,ST2A1,ST2A3,STD,Sulfotransferase 2A1,SULT2A1Biotin-linked Antibody to Dehydroepiandrosterone (DHEA); Reactivity: Homo sapiens (Human) Clonality: Polyclonal Source: RabbitBovine Dehydroepiandrosterone ELISA , DHEABovine Dehydroepiandrosterone ELISA , DHEABovine Dehydroepiandrosterone(DHEA)ELISA Kit Related articles to: DHEA_S
- Non-alcoholic fatty liver disease (NAFLD) frequently coexists with type 2 diabetes mellitus (T2DM), posing a significant metabolic disorder with limited dietary intervention options. Cordycepin, a food‑derived nucleoside from the edible fungus Cordyceps militaris, exhibits hypoglycemic and hypolipidemic effects, but its role in T2DM combined with NAFLD remains unknown. Here, we established a mouse model of T2DM combined with NAFLD in male KM mice using high-fructose and high‑fat diet, and streptozotocin. Both cordycepin (COR) and Cordyceps militaris water extract (CWE) attenuated glucose intolerance, dyslipidemia, hepatic steatosis, liver injury, inflammatory response and oxidative stress, with cordycepin showing superior efficacy. Multi‑omics analysis revealed that cordycepin uniquely reshaped the gut microbiota by significantly enriching the c__Clostridia, including g__Acetatifactor, g__Anaerovorax, g__Monoglobus, s__Acutalibacter_muris, and further affected liver metabolism, which was characterized by enrichment of bile acid metabolism-related pathways. Targeted bile acid metabolomics demonstrated that cordycepin specifically promoted the production of cholic acid‑7‑sulfate (CA7S), a gut‑restricted secondary bile acid, through activation of the hepatic PXR/Sult2a1 pathway. Notably, integrated correlation analysis revealed a significant positive association between CA7S and c__Clostridia (e.g., g__Monoglobus, g__Lachnoclostridium, and g__Anaerovorax), suggesting that cordycepin enhances CA7S production by enriching these Clostridia members. And CA7S activated TGR5 to stimulate glucagon‑like peptide‑1 (GLP‑1) secretion, thereby improving glucose and lipid homeostasis. Therefore, these findings demonstrate that dietary cordycepin improves T2DM combined with NAFLD by modulating gut microbiota, particularly Clostridia, and affecting the PXR/Sult2a1/CA7S/GLP‑1 pathway, thereby exerting beneficial effects on glucose and lipid homeostasis. - Source: PubMed
Publication date: 2026/09/05
Meng YingDun MengqianLiu XinyuanChen WeiboZhang ZhongmingLu ShengyuZhang GuoyingLing Jianya - The objective of this study was to assess the effects of short-chain fatty acids (SCFAs) on androstenone metabolism and associated gene expression in hepatocytes isolated from intact (boars) and castrated (barrows) male pigs. Isolated porcine hepatocytes were treated with the SCFAs acetate, propionate, and butyrate, both individually and in combination, and then incubated with androstenone. Androstenone metabolism and gene expression were subsequently assessed. Androstenone metabolism was significantly increased by propionate (P < 0.01) and all SCFA combination treatments (P < 0.0001) in hepatocytes from both boars and barrows, and by butyrate in hepatocytes from boars (P = 0.009). Several key genes were upregulated in hepatocytes from barrows; this included AKR1C1 following all SCFA combination treatments (P ≤ 0.01), UGT2A1 and SULT2A1 following treatment with the combination of propionate and butyrate (P < 0.05) and the combination of all three SCFAs (P < 0.05), and SULT1E1 following treatment with the combination of acetate and butyrate (P = 0.005). Short-chain fatty acid treatments did not alter gene expression in hepatocytes from boars; however, plasma levels of estrone-1-sulfate, an abundant testicular steroid in boars, were positively correlated (P < 0.05) with UGT1A1, SULT1E1, and UGT2A1 expression in response to treatment with different SCFAs. These results suggest that SCFA-induced effects on hepatic androstenone metabolism and gene expression depend on the specific SCFA profile and are influenced by testicular steroid hormones. - Source: PubMed
Publication date: 2026/09/04
Lawson AustinBone ChristineParent MelissaSquires E James - Digestive system disorders (DSDs) are prevalent and burdensome conditions worldwide. The human proteome serves as a primary source for designing disease treatment targets and holds great potential for drug repurposing. We applied Mendelian randomization analyses to examine the genetic associations between 2321 plasma proteins and 47 DSDs using data from the FinnGen project, identifying 12 causal proteins and validating four (Tripartite Motif Containing 40, Sulfotransferase Family 2A Member 1, Peptidase Inhibitor 16, MHC Class I Polypeptide-Related Sequence B) of them in the UK Biobank. Mediation analysis showed that SULT2A1 may increase the risk of cholelithiasis by reducing 25-hydroxyvitamin D levels. Molecular interaction simulations indicated that the interaction between SULT2A1 and 25-hydroxyvitamin D is comparable to that with the defined substrate 24-OHChol-24-sulfate. We found that elevated levels of SULT2A1 may increase metabolism of approved drugs for cholelithiasis (i.e., ursodeoxycholic acid and chenodeoxycholic acid) by binding deoxycholic acid, thus reducing drug efficacy. We applied the AlphaFold3 strategy to simulate interactions between SULT2A1 and 10,052 small molecules, identifying 5 molecules that may competitively bind to SULT2A1, potentially enhancing the treatment efficacy of deoxycholic acid for cholelithiasis. Overall, our study reveals several causal associations between plasma proteins and DSDs and identifies SULT2A1 as a promising drug repurposing target for cholelithiasis. - Source: PubMed
Publication date: 2026/04/17
Zhang ShixuanLiu ZhenqiuSun DayanWu FeiWei YangJin LiYang ShenHuang JinshiWang Jiucun - Given the existing uncertainties regarding the link between Di(2-ethylhexyl) phthalate (DEHP) exposure and gastric cancer (GC) progression, this study aimed to clarify their association, identify the toxic targets of DEHP, and elucidate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/07/16
Li ShenghaoPeng QingHao LiyuanMao JingyuHuo Bingjie - Disruption of bile acid (BA) homeostasis and circadian rhythm are interconnected in chronic liver diseases, yet how circadian dysfunction exacerbates cholestasis remains unclear. This study demonstrates that hepatocyte-specific knockout of the core clock gene Bmal1 in female mice markedly aggravates liver injury, inflammation, and fibrosis in an α-naphthylisothiocyanate (ANIT)-induced intrahepatic cholestasis model. The pathological exacerbation is attributed to a profound loss of circadian oscillation and reduced expression of the detoxification enzyme sulfotransferase family 2A member 1 (SULT2A1), resulting in deficient sulfation and hepatic accumulation of cytotoxic bile acids. This hypersusceptibility was further validated in primary hepatocytes under BA overload. Notably, specific in vivo restoration of hepatic SULT2A1 significantly reversed these pathological progressions. Mechanistically, BMAL1 transcriptionally activates Sult2a1 by directly binding to the E-box element within its promoter region. Taken together, our work elucidates the BMAL1-SULT2A1 axis as an essential circadian defense mechanism that maintains hepatic bile acid detoxification homeostasis in female mice, providing a novel theoretical basis for chronotherapeutic strategies in cholestatic liver diseases. - Source: PubMed
Publication date: 2026/07/15
Xiao YifeiHe JiatianZheng YiZhang XinyuLi JintaoJin MengChen MinWu YushanLiu XiaowenXu HaimanLin LuominWu BaojianGuo LianxiaDong Dong