ADIPOR1 ELISA kit
- Known as:
- ADIPOR1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADIPOR1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADIPOR1 ELISA kit
Related genes to: ADIPOR1 ELISA kit
- Gene:
- ADIPOR1 NIH gene
- Name:
- adiponectin receptor 1
- Previous symbol:
- -
- Synonyms:
- PAQR1, ACDCR1
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-23
- Date modifiied:
- 2018-05-03
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- The aim of this study was to perform multivariate analysis of correlation between gene expression of leptin, leptin receptor (ObRb), adiponectin, adiponectin receptor (Adipo R1), and resistin in placental tissue with biochemical variables of the energy, protein, enzymatic, hormonal, and mineral profile, through multivariate analysis, in cows with and without hyperketonemia. Samples from 135 cows were collected during calving and subsequently distributed into two groups: G1 = control (β-hydroxybutyrate <1.2 mmol/L / n = 120); and G2 = with hyperketonemia (β-hydroxybutyrate ≥1.2 mmol/L / n = 15). Biochemical and hormonal indicators (NEFA, β-hydroxybutyrate, glucose, total protein, albumin, urea, creatinine, GGT, AST, chlorides, phosphorus, ionizable calcium, potassium, sodium, insulin, and cortisol ions) were evaluated, as well as insulin sensitivity. Placental fragments were collected and processed for mRNA analysis by qPCR, with 38 samples analyzed (G1 =23; G2 =15). The data were analyzed using SAS PROC MIXED, with normality checks and transformations applied when necessary. F/SNK or Mann-Whitney tests were used according to the data distribution. In the multivariate analysis, data imputation, SMOTE, and autoscaling were performed, followed by analyses using PCA, HCA, and PLS. A significance level of 5% was adopted. Hyperketotic cows showed higher expression of leptin (p = 0,0174) and ObRb (p < 0,0001), while healthy cows showed higher expression of AdipoR1 and resistin (p < 0,0001). Multivariate analyses indicated ObrRb, AdipoR1, and β-hydroxybutyrate as key variables in differentiating the groups, being representative of the hyperketonemia condition in cows at calving, highlighting the potential of placental adipokines as tools for diagnosis and prognosis of this metabolic disorder in these females. - Source: PubMed
Publication date: 2026/04/13
Conceição Ângela Imperiano daDantas João Victor José de BarrosMendonça Carla Lopes deCajueiro Jobson Filipe de PaulaSouto Rodolfo José CavalcantiSouza Paulo Roberto Eleutério dePinto LicarionAfonso José Augusto BastosSoares Pierre Castro - Opioid use disorder (OUD) has been linked to cardiometabolic diseases in adults through reductions in adiponectin-an adipocytokine with insulin-sensitizing effects. Opioid use during pregnancy dysregulates neonatal growth and may predispose to adult-onset diseases, but the impact of maternal OUD on neonatal adiponectin signaling has not been studied. As receptor activation is important for physiological effects, we made decision to measure adiponectin receptor expression. We hypothesize that maternal OUD also reduces adiponectin receptor level in offspring (primary outcome) and alters growth (secondary outcome). To test our hypothesis, we conducted a prospective, observational pilot study and compared the expression of salivary adiponectin receptor 1/ and anthropometric and body composition (fat and fat-free mass) measurements between opioid-exposed and age-matched non-exposed neonates born at ≥34 weeks' gestation. Data were stratified by exposure and sex using a Student's -test. Significance was set at < 0.05. A total of 67 neonates (35 opioid-exposed, 32 non-exposed neonates) were enrolled. Compared to healthy, non-exposed neonates, the expression of was reduced in opioid-exposed neonates (0.27-fold, < 0.01), with the lowest expression in those requiring pharmacotherapy (0.048-fold, < 0.001). Despite the smaller anthropometric measurements in the exposed than non-exposed neonates (2,915 ± 625 grams vs. 3,209 ± 345 grams, = 0.02), opioid-exposed neonates had comparable adiposity to non-exposed neonates (fat mass percentage 8.60 ± 4.52% vs. 8.53 ± 4.00%, = 0.95). Less breast milk was used in the exposed than non-exposed group (25.7% vs. 71.9%, < 0.01). Maternal OUD may be associated with aberrant growth and excess adiposity in offspring through its effect on adiponectin signaling, predisposing these neonates to cardiometabolic risks. - Source: PubMed
Publication date: 2026/04/01
Yen ElizabethSingh KiranChow MarissaCarasi-Schwartz FrancescaCordova MarioKaneko-Tarui TomokoBrew EmilyMahmoud TaysirReddy PratikRodday Angie MaeMaron Jill LDavis Jonathan MO'Tierney-Ginn Perrie - Pathological intramuscular lipid deposition (myosteatosis) and exercise intolerance are hallmarks of metabolic disorders, including diabetes and metabolic dysfunction-associated steatotic liver disease (MASLD), yet their underlying mechanisms remain unclear. Our previous work has confirmed that hypertriglyceridemia-driven kallistatin (KAL) elevation is present in the peripheral blood of patients with MASLD and diabetes and is a causative factor in hepatic steatosis and MASH pathogenesis. Here, we aim to evaluate this elevated KAL on myosteatosis and exercise function. - Source: PubMed
Hong FuyanFang ZhenzhenShen GangWang YanLi YunhuaZhong YoubinDai JunzeZhang ChengweiZhang JingChen WencanQi WeiweiYang XiaGao GuoquanZhou Ti - Adipokines secreted by adipocytes have emerged as critical modulators of cancer progression, particularly in obesity-associated malignancies. However, their therapeutic relevance and the tumor types responsive to adipokine pathways remain unclear. To identify adipokine-driven cancers and assess the therapeutic potential of adipokine signaling, we conducted a pan-cancer transcriptome analysis of the expression of various adipokine receptors in 31 tumor types. AdipoR1 was most frequently amplified and overexpressed in breast cancer across molecular subtypes. In the functional analysis, AdipoR1 stimulation using the agonist AdipoRon activated AMPK signaling, suppressed proliferation and migration, and induced apoptosis in both hormone receptor (HR)-positive (MCF7, T47D) and triple-negative (MDA-MB-231, MDA-MB-468) breast cancer cells. Notably, RNA-Seq analysis revealed that AdipoR1 stimulation upregulated ferroptosis-related genes, DDIT3, HMOX1, and IRE1α, and downregulated proliferation-related genes, estrogen receptor and TROP2, in breast cancer cell lines. Immunoblotting confirmed these changes at the protein level. AdipoR1 activation enhanced the efficacy of chemotherapeutic agents. In vivo, AdipoRon significantly reduced tumor growth and induced necrotic cell death. AdipoR1 activation exerts multimodal antitumor effects by engaging cell death and hormone receptor signaling. These findings establish AdipoR1 as a valuable therapeutic target in breast cancer and support further development of adipokine receptor-targeting therapies. - Source: PubMed
Publication date: 2026/03/26
Sato ShinyaYamanaka TakashiKomori YukakoIshida MutsumiNakamura YoshiyasuYamashita ToshinariMiyagi Yohei - Psoriasis is a recurrent immune-mediated systemic disease. Adiponectin (APN), a key regulator of metabolism, is also known for its anti-inflammatory properties in several inflammatory disorders. The study aims to investigate the anti-inflammatory properties of APN on human immortalized keratinocyte cells (HaCaT) and to evaluate its therapeutic potential in an imiquimod (IMQ)-induced psoriasis mouse model. - Source: PubMed
Zhang LinglingKe ChunxiShen YunShi FengJiao QingqingJi Jiang