ADIPOR1 ELISA kit
- Known as:
- ADIPOR1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADIPOR1-Si
- 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
Related products to: ADIPOR1 ELISA kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: ADIPOR1 ELISA kit
- This study aimed to identify potential genetic variants and candidate genes associated with feed efficiency (FE), production, and feeding behaviour traits in Canadian purebred Duroc pigs. Genome-wide association studies (GWAS) were conducted using 8,861 individuals and an imputed Affymetrix PigGen Canada 50K panel v2.0 using a linear mixed model (LMM) and a Bayesian B model. This analysis used an adjusted p-value threshold (ranging from 6.6 × 10-5 to 1.3 × 10-4) using false-discovery rate to determine significance. The number of significant SNPs identified for each trait was as follows: average daily gain (ADG, 48), daily feed intake (DFI, 85), feed conversion ratio (FCR, 101), residual feed intake (RFI, 37), residual gain (RG, 64), residual intake and gain (RIG, 55), backfat thickness (BF, 100), loin depth (LD, 6), Keibler ratio (KR, 0), total time spent eating per day (TPD, 7), and number of visits to the feeder per day (NVD, 6). Several traits (BF, DFI, FCR, RFI, RG, and RIG) showed strong overlapping signals on chromosomes 7 and 10 with 24 shared significant SNPs, indicating potential shared genetic mechanisms. These traits also had 71 overlapping candidate genes such as PACSIN1, PTCH1, ADIPOR1 and ITPR3, associated with glucose, lipid and cholesterol metabolism. Well known candidate genes in literature associated with growth and fatness such as MC4R and CDH20 were also identified to be associated with ADG, BF, FCR and DFI in this study. Gene Ontology enrichment analysis revealed a set of the candidate genes were involved in the gonadotropin-releasing hormone (GnRH) and the platelet-derived growth factor (PDGF) signaling pathways. Overall, this study contributed to understating the genetic architecture and provided a biological foundation for improving FE, production and feeding behaviour traits in Canadian Duroc pigs facilitating the selection of more efficient pigs. - Source: PubMed
Publication date: 2026/05/09
Kim BelleDo Duy NgocJafarikia MohsenTulpan DanAdewole DeborahManafiazar GhaderSullivan BrianHoll JustinMiar Younes - Type 2 diabetes mellitus (T2DM) is closely related to cognitive impairment, with underlying pathological mechanisms including chronic inflammation, synaptic dysfunction, and microglial dysregulation. Although microRNA-144 (miR-144) has been implicated in these processes, its precise role and molecular mechanisms remain unclear. T2DM mouse models were established using a high-fat diet combined with low-dose streptozotocin, and microglia-specific miR-144 intervention was achieved in the hippocampus via bilateral injection of adeno-associated virus. Cognitive function was assessed using the novel object recognition and Morris water maze tests, while synaptic plasticity, microglial phenotype, neuroinflammation, and Tau pathology were evaluated by immunofluorescence, Western blot, Golgi staining, transmission electron microscopy, and electrophysiology. Our results showed that overexpression of miR-144 mimicked the pathological state of T2DM, leading to impaired learning and memory, neuronal dysfunction, reduced expression of synaptic proteins, and decreased dendritic spine density. Additionally, miR-144 overexpression significantly suppressed FoxO1 and AdipoR1/AdipoR2 expression while inducing microglial M1 polarization, activating downstream NLRP3-mediated neuroinflammatory responses, and increasing Tau phosphorylation. Conversely, miR-144 knockdown effectively ameliorated these pathological changes and provided neuroprotection. These findings suggest that miR-144 could serve as a promising biomarker and therapeutic target for T2DM-related cognitive impairment. This study offers novel insights into the underlying mechanisms of T2DM-related cognitive impairment and provides an experimental foundation for exploring miR-144-based intervention strategies. - Source: PubMed
Publication date: 2026/05/05
Zhao JinyingZhou YuliangCheng ShiShen JiaLi YahongXu Zhipeng - 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