Chicken Adiponectin Receptor 1 ELISA , ADIPOR1
- Known as:
- Chicken Adiponectin Receptor 1 Enzyme-linked immunosorbent assay test , ADIPOR1
- Catalog number:
- E12A0524
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Chicken Adiponectin Receptor 1 ELISA ADIPOR1
Related genes to: Chicken Adiponectin Receptor 1 ELISA , ADIPOR1
- 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: Chicken Adiponectin Receptor 1 ELISA , ADIPOR1
Related articles to: Chicken Adiponectin Receptor 1 ELISA , ADIPOR1
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by amyloid-β buildup, tau pathology, neuroinflammation, and declining cognition. Adiponectin, a hormone produced by adipose tissue with insulin-sensitizing, anti-inflammatory, and antioxidant effects, may link peripheral metabolic health to brain function. Studies show that adiponectin helps neurons survive, improves synaptic plasticity, maintains blood-brain barrier integrity, and reduces amyloid-β and tau damage via AdipoR1/R2 signaling. Clinical studies evaluating circulating adiponectin have yielded inconsistent findings, giving rise to the 'adiponectin paradox' whereby elevated adiponectin levels in older adults and patients with AD may reflect frailty, weight loss, systemic inflammation, or compensatory responses rather than direct neuroprotective effects. Studies indicate that vitamin D (VD) and L-cysteine (L-Cys), a precursor to glutathione, act synergistically to modulate oxidative stress, inflammation, and adiponectin levels. VD increases circulating adiponectin and benefits metabolism, while L-Cys boosts glutathione, restores redox balance, and promotes adiponectin secretion by affecting fat cell function. Emerging experimental evidence, together with clinical observations from metabolic disorders, suggests that VD and L-Cys may influence adiponectin-related pathways, oxidative stress, and inflammation, which are implicated in AD pathogenesis. However, direct clinical evidence demonstrating that combined VD and L-Cys supplementation modulates these pathways or alters AD progression in humans is currently lacking. This narrative review covers current knowledge of adiponectin and its links to obesity, metabolic issues, and AD, and it also explores the roles of VD and L-Cys as regulators of adiponectin signaling. Overall, the available evidence supports the proposed interaction among VD-L-Cys and adiponectin, which warrants further mechanistic investigation and well-designed clinical studies to determine its therapeutic relevance in AD. - Source: PubMed
Publication date: 2026/07/26
Justin Margret JeffreyJain Sushil K - The objective was to analyze the mRNA expression of leptin, leptin receptor (ObRb), adiponectin, adiponectin receptor (AdipoR1), and resistin in the placental tissue of cows with and without hyperketonemia, relating it to their metabolic profile. Samples were collected from 135 cows during birth, divided into two groups: G1: without hyperketonemia (n = 120) and G2: with hyperketonemia (n = 15). Biochemical and hormonal indicators and insulin sensitivity were evaluated. Placental fragments were analyzed by qPCR. The variables were tested for normality and Pearson's correlation coefficient was applied. The significance level was 5%. Cows with hyperketonemia showed increased concentrations of NEFA (p = 0.0002), urea (p = 0.0302), higher expressions of leptin (p = 0.0174) and ObRb (p < 0.0001), while healthy cows showed higher expression of AdipoR1 (p < 0.0001) and resistin (p = 0.0435). Glucose concentrations were lower in G2 (p = 0.0132), as were the percentages of RQUICKI (p < 0.0001). Among the varying degrees of correlations between the variables, the following stand out: positive correlation of leptin expression with β-Hydroxybutyrate and ObRb expression; positive correlation of ObRb expression with β-hydroxybutyrate, NEFA, GGT and AST, and negative correlation with glucose; positive correlation of AdipoR1 expression with glucose, RQUICK and RQUICK, and negative correlation with β-Hydroxybutyrate, NEFA and GGT. Gene expression analysis of adipokines in the placenta is a promising tool to understand their role in metabolic regulation in cows, especially in the dynamics of hyperketonemia. It is concluded that the placental production of these hormones has an important contribution to metabolic conditions in the transition period, bringing implications for the physiology, health and productivity of females. - Source: PubMed
Publication date: 2026/08/10
da Conceição Ângela Imperianode Barros Dantas João Victor Joséde Mendonça Carla Lopesde Paula Cajueiro Jobson FilipeSouto Rodolfo José CavalcantiPinto Licarionde Araújo Gonçalves Daniel Nunesde Souza Paulo Roberto EleutérioAfonso José Augusto BastosSoares Pierre Castro - Feed efficiency (FE) is recognized as a vital component of sustainable dairy production, with residual feed intake (RFI) serving as a key metabolic indicator of FE independent of production levels. However, the genetic improvement of this complex trait is limited by the inability of conventional genomic Best Linear Unbiased Prediction (gBLUP) model to capture complex, non-linear genetic architectures and epistatic interactions. To address these limitations, this study aims to compare the predictive performance of machine learning (ML) approaches, specifically Random Forest (RF) and Multi-Layer Perceptron (MLP) models, against standard gBLUP using genomic data from 220 UK Holstein cows genotyped with the BovineSNP50 v3 BeadChip with 47,446 quality-controlled single nucleotide polymorphisms (SNPs), phenotyped for RFI from 1996-2023. SHapley Additive exPlanations (SHAP) were applied to interpret SNP feature importance from the ML models, and an ensemble framework was implemented to leverage the complementary strengths of RF and MLP. - Source: PubMed
Publication date: 2026/08/08
Ong Edwin Jun KiatMooney Mark HRezwan Faisal IWang HuiShirali Masoud - Necroptosis is implicated in the pathogenesis of various inflammatory diseases, including periodontitis. This study aimed to investigate the molecular mechanisms underlying necroptosis in gingival fibroblasts (GFs) and to evaluate the therapeutic potential of AdipoAI, a novel adiponectin receptor agonist, administered locally, along with its regulatory effect on necroptosis. - Source: PubMed
Publication date: 2026/07/27
Qiu WeiDing DianShao JunHuang YuxuanChen ZehaoGuo RuimingZhao HuaxuanWu HongleFang Fuchun - Ischemia with non-obstructive coronary arteries (INOCA)/myocardial infarction with non-obstructive coronary arteries (MINOCA) affects a substantial proportion of patients undergoing coronary angiography; however, its pathophysiology remains incompletely understood, and evidence-based management remains limited. This narrative review synthesizes mechanistic, translational, and clinical evidence linking pericoronary perivascular adipose tissue (PVAT) dysfunction to coronary microvascular dysfunction (CMD) and vasomotor dysregulation in the absence of epicardial stenosis. A comprehensive literature search was conducted across PubMed/MEDLINE, Scopus, the Cochrane Library, and Google Scholar up to March 2025, encompassing preclinical studies, observational cohorts, imaging studies, and clinical trials across five thematic domains: PVAT physiology, adiponectin signaling, PVAT phenotypic transition in INOCA/MINOCA, pericoronary fat attenuation index (FAI), and endocrine-metabolic therapeutic targets. In healthy individuals, PVAT maintains coronary homeostasis through adiponectin-mediated AMP-activated protein kinase (AMPK)-endothelial nitric oxide synthase (eNOS)-nitric oxide signaling and anti-inflammatory paracrine effects. Under metabolic dysfunction, PVAT undergoes a phenotypic transition characterized by reduced adiponectin secretion and increased production of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and reactive oxygen species, thereby impairing endothelium-dependent vasodilation and promoting microvascular dysfunction. In MINOCA, distinct mechanisms including Rho-kinase activation and TNF-α-driven α1-adrenergic upregulation drive vasospasm. Pericoronary FAI has demonstrated independent prognostic value across obstructive and non-obstructive coronary disease. Therapeutic strategies including sodium-glucose cotransporter-2 (SGLT-2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and peroxisome proliferator-activated receptor gamma (PPAR-γ) agonists show mechanistic promise for PVAT remodeling, though dedicated randomized evidence in non-diabetic INOCA populations remains limited. These findings support repositioning PVAT as a therapeutic target in non-obstructive ischemic disease, pending prospective validation. - Source: PubMed
Publication date: 2026/06/29
Cisneros Clavijo Paulina ElizabethPinzón Tejada Diego FernandoDorado Ramírez John ManuelZabaleta Orozco Sergio DanielSeidlitz Arteaga Nataisha MichaellaMartínez Hernández AdolfoVimos Congacha Diego AdolfoGranados Villa Rodolfo