Chicken ADIPOR1 (Adiponectin Receptor 1) ELISA Kit
- Known as:
- Chicken ADIPOR1 (Adiponectin Receptor 1) Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E-EL-Ch0462
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- Elabscience
- Gene target:
- Chicken ADIPOR1 (Adiponectin Receptor 1) ELISA Kit
Related genes to: Chicken ADIPOR1 (Adiponectin Receptor 1) 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: Chicken ADIPOR1 (Adiponectin Receptor 1) ELISA Kit
Related articles to: Chicken ADIPOR1 (Adiponectin Receptor 1) ELISA Kit
- Type 2 diabetes mellitus is characterized by chronic hyperglycemia and impaired glucose homeostasis. This study evaluated the anti-diabetic effects of B-3 using models and db/db mice. B-3 inhibited α-amylase activity and enhanced insulin-stimulated glucose uptake in palmitic acid-induced insulin-resistant C2C12 myotubes. Metabolite profiling also showed distinct strain-associated metabolic characteristics of B-3. In db/db mice, oral administration of B-3 significantly reduced fasting blood glucose levels and improved oral glucose tolerance without affecting body weight. These effects were accompanied by changes in incretin-related endocrine responses, including increased serum GLP-1 levels and decreased DPP-4 activity. B-3 also increased serum insulin and C-peptide levels and partially preserved pancreatic insulin immunoreactivity. In addition, mild diabetes-associated intestinal morphological alterations and glucose-regulatory marker expression were partially normalized after administration. In skeletal muscle, B-3 was associated with increased expression of glucose uptake- and metabolic signaling-related markers, including AKT/GLUT4 and ADIPOR1/AMPK pathways. Overall, these findings suggest that B-3 improves glycemic control in db/db mice in association with changes in incretin-related endocrine responses and glucose-regulatory signaling markers. - Source: PubMed
Publication date: 2026/08/18
Cho SungminJeong YewonKim Jae-HoonGwon YuriShin HakdongLim WonchulLim Tae-Gyu - Colorectal cancer (CRC) remains one of the most prevalent and lethal malignancies worldwide. Adiponectin, a hormone secreted by adipose tissue, has been increasingly recognized for its pleiotropic effects in several malignancies. In particular, an inverse association between circulating adiponectin levels and CRC incidence supports a potential protective role for adiponectin and its receptors (AdipoR1, AdipoR2). The aim of this study was to investigate the effects of adiponectin on Caco-2 cells, a human CRC cell line, by examining intestinal epithelial differentiation using AdipoRon (AR), a synthetic adiponectin receptor agonist. The effects of AR on Caco-2 cells were assessed by evaluating dome formation and the expression of key molecular markers involved in intestinal epithelial differentiation, including KLF-4, DPPIV, SI, and KRT20, at both transcriptional levels using qRT-PCR and at protein levels using immunofluorescence and Western blot analysis. In addition, mitochondrial reactive oxygen species (ROS) production was assessed using MitoSOX™ Red. Our findings showed that AR administration was associated with a dose-dependent increase in AdipoR1 and AdipoR2 expression as well as with dome formation in Caco-2 cells. Furthermore, AR administration reduced Ki-67 expression with no changes in cell cycle and an increase in the differentiation markers DPPIV and SI, while KRT20 remained unchanged. Finally, AR decreased mitochondrial ROS levels during differentiation. Our findings provide new evidence that AR contributes to intestinal epithelial differentiation and may represent a potential therapy for colorectal cancer. AdipoRon may contribute to the regulation of intestinal epithelial differentiation and may contribute to restoring epithelial homeostasis in tumor cells. Further research is needed to clarify the underlying mechanisms and assess the translational relevance of adiponectin-based therapies. - Source: PubMed
Publication date: 2026/07/28
Mallardo MartaMemon FurqanD'Auria LudovicaPagliaro RaffaellaDaniele AuroraNigro Ersilia - Nutritional status and adipose tissue-derived mediators have been implicated in the development and clinical characteristics of epithelial ovarian carcinoma; however, studies integrating circulating adipokines, adipokine receptor expression, and nutritional status remain limited. This study aimed to evaluate circulating adipokine concentrations, adipokine receptor expression, nutritional status parameters, and their associations with clinically relevant features and disease stage in women with epithelial ovarian carcinoma. - Source: PubMed
Publication date: 2026/08/21
Aguilar-Vazquez Lizeth MontserratEspinoza-de-León Gabriela NohemiAlemán-Montes Ricardo MisaelMorales-Soto Diego AlbertoLopez-Lopez Jose RamonGonzález-Amézquita BenjamínVillegas-Pacheco RaquelAlcaraz-Wong Aldo AntonioLlamas-Covarrubias Iris MonserratMartínez-López ErikaAguilar-Lemarroy AdrianaJave-Suárez Luis Felipe - Skeletal muscle atrophy is a hallmark of ageing and chronic diseases, yet effective pharmacotherapies remain unavailable. Adiponectin signalling through AdipoR1 and AdipoR2 regulates skeletal muscle metabolism, regeneration and oxidative capacity, but the therapeutic use of adiponectin is limited by its large size and complex multimeric structure. Small-molecule AdipoR agonists, therefore, represent an attractive therapeutic strategy. - Source: PubMed
Das ShubhrajyotiAwasthi PallaviMoin Md RameezPal ShyamalTalukdar AnushkaKumar AkhileshNikolas NikhilVarode Shruti SuhasKhatoon ShamimaDas NabanitaChattopadhyay SouravMugale Madhav NilkanthGuha RajdeepSanyal SabyasachiGoel Atul - 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