Rat Adiponectin Receptor 1,ADIPOR1 ELISA Kit
- Known as:
- Rat Adiponectin Receptor 1,ADIPOR1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- dl-adipor1-ra
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Wuxi donglin
- Gene target:
- Rat Adiponectin Receptor 1 ADIPOR1 ELISA Kit
Related genes to: Rat Adiponectin Receptor 1,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: Rat Adiponectin Receptor 1,ADIPOR1 ELISA Kit
Related articles to: Rat Adiponectin Receptor 1,ADIPOR1 ELISA Kit
- Fibromyalgia (FM) is a difficult-to-cure disease, and finding effective pain management methods is crucial for providing clinicians and healthcare. Adiponectin (ADP) is considered a peripheral metabolic hormone, but its role in the central nervous system remains unknown, especially in pain management. Electroacupuncture (EA) has long been scientifically proven as an effective therapy for pain relief. - Source: PubMed
Liao Hsien-YinChae YounbyoungHo Chien-YiHsiao I-HanLin Ming-ChiaWang Yu-ChingLin Yi-Wen - Insulin resistance has been independently associated with cardiac diseases. Free fatty acids (FFAs) are known to induce cardiac insulin resistance via low-grade inflammation. Therefore, lowering FFA levels may improve cardiac insulin resistance. This study investigated the effects of a combination of green tea and decaffeinated light-roasted green coffee extract on free fatty acid-induced cardiac insulin resistance by modulating the adiponectin/FAS pathways. - Source: PubMed
Publication date: 2026/07/03
Lukitasari MifetikaRohman Mohammad SaifurNugroho Dwi AdiNur Kholis MukhamadWahyuni Nila AisyahWidodo Nashi - 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
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