Monkey adiponectin,ADP ELISA Kit
- Known as:
- Monkey adiponectin,ADP Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0008MK
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Monkey adiponectin ADP ELISA Kit
Related genes to: Monkey adiponectin,ADP ELISA Kit
- Gene:
- ADIPOQ NIH gene
- Name:
- adiponectin, C1Q and collagen domain containing
- Previous symbol:
- ACDC
- Synonyms:
- ACRP30, AdipoQ, apM1, GBP28, adiponectin
- Chromosome:
- 3q27.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-26
- Date modifiied:
- 2016-10-05
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- Free fatty acid receptor 4 (FFAR4) activation modulates adipogenesis, but this pathway has not been explored in the context of perivascular adipose tissue (PVAT) dysfunction and vascular remodeling. - Source: PubMed
Publication date: 2026/09/01
Jiang AiWang TianjiaoXu XiaobingChen ZhangLi YujuanDu JiaheJiang YixuanLi Xinzhi - Leptin, secreted by adipocytes, conveys the status of peripheral energy stores to the brain to regulate appetite and metabolism. Although sympathetic activation via β3-adrenergic receptors (β3-ARs) has been shown to suppress leptin expression, it remains unclear whether this regulation arises directly within adipocytes or through other populations. Additionally, it is unclear whether β3-AR signaling contributes to the fasting-induced reduction in leptin. To address this, we generated a novel Adrb3 transcriptional block mouse () enabling global β3-AR inactivation and adipocyte-specific re- expression (; Adipoq-Cre). Global loss of Adrb3 increased plasma leptin levels, while re-expression in adipocytes normalized leptin and restored β3-AR agonist-induced leptin suppression. Analysis of Lep mRNA revealed depot specific regulation, with β3-AR signaling predominantly affecting gonadal and subcutaneous white adipose tissue, while brown adipose tissue responses were modest and variable. Despite these effects, fasting for 48 hours comparably reduced plasma leptin and Lep mRNA in both wild-type (WT) and mice, indicating that β3-AR signaling is not required for the fasting-induced decline in leptin. Collectively, these findings establish adipocyte β3-AR signaling as a key regulator that constrains leptin synthesis under basal and stimulated conditions in male mice, but not during energy deprivation. Together, these findings clarify the role of adipocyte β3-adrenergic signaling in leptin regulation and provide new insight into the sympathetic control of adipose tissue function. - Source: PubMed
Publication date: 2026/09/01
Heaselgrave Samuel RWyler Steven CThomas ShreyaTinajero ArelyGalvan MarcoMihaila EmmaFan RogerFujikawa TeppeiScherer Philipp EElmquist Joel K - Gestational diabetes mellitus (GDM) is linked to poor infant metabolic outcomes, potentially via altered human milk (HM) hormones and microRNAs. Since their specific roles remain unclear, this study synthesizes current evidence on HM adipose tissue-derived hormones (particularly adiponectin, leptin, and resistin) and microRNA modifications during gestational diabetes. Firstly, a systematic review following PRISMA 2020 guidelines was conducted (PROSPERO: CRD42024612813). Searches in major databases identified studies comparing HM adiponectin, leptin, or resistin concentrations and/or miRNA profiles between GDM and normoglycemic mothers. Secondly, bioinformatics analysis using miRWalk 3.0, functional enrichment, and network topology mapping examined miRNA interactions with , and genes. Twelve studies were included. Adiponectin showed the most consistent GDM-associated reductions, though findings were context-dependent. Leptin was primarily associated with maternal adiposity rather than GDM status. Resistin evidence was insufficient. Three miRNA studies revealed stage-dependent dysregulation in GDM, with , and linked to infant growth outcomes during the first 6 months. Bioinformatics identified and as targeting all three adipokine genes, with enrichment in glucose homeostasis and insulin resistance pathways. Network analysis highlighted , and as central nodes. GDM is associated with selective alterations in HM adipokines and miRNAs, with adiponectin and specific miRNAs showing the strongest signals. These findings support a conceptual model where GDM shapes HM's molecular composition through interacting endocrine and posttranscriptional mechanisms, potentially influencing infant metabolic programming. Larger longitudinal studies are needed to validate these observations and determine clinical relevance. - Source: PubMed
Publication date: 2026/08/31
Zhang ZhijunDavoudi MaryamGhafourian AmirrezaDehghan ParmidaAhmadi MojdeAyyoubzadeh Seyed MohammadMiao XiaoleiChoobineh HamidAfrisham Reza - Osteoporosis (OP) is often underdiagnosed, highlighting the need for tools that can both detect existing disease and predict future risk; large-scale plasma proteomics combined with explainable machine learning enables integrated diagnostic and prognostic modeling while prioritizing clinically relevant protein markers. This study aims to develop and validate an explainable plasma proteomics machine-learning framework for osteoporosis diagnosis, future risk prediction, and biomarker discovery. We further tested whether a combined marker panel could distinguish normal, prevalent OP, and future incident OP states from baseline samples. Using UK Biobank plasma proteomic data, we established SPX-OP, which separately models prevalent OP and incident OP based on Extreme Gradient Boosting (XGBoost) and SHapley Additive exPlanations (SHAP), and then evaluates whether the union of diagnostic and prognostic markers supports integrated baseline stratification. In the experiments, both the diagnostic and prognostic XGBoost models showed robust discrimination for osteoporosis status and future risk, respectively. SHAP-derived protein markers, including FSHB, ADIPOQ, SOST, COL9A1, and CHAD, were linked to osteoporosis and enriched in bone-related pathways involving bone development and remodeling, extracellular matrix organization, and inflammatory processes. Using only these SHAP-selected protein markers, the XGBoost model outperformed the full-proteome models and provided robust, simultaneous diagnostic and prognostic prediction of osteoporosis. In summary, this work transforms high-dimensional proteomic data into interpretable marker sets, paving the way for improved risk stratification and further validation of plasma protein biomarkers in osteoporosis. - Source: PubMed
Zhang WenxiangZhang WenjingCheng HanwenGong WeijieKou YuhuiJiang Baoguo - Bone marrow Adipoq-lineage cells refer to all cells that have ever expressed Adipoq (Adiponectin) and their progeny. They contribute not only to marrow adipogenesis but also to osteoclast regulation, hematopoietic support, vascular maintenance, and post-injury regeneration. Recent single-cell transcriptomic and genetic fate-mapping studies have revealed unexpected heterogeneity within this lineage, such as genuine adipogenic precursors (MALPs), bipotent adipo-osteoprogenitors (AdipoqOsx cells), and their differentiated progeny (including mature marrow adipocytes and, in some contexts, osteoblasts). The progenitor subsets partly overlap with well-characterized SSPC subsets such as CXCL12-abundant reticular cells and leptin receptor-expressing cells, yet they exhibit distinct functional properties. This review synthesizes current knowledge on the identity, differentiation potential, and multifaceted functions of bone marrow Adipoq-lineage cells, with a focus on their roles in promoting osteoclastogenesis, regulating osteogenesis, supporting hematopoiesis and vascular integrity, and mediating bone marrow repair after injury. We also discuss how these cells are regulated by intrinsic factors that either control cell-autonomous fate or modulate secretory phenotype, and highlight key unresolved questions. By integrating these findings into a unified conceptual framework, this review aims to guide future research and therapeutic development targeting these cells in skeletal and hematopoietic disorders. - Source: PubMed
Publication date: 2026/08/13
Zhang ChunyanGu XiaohuiXiang YuyanZheng ChanchanYang LeiChen Jianquan