Ask about this productRelated genes to: ADIPOR2 Blocking Peptide
- Gene:
- ADIPOR2 NIH gene
- Name:
- adiponectin receptor 2
- Previous symbol:
- -
- Synonyms:
- PAQR2, ACDCR2
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-23
- Date modifiied:
- 2018-05-03
Related products to: ADIPOR2 Blocking Peptide
Related articles to: ADIPOR2 Blocking Peptide
- Adiponectin signaling is essential for hepatic glucose homeostasis, yet the molecular basis of adiponectin receptor responsiveness remains incompletely understood. Here, we identify the Nogo-B receptor (NgBR; NUS1) as a regulator of hepatic adiponectin sensitivity. Across human, cynomolgus monkey, and mouse datasets, hepatic NgBR expression is consistently reduced in obesity-associated diabetes, indicating a conserved metabolic signature. Hepatocyte-specific NgBR deletion abolishes the metabolic effects of the adiponectin agonist AdipoRon, resulting in impaired AMPK activation, persistent gluconeogenesis, and ceramide accumulation. Mechanistically, NgBR loss suppresses KAT7 expression and reduces histone acetylation at AdipoR1 and AdipoR2 promoters, thereby limiting receptor expression. Adeno-associated virus (AAV)-mediated restoration of hepatic NgBR reinstates KAT7-dependent chromatin activation, adiponectin receptor expression, and glucose homeostasis. These findings support a hepatocellular mechanism in which NgBR maintains adiponectin receptor competence and suggest a potential therapeutic strategy for restoring adiponectin responsiveness in metabolic disease. - Source: PubMed
Publication date: 2026/05/22
Mohiuddin Mohammad SarifTirumalasetty Munichandra BabuHu WenquanBarua RashuWahiduzzaman MdChoubey MayankSchwartz Gary JMiao Qing Robert - Periodontitis is a chronic inflammatory disease which is initiated by dysbiotic biofilms and maintained by a host who is permissive to inflammation resulting in continuous destruction of periodontal supporting structures. Periodontitis occurs frequently with obesity and type 2 diabetes mellitus and the broader cardiometabolic risk state leading to investigations into the common immunometabolic pathways that link these conditions. Adiponectin, an insulin sensitizing and anti-inflammatory adipokine which can also act as a vasculoprotective and bone-related factor, has been studied as a potential modulator of the relation between periodontal inflammation and systemic metabolic disturbance. This narrative review summarizes the biology of adiponectin and its receptors, human findings relating to both the local and circulating forms of adiponectin in periodontal health and disease, the mechanism in cell and animal models and translational implications and limitations. The literature was reviewed in a narrative manner with particular attention to study quality, compartment-specific biology and any conflicts in evidence and the difference between biological plausibility and clinical relevance. A tendency for a reduction in the circulating, saliva and gingival crevicular fluid levels of adiponectin in periodontitis in human studies, particularly those with co-existing obesity and type 2 diabetes mellitus, can be demonstrated but these finding are often disparate due to variable methods in case definitions, assay techniques, metabolic background of subjects and other confounders. Experimental findings may establish biological plausibility by linking adiponectin signalling with the mechanisms which affect inflammatory responses, endothelial function and matrix homeostasis, osteoclastogenesis and subsequent alveolar bone loss, although adiponectin signalling appears context-specific in its actions and this does not confirm clinical relevance. Evidence suggests adiponectin is a biologically significant, but context-dependent factor within the immunometabolic network which connects periodontal disease with the systemic condition, rather than a sole marker or clinically recognized target for therapeutic intervention. - Source: PubMed
Publication date: 2026/05/08
Mochol MartynaDura WłodzimierzLodigkeit MaikeAndrzejewski PiotrLipski MariuszMazurek-Mochol Małgorzata - Disruptions in structure-function coupling (SFC) in major depressive disorder (MDD) have been reported. Given the brain functional dynamics over time, whether/how dynamic SFC changes in MDD and its associated molecular signatures is still elusive. Here, we integrate multimodal neuroimaging, neurotransmitter density maps, transcriptome, and plasma proteome to investigate the biological correlates of abnormal dynamic SFC in MDD. Using resting-state functional and structural connectivity data of 21,030 individuals (19,107 healthy controls and 1923 MDD patients) from UK Biobank, we identified a robust reductions of dynamic SFC in cortical regions primarily localized in the somatomotor and dorsal attention networks. Spatial association analyses further showed associations between these alterations and the neurotransmitters of norepinephrine, GABA and histamine, the genes regulating neurodevelopment and energy metabolism, the cell types of oligodendrocyte and astrocyte, and the neuropeptide of MCHR1 and ADIPOR2. Moreover, we found that the immune- and inflammation-related proteins were associated with regional abnormal dynamic SFC, which showed overlap with known drug targets, suggesting potential therapeutic relevance. In summary, our research provides evidence for abnormal dynamic SFC in MDD and identifies associated multimodal molecular signatures, highlighting the importance of dynamic structure-function relationships in MDD-related brain dysfunction and contributing to a better understanding of its neurobiological basis. - Source: PubMed
Publication date: 2026/05/16
Zhang JiangLi JiananSun HuiLi WeiChen JinZhang HengShang WeiWang LiboWu ZheWang Jiaojian - 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 - Major depressive disorder (MDD) is a disabling psychiatric disease featuring altered adiponectin signaling, evidenced by changes in peripheral adiponectin levels and receptor activation-both potentially predictive of treatment response. While adiponectin's therapeutic role in MDD is established, specific molecular mechanisms, particularly relating to neuroinflammation, remain unclear. - Source: PubMed
Publication date: 2026/04/27
Chang JinlongZhu WenhuiLi TianxiangCui DanXie HaierZhu ZiLi Weifen