Last update 01 Nov 2024

ADIPOR1

Last update 01 Nov 2024

Basic Info

Synonyms

ACDCR1, adiponectin receptor 1, Adiponectin receptor protein 1

+ [5]

Introduction

Receptor for ADIPOQ, an essential hormone secreted by adipocytes that regulates glucose and lipid metabolism (PubMed:25855295, PubMed:12802337). Required for normal glucose and fat homeostasis and for maintaining a normal body weight. ADIPOQ-binding activates a signaling cascade that leads to increased AMPK activity, and ultimately to increased fatty acid oxidation, increased glucose uptake and decreased gluconeogenesis. Has high affinity for globular adiponectin and low affinity for full-length adiponectin (By similarity).

Drugs associated with ADIPOR1

BHD-1028

Target

ADIPOR1 x ADIPOR2

Mechanism

ADIPOR1 agonists [+1]

Active Org.

EncuraGen Co., Ltd.

Originator Org.

EncuraGen Co., Ltd.

Active Indication

Insulin Resistance [+4]

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AdipoRon

Target

ADIPOR1 x ADIPOR2

Mechanism

ADIPOR1 agonists [+1]

Active Org.

University of Tokyo

Originator Org.

University of Tokyo

Active Indication

Diabetes Mellitus, Type 2 [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Arctigenin

Target

ADIPOR1 x PP2A

Mechanism

ADIPOR1 agonists [+2]

Active Org.

Icahn School of Medicine at Mount Sinai [+2]

Originator Org.

Kracie Ltd.

Active Indication

Diabetic Nephropathies [+2]

Inactive Indication

Pancreatic Cancer

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with ADIPOR1

NCT06563115 / CompletedPhase 1

A Randomized, Double-Blinded, Placebo-Controlled, Single and Multiple Ascending Dose Study in Overweight/Obese Subjects to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of (PEG)-BHD1028

Adiponectin has been known to play critical roles in various physio-regulatory processes, and adiponectin deficiency may contribute to insulin resistance. (PEG)-BHD1028 was developed as an agonist of adiponectin receptors.
This first-in-human study evaluates the safety, tolerability, pharmacokinetics, and pharmacodynamics of (PEG)-BHD1028 in healthy overweight/obese subjects with insulin resistance.

Start Date18 Apr 2022

Sponsor / Collaborator

EncuraGen Co., Ltd.

JPRN-UMIN000050011 / CompletedPhase 2IIT

Efficacy and safety of HMB/Gln/Arg for the prophylaxis of chemoradiation -induced mucositis in head and neck squamous cell carcinoma: Randomized Phase II Clinical Study - Efficacy and safety of HMB/Gln/Arg for the prophylaxis of chemoradiation -induced mucositis in head and neck squamous cell carcinoma: Randomized Phase II Clinical Study

Start Date01 Mar 2018

Sponsor / Collaborator-

JPRN-UMIN000010111 / CompletedPhase 2IIT

Phase 2a trial of GBS-01 for advanced pancreatic cancer refractory to gemcitabine and fluoropyrimidine chemotherapy. - GBS-01 Phase IIa

Start Date11 Mar 2013

Sponsor / Collaborator

National Cancer Center Hospital East

[+1]

100 Clinical Results associated with ADIPOR1

100 Translational Medicine associated with ADIPOR1

0 Patents (Medical) associated with ADIPOR1

1,288

Literatures (Medical) associated with ADIPOR1

01 Jan 2025·Gene

Association of adiponectin gene single nucleotide polymorphisms with environmental risk factors in type 2 diabetes mellitus: An updated evidence of haplotype-based analysis study

Article

Author: Siahkouhian, Marefat ; Ramezanzade, Raziye ; Mamashli, Elahe ; Davarnia, Behzad ; Jaspers, Richard T ; Iranparvar, Manouchehr ; Goulding, Richie P ; Skishahr, Farnaz Seifi

BACKGROUND AND AIMAdiponectin (ADIPOQ) gene is considered to be one of the promising players in deciphering the genetic bases of type 2 diabetes. This study investigated the associations between haplotype combinations of three single nucleotide polymorphisms (SNPs) of the ADIPOQ gene and two SNPs of the adiponectin receptor 1 (AdipoR1) and 2 (AdipoR2) genes with environmental risk factors for the prediction of T2DM disorder susceptibility in the Iranian population.METHODSThis case-control and cross-sectional study was conducted on 182 patients with T2DM and 155 healthy controls. Genotyping was performed using amplification refractory mutation system-PCR (ARMS-PCR) for rs17300539G/A, rs2241766T/G, and rs1501299G/T of the ADIPOQ gene, rs1342387C/T of the AdipoR1 gene, and rs10773989T/C of the AdipoR2 gene.RESULTSAll polymorphisms met the Hardy-Weinberg equilibrium (p> 0.05). The studied SNPs; rs17300539, rs2241766 of the ADIPOQ gene and rs10773989 of the AdipoR2 gene, were significantly associated with an increased risk of T2DM. Two-way ANOVA analysis indicated that GG carriers of rs2241766T/G had a significantly lower waist-to-hip ratio (P= 0.049) and body mass index (P= 0.011) and higher HbA1c (P= 0.048) compared to TT carriers, while TT genotype carriers of rs2241766T/G showed the higher plasma adiponectin concentration compared to TG and GG carriers (P= 0.009 and P= 0.013, respectively). CC carriers of rs10773989T/C displayed a significantly higher LDL level compared to the TT genotype carries (P= 0.036). Also plasma adiponectin concentrations were significantly lower in AA genotype carriers of rs17300539G/A compared to GG and GA genotypes carriers in the control group only (P= 0.005 and P= 0.016, respectively). According to Combined Haplotype ([rs17300539, rs2241766, rs1501299]/[rs17300539, rs2241766, rs1501299]) analysis, GTT-homozygote carriers displayed the highest plasma adiponectin concentration and in contrast, GGG/GTG, ATG/GTG, and GGG/GGG showed the lowest plasma adiponectin concentration in the controls (p> 0.05).CONCLUSIONThe adiponectin gene haplotype combinations were associated with plasma adiponectin concentration in healthy individuals. In T2DM, adiponectin genetic variants displayed less effect on adiponectin plasma concentration.

01 Jan 2025·Journal of Ethnopharmacology

Integration of network pharmacology, UHPLC-Q exactive orbitrap HRMS technique and metabolomics to elucidate the active ingredients and mechanisms of compound danshen pills in treating hypercholesterolemic rats

Article

Author: Guo, Zhuoqian ; Xu, Bing ; Dai, Ziqi ; Cheng, Xuehao ; Xiong, Xiaomin ; Cheng, Sijin ; Li, Shanlan ; Zhang, Tong ; An, Jin ; Chen, Guangyun ; Wang, Nan ; Zhang, Zixuan ; Jiang, Guanghui ; Lei, Haimin

ETHNOPHARMACOLOGICAL RELEVANCEHypercholesterolemia (HLC) was a key risk factor for cardiovascular disease (CVD) characterized by elevated cholesterol levels, particularly LDL. While traditional Chinese medicine preparations Compound Danshen Pills(CDP) has been clinically used for hypercholesterolemia and coronary heart disease, its specific therapeutic effect on HLC remains understudied, necessitating further investigation into its mechanisms.AIM OF THE STUDYThe aim of this study was to explore the potential of CDP in treating HLC and elucidate its underlying mechanisms and active components.MATERIALS AND METHODSA hypercholesterolemic lipemia rat model induced by a high-fat diet was employed. Network pharmacology combined with UHPLC-Q exactive orbitrap HRMS technique was used to predict the active components, targets and mechanisms of CDP for HLC. Histological analysis and serum biochemical assays were used to assess the therapeutic effect of CDP and its main active ingredient Sa B on hypercholesterolemic lipemia rat model. Immunofluorescence assays and western blotting were used to verify the mechanism of CDP and Sa B in the treatment of HLC. Metabolomics approach was used to demonstrate that CDP and Sa B affected the metabolic profile of HLC.RESULTSOur findings demonstrated that both CDP and its main active ingredient Sa B significantly ameliorated hypercholesterolemic lipemic lesions, reducing levels of TC, LDL, AST, ALT, and ALP. Histological analysis revealed a decrease in lipid droplet accumulation and collagen fiber deposition in the liver, as well as reduced collagen fiber deposition in the aorta. Network pharmacology predicted potential targets such as PPARα and CYP27A1. Immunofluorescence assays and western blotting confirmed that CDP and Sa B upregulated the expression of Adipor1, PPARα and CYP27A1. Metabolomics analyses further indicated improvements in ABC transporters metabolic pathways, with differential metabolites such as riboflavin, taurine, and choline showed regression in levels after CDP treatment and riboflavin, L-Threonine, Thiamine, L-Leucine, and Adenosine showed improved expression after Sa B treatment.CONCLUSIONCDP and Sa B have been shown to alleviate high-fat diet-induced hypercholesterolemia by activating the PPAR pathway and improving hepatic lipid metabolism. Our study demonstrated, for the first time, the complex mechanism of CDP, Sa B in the treatment of hypercholesterolemia at the protein and metabolic levels and provided a new reference that could elucidate the pharmacological effects of traditional Chinese medicine on hypercholesterolemia from multiple perspectives.

01 Nov 2024·Biomedicine & Pharmacotherapy

6-Gingerol improves lipid metabolism disorders in skeletal muscle by regulating AdipoR1/AMPK signaling pathway

Article

Author: Peng, Ze ; Zeng, Yan ; Zeng, Xin ; He, Qifeng ; Wang, Jianwei ; Wang, Shang ; Tan, Qi

BACKGROUNDTo delve into the precise mechanisms by which 6-gingerol ameliorates lipid metabolism disorders in skeletal muscle.METHODSThe level of triglycerides (TG) was used to evaluate lipid deposition. In skeletal muscle, transmission electron microscopy (TEM) was employed to observe mitochondrial morphology. Additionally, PCR was applied to detect mitochondrial biogenesis, and levels of malondialdehyde (MDA), catalase (CAT), glutathione, r-glutamyl cysteingl+glycine (GSH) and nicotinamide adenine dinucleotide (NADH) were measured to assess mitochondrial oxidative stress levels. In vivo, flow cytometry and immunofluorescence assays were conducted to quantify reactive oxygen species (ROS) and mitochondrial membrane potential (MMP). Furthermore, the Seahorse XF assays was utilized to assess mitochondrial respiratory capacity. Fluorescence confocal microscopy and molecular docking were applied to analyze the binding of 6-gingerol and adiponectin receptor 1 (AdipoR1). The expression of AdipoR1, AMPK, PGC-1α and SIRT1 were detected by Western Blot.RESULTSIn vivo, 6-gingerol could reduce body weight in mice induced by a high-fat diet, enhance metabolic profiles in plasma, decrease lipid accumulation in skeletal muscle and liver, and elevate adiponectin levels. In skeletal muscle, it could restore mitochondrial morphology, boost mitochondrial copy number and biogenesis, and mitigate oxidative stress. In vitro, 6-gingerol may directly interact with AdipoR1 to upregulate the expression of downstream proteins p-AMPK, SIRT1, and PGC-1α, leading to a reduction in lipid deposition, a decrease in ROS production, an increase in mitochondrial membrane potential, and an enhancement of mitochondrial respiratory capacity in C2C12 myotubes.CONCLUSION6-Gingerol ameliorated lipid metabolism in skeletal muscle by regulating the AdipoR1/AMPK signaling pathway.

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ADIPOR1

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