Last update 01 Nov 2024

ADIPOR2

Last update 01 Nov 2024

Basic Info

Synonyms

ACDCR2, adiponectin receptor 2, Adiponectin receptor protein 2

+ [4]

Introduction

Receptor for ADIPOQ, an essential hormone secreted by adipocytes that regulates glucose and lipid metabolism (PubMed:12802337, PubMed:25855295). Required for normal body fat and glucose homeostasis. ADIPOQ-binding activates a signaling cascade that leads to increased PPARA activity, and ultimately to increased fatty acid oxidation and glucose uptake. Has intermediate affinity for globular and full-length adiponectin. Required for normal revascularization after chronic ischemia caused by severing of blood vessels (By similarity).

Drugs associated with ADIPOR2

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

AdipoRaMab(Mitsubishi Tanabe Pharma)

Target

ADIPOR1 x ADIPOR2

Mechanism

ADIPOR1 agonists [+1]

Active Org.

Mitsubishi Tanabe Pharma Corp.

Originator Org.

Mitsubishi Tanabe Pharma Corp.

Active Indication

Diabetes Mellitus, Type 2 [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with ADIPOR2

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.

100 Clinical Results associated with ADIPOR2

100 Translational Medicine associated with ADIPOR2

0 Patents (Medical) associated with ADIPOR2

972

Literatures (Medical) associated with ADIPOR2

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.

15 Oct 2024·The FASEB Journal

Trophoblast‐specific overexpression of adiponectin receptor 2 causes fetal growth restriction in pregnant mice

Article

Author: Barentsen, Kenneth ; Urschitz, Johann ; Jansson, Thomas ; Rosario, Fredrick J. ; Powell, Theresa L. ; Dumolt, Jerad H.

AbstractMaternal obesity in pregnancy is strongly associated with complications such as fetal overgrowth and infants of obese mothers have an increased risk to develop obesity, diabetes, and cardiovascular disease later in life. However, the underlying mechanisms are not well established. Circulating levels of adiponectin are low in obese pregnant women and maternal circulating adiponectin is negatively associated with birth weight. We have reported that normalizing maternal adiponectin in obese pregnant mice prevents placental dysfunction, fetal overgrowth, and programming of offspring cardio‐metabolic disease. However, the mechanistic link between maternal adiponectin, placental function, and fetal growth remains to be established. We hypothesized that trophoblast‐specific overexpression of the adiponectin receptor 2 (Adipor2) in healthy pregnant mice inhibits placental mTORC1 signaling and nutrient transport, resulting in fetal growth restriction. Using lentiviral transduction of blastocysts with a mammalian gene expression lentiviral vector for up‐regulation of Adipor2 (Adipor2‐OX), we achieved a ~ 3‐fold increase in placenta Adipor2 mRNA levels and a 2‐fold increase of the ADIPOR2 protein in the trophoblast plasma membrane. Placenta‐specific Adipor2‐OX increased placental peroxisome proliferator‐activated receptor‐α phosphorylation, ceramide synthase expression and ceramide concentrations. Furthermore, Adipor2‐OX inhibited placental mTORC1 signaling and reduced in vivo placental transport of glucose and amino acids. Lastly, Adipor2‐OX reduced fetal weight by 11%. These data provide mechanistic evidence that placental Adipor2 signaling directly affects fetal growth. We propose that low circulating adiponectin in maternal obesity causes fetal overgrowth and programs the offspring for cardio‐metabolic disease mediated by a direct effect on placental function.

01 Oct 2024·Molecular and Cellular Endocrinology

Reduced hepatic AdipoR2 by increased glucocorticoid mediates effect of psychosocial stress to elevate serum cholesterol

Article

Author: Wang, Jin Hua ; Zhang, Ji Cheng ; Fang, Ding Zhi ; Tang, Hui ; Zheng, Yan Jiang ; Chen, Xu ; Shen, Yi Lin ; Su, Guo Ming ; Su, Mi ; Guo, Qi Wei ; Lin, Jia ; Li, Zheng Ke

Understanding the effects of psychosocial stress on serum cholesterol may offer valuable insights into the relationship between psychological disorders and endocrine diseases. However, these effects and their underlying mechanisms have not been elucidated yet. Here we show that serum corticosterone, total cholesterol and low-density lipoprotein cholesterol (LDL-C) are elevated in a mouse model of psychosocial stress. Furthermore, alterations occur in AdipoR2-mediated AMPK and PPARα signaling pathways in liver, accompanied by a decrease in LDL-C clearance and an increase in cholesterol synthesis. These changes are further verified in wild-type and AdipoR2 overexpression HepG2 cells incubated with cortisol and AdipoR agonist, and are finally confirmed by treating wild-type and hepatic-specific AdipoR2 overexpression mice with corticosterone. We conclude that increased glucocorticoid mediates the effects of psychosocial stress to elevate serum cholesterol by inhibiting AdipoR2-mediated AMPK and PPARα signaling to decrease LDL-C clearance and increase cholesterol synthesis in liver.

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ADIPOR2

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