Gene Symbol RhesusBase Transcript ID Entrez ID Location Gene Type Gene Full Name RefSeq RNA/Protein Ensembl ID UniProt Accession InterPro Acc/Name/Signatures PubMed ID GO ID CAM ID

Gene Symbol	INSR
RhesusBase Transcript	IMMRT10011037116
Entrez ID	706009
Location	chr1:1-100000 / chr1:1+9999
Gene Type	protein-coding/tRNA
Gene Full Name	insulin receptor
RefSeq ID	NM_001032803/NP_001027975
Ensembl ID	ENSMMUG00000000001/ENSMMUT00000000001 /ENSMMUP00000000001
UniProt Accession	A0MJA5
InterPro Acc/Name/Signatures	IPR000001/Kringle/PR00545
PubMed ID	1301735
GO ID	0002001
CAM ID	CAM:0000123

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As reported in the online edition of Circulation on June 20, 2012, researchers in Institute of Molecular Medicine (IMM) at Peking University have successfully established rhesus macaque model for develop metabolic syndrome. Studying in coemergence of metabolic, cardiovascular components during metabolic syndrome, and vascular dysfunction, they suggested that all of them shared underlying mechanisms. Rhesus macaques models of metabolic syndrome should be provide a valuable platform to study the pathogenesis of metabolic syndrome in relation to cardiovascular disease and diabetes mellitus.

For details, refer to the publication:

Rhesus Macaques Develop Metabolic Syndrome with Reversible Vascular Dysfunction Responsive to Pioglitazone. Circulation (2012) doi: 10.1161/CIRCULATIONAHA.110.990333.

Xiuqin Zhang, Rongli Zhang, Susanne Raab, Wen Zheng, Jue Wang, Na Liu, Tiangang Zhu, Lifang Xue, Zhentao Song, Jiaming Mao, Kaitao Li, Huiliang Zhang, Yan Zhang, Chao Han, Yi Ding, Hui Wang, Ning Hou, Yuli Liu, Shujiang Shang, Chuanyun Li, Elena Sebokova, Heping Cheng and Paul L. Huang

Background

The metabolic syndrome (MetS) is a constellation of clinical features that include central obesity, hypertension, atherogenic dyslipidemia, and insulin resistance. However, the concept remains controversial; it has been debated whether MetS represents nothing more than simultaneous co-occurrence of individual risk factors or whether there are common shared pathophysiological mechanisms that link the individual components.

Methods and Results

To investigate the emergence of metabolic and cardiovascular components during the development of MetS, we identified MetS-predisposed animals (n=35) in a large population of rhesus macaques (Macaca mulatta, 12.7±2.9 years old, n=408), acclimated them to standardized conditions, and monitored the progression of individual component features over 18 months. In 18 MetS animals with recently developed fasting hyperinsulinemia, central obesity, hypertension, and atherogenic dyslipidemia, we found that individual metabolic and cardiovascular components track together during the transition from pre-MetS to onset of MetS; MetS was associated with a 60% impairment of flow-mediated dilation, establishing the mechanistic link with vascular dysfunction. Pioglitazone treatment (3 mg/kg body weight/d for 6 weeks), a peroxisome proliferator-activated receptor γ agonist, reversibly improved atherogenic dyslipidemia and insulin resistance and fully restored flow-mediated dilation with persistent benefits.

Conclusions

Coemergence of metabolic and cardiovascular components during MetS progression and complete normalization of vascular dysfunction with peroxisome proliferator-activated receptor γ agonists suggest shared underlying mechanisms rather than separate processes, arguing for the benefit of early intervention of MetS components. Predictive nonhuman primate (NHP) models of MetS should be highly valuable in mechanistic and translational studies on the pathogenesis of MetS in relation to cardiovascular disease and diabetes mellitus.