Original Data

Rev Diabet Stud, 2017, 14(2-3):311-328 DOI 10.1900/RDS.2017.14.311

Variations in ADIPOR1 But Not ADIPOR2 are Associated With Hypertriglyceridemia and Diabetes in an Admixed Latin American Population

Gustavo Gustavo Mora-García1, María S. Ruiz-Díaz1, Fabian Espitia-Almeida2, Doris Gómez-Camargo1

1Doctorate in Tropical Medicine, Faculty of Medicine, Universidad de Cartagena. Cartagena de Indias, Colombia
2Biochemistry Master Program, Faculty of Medicine, Universidad de Cartagena. Cartagena de Indias, Colombia
Address correspondence to: Gustavo Mora-García, e-mail: gmorag@unicartagena.edu.co

Manuscript submitted May 3, 2017; resubmitted July 17, 2017; accepted August 29, 2017.

Keywords: diabetes mellitus, adiponectin, adiponectin receptor, ADIPOR1, ADIPOR2, hypertriglyceridemia, genetic association study

Abstract

BACKGROUND: Adiponectin is a hormone secreted by adipose tissue. It regulates glycolysis and lipolysis and is involved in the pathophysiology of diabetes and related disorders. Its activity is mainly mediated by the transmembrane receptors AdipoR1 and AdipoR2, which are encoded by ADIPOR1 (1q32.1) and ADIPOR2 (12p13.33) genes, respectively. In genetic association studies, single nucleotide polymorphisms (SNPs) in or near these genes have been associated with metabolic alterations. However, these relationships are still controversial. AIM: The aim of this work was to analyze possible associations between ADIPOR1/2 and diabetes and other metabolic disorders. METHODS: A genetic association study was carried out in an admixed Latin American population. A sample of 200 adults was analyzed. Clinical and serum-biochemical characteristics were measured to diagnose obesity, abdominal obesity, hypertension, hyperglycemia, hypertriglyceridemia, low HDLc, insulin resistance (HOMA-IR), and diabetes. Three SNPs were genotyped in ADIPOR1 (rs10494839, rs12733285, and rs2275737) and ADIPOR2 (rs11061937, rs11612383, and rs2286383). For the association analysis, an additive model was assessed through logistic regression. An admixture adjustment was performed using a Monte-Carlo-Markov-Chain method, assuming a three-hybrid substructure (k = 3). RESULTS: Two SNPs in ADIPOR1 were associated with diabetes: rs10494839 (OR = 3.88, adjusted p < 0.03) and rs12733285 (OR = 4.72, adjusted p < 0.03). Additionally, rs10494839 was associated with hypertriglyceridemia (OR = 2.16, adjusted p < 0.01). None of the SNPs in ADIPOR2 were associated with metabolic disorders. CONCLUSIONS: ADIPOR1 was consistently associated with diabetes and hypertriglyceridemia. This association was maintained even after adjusting for genetic stratification. There were no significant associations involving ADIPOR2.

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