Dongdong Zhang1, Ruiyuan Zhang2, Yu Liu3, Xizhuo Sun3, Zhaoxia Yin3, Honghui Li3, Yang Zhao2, Bingyuan Wang2, Yongcheng Ren2, Cheng Cheng2, Xuejiao Liu2, Dechen Liu2, Feiyan Liu2, Xu Chen2, Leilei Liu2, Qionggui Zhou2, Yihan Xiong4, Qihuan Xu4, Jiali Liu4, Shihao Hong4, Ziyang You4, Dongsheng Hu2, Ming Zhang5. 1. Department of Preventive Medicine, Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China; Guangdong Key Laboratory for Genome Stability & Disease Prevention, Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China; The Affiliated Luohu Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China. 2. Department of Preventive Medicine, Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China; Guangdong Key Laboratory for Genome Stability & Disease Prevention, Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China. 3. The Affiliated Luohu Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China. 4. Department of Clinical Medicine, Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China. 5. Department of Preventive Medicine, Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China; Guangdong Key Laboratory for Genome Stability & Disease Prevention, Shenzhen University Health Science Center, Shenzhen, Guangdong, People's Republic of China. Electronic address: zhangming@szu.edu.cn.
Abstract
BACKGROUND: Evidences show that cluster determinant 36 (CD36) protein plays a role in lipid metabolism and insulin resistance, and the expression of CD36 is inducible in obesity. The present study evaluated the association of CD36 variants and the interaction with obesity on type 2 diabetes mellitus (T2DM) risk. METHODS: We performed a case-control study nested in the Rural Chinese Cohort Study. We included 546 incident T2DM cases matched with non-T2DM controls in a 1:1 ratio by sex, age (within 2 years), marital status, and residence village. Four loci in CD36 (rs1194197, rs2151916, rs3211956, and rs7755) were genotyped by SNPscanTM Genotyping system. RESULTS: After adjusting for potential confounding, we observed no statistically significant association between the CD36 polymorphisms and T2DM risk. Compared to wild-type homozygous carriers with normal weight, overweight/obesity participants carrying the mutational allele rs7755 showed increased risk of T2DM, by 114% (OR = 2.14, 95% CI: 1.33-3.46; Pinteraction = 0.007); abdominal obesity participants carrying the mutational allele rs7755 showed increased risk of T2DM, by 133% (OR = 2.33, 95% CI: 1.48-3.66; Pinteraction = 0.002). Furthermore, rs2151916 polymorphism was associated with triglycerides level (P = 0.019), and the rs1194197 variant was related to systolic blood pressure (P = 0.023) within the group of controls. CONCLUSIONS: CD36 genotypes were not associated with the progression to T2DM independently. However, our results suggested a positive interaction between the CD36 variants and obesity on T2DM susceptibility, which might be through a cardiometabolic disorder.
BACKGROUND: Evidences show that cluster determinant 36 (CD36) protein plays a role in lipid metabolism and insulin resistance, and the expression of CD36 is inducible in obesity. The present study evaluated the association of CD36 variants and the interaction with obesity on type 2 diabetes mellitus (T2DM) risk. METHODS: We performed a case-control study nested in the Rural Chinese Cohort Study. We included 546 incident T2DM cases matched with non-T2DM controls in a 1:1 ratio by sex, age (within 2 years), marital status, and residence village. Four loci in CD36 (rs1194197, rs2151916, rs3211956, and rs7755) were genotyped by SNPscanTM Genotyping system. RESULTS: After adjusting for potential confounding, we observed no statistically significant association between the CD36 polymorphisms and T2DM risk. Compared to wild-type homozygous carriers with normal weight, overweight/obesityparticipants carrying the mutational allele rs7755 showed increased risk of T2DM, by 114% (OR = 2.14, 95% CI: 1.33-3.46; Pinteraction = 0.007); abdominal obesityparticipants carrying the mutational allele rs7755 showed increased risk of T2DM, by 133% (OR = 2.33, 95% CI: 1.48-3.66; Pinteraction = 0.002). Furthermore, rs2151916 polymorphism was associated with triglycerides level (P = 0.019), and the rs1194197 variant was related to systolic blood pressure (P = 0.023) within the group of controls. CONCLUSIONS:CD36 genotypes were not associated with the progression to T2DM independently. However, our results suggested a positive interaction between the CD36 variants and obesity on T2DM susceptibility, which might be through a cardiometabolic disorder.