The Association Between the Uncoupling Protein-1 Gene A-3826G Polymorphism and High-density Lipoprotein Cholesterol in A General Japanese Population: A Consideration of the Obesity Status

Abstract

BackgroundLimited studies have shown inconsistent data about the association between the uncoupling protein 1 (UCP1) gene A-3826G polymorphism and high-density lipoprotein (HDL) cholesterol levels. The present study investigated the association between the A-3826G polymorphism and low HDL-cholesterolemia in non-obese and obese subjects.MethodsAnthropometric and biochemical factors, in addition to genotyping by an allele-specific DNA assay, were measured in 294 community-dwelling Japanese subjects (male/female: 127/167, mean age: 65 years). Obesity was defined as a body mass index (BMI) ≥ 25 kg/m2, and low HDL-cholesterolemia was defined as < 1.04 mmol/L of HDL-cholesterol.ResultsThe subjects with the G/G genotype (n = 27) showed a significantly higher prevalence of low HDL-cholesterolemia (37%) than those with the A/A + A/G genotype (13%) in the obese group (n = 102). There was a non-significant difference in the prevalence of low HDL-cholesterolemia between subjects with the G/G genotype (n = 45, 13%) and with the A/A + A/G genotype (15%) in the non-obese group (n = 192). A multivariate-adjusted logistic regression analysis of the presence of low HDL-cholesterolemia revealed that carrying the G/G genotype was an independent and significant factor positively associated with low HDL-cholesterolemia [odds ratio (OR): 6.85, 95% confidence interval (CI): 1.65-28.49] in the obese group, while carrying the G/G genotype exhibited a non-significant but reduced OR, by one-half, for low HDL-cholesterolemia (OR: 0.51, 95% CI: 0.13-1.96) in the non-obese group.ConclusionsThe obesity status could have opposing impacts on the relationship between the G/G genotype and low HDL-cholesterolemia, providing insight into the need to consider the obesity levels when studying the association between the UCP-1 gene A-3826G polymorphism and HDL-cholesterol.KeywordsObesity; Body mass index; HDL-C; Atherosclerotic risk

Effect of the beta-3 adrenergic receptor Trp64Arg and uncoupling protein 1–3826 A > G genotypes on lipid and apolipoprotein levels in overweight/obese and non-obese Chinese subjects

“…Kotani et al reported that the UCP1 -3826A > G polymorphism was associated with low HDL-cholesterolemia in obese Japanese patients [ 32 ]. In the current study we are unable to find a similar effect in overweight/obese subjects (OR = 1.296, CI = 0.743-2.261, P = 0.360), suggesting that UCP1 gene variation might not predispose overweight/obese Chinese subjects to the development of low HDL-cholesterolemia.…”

Association of the UCP-1 single nucleotide polymorphism A-3826G with the dampness-phlegm pattern among Korean stroke patients

“…Therefore, this mechanism to control blood lipids may be affected by genetic polymorphisms such as A-3826G polymorphism of UCP-1 gene [27]. This was proved by a study that showed lowered activation of sympathetic nerve and declined expression of UCP-1 in BAT of obese rats and by another in vivo study that reported overexpression of UCP-1 reduced degree of obesity induced by high fat diet.…”

Investigation of Urinary Sestrin2 in Patients with Obstructive Sleep Apnea

“…The HDL played an antioxidant role [ 38 ], and the HDL levels were positively correlated with obesity status [ 39 , 40 ]. Moreover, Sestrin2 regulated the PERK-c/EBPβ pathway by mediating mTORCI [ 41 , 42 ], and inhibited the ROS-mediated p38 MAPK activation and interfered the expression of uncoupling protein 1 (Ucp1), subsequently resulting in the decrease of heat production and the increase of adipose tissue, which led to obesity [ 43 , 44 ]. In addition, HDL was reduced in inflammatory conditions [ 45 ], while Sestrin2 could inhibit TLR-mediated inflammatory responses in macrophages [ 46 ].…”