%0 Journal Article
%T The association of the Clock 3111 T/C SNP with lipids and lipoproteins including small dense low-density lipoprotein: results from the Mima study
%A Kokoro Tsuzaki
%A Kazuhiko Kotani
%A Yoshiko Sano
%A Shinji Fujiwara
%A Kaoru Takahashi
%A Naoki Sakane
%J BMC Medical Genetics
%D 2010
%I BioMed Central
%R 10.1186/1471-2350-11-150
%X In 365 community-dwelling subjects (170 men and 195 women, mean age 63 ¡À 14 years), the 3111 T/C SNP was genotyped using a fluorescent allele-specific DNA primer assay system. The levels of sdLDL were measured with the electrophoretic separation of lipoproteins employing the Lipoprint system.The frequency of the Clock 3111 C allele was 0.14. The area of sdLDL did not differ between the subjects with obesity and those without. In carriers of T/T homozygotes, the area of sdLDL was significantly higher compared with carriers of the C allele (T/C or C/C) (1.7 ¡À 3.4 vs. 0.8 ¡À 1.9%; p < 0.05). A multiple regression analysis showed that the area of sdLDL was significantly and negatively correlated with the Clock 3111 T/C SNP (¦Â = -0.114, p < 0.05), independently of age, sex, body mass index, and exercise habits.Our findings indicated that the Clock 3111 T/C SNP might be associated with the existence of sdLDL.Sleep can be interrelated with various lifestyle and genetic factors. The sleep-wake cycle is generated through circadian rhythmicity and homeostasis [1,2]. In mammals, physiological processes show approximate 24-hour rhythms [3] derived by the clock molecules controlled not only by the master circadian clock in the suprachiasmatic nucleus (SCN) [4-6] but also by peripheral clocks in the liver, muscle, and adipose tissue [7-9]. The clock molecule groups, such as brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor output cycles protein kaput (CLOCK), also play major roles in circadian rhythmicity and regulating lipid and glucose metabolism in peripheral organs [10]. The human Clock gene located on chromosome 4q12 has a basic helix-loop-helix domains (for binding DNA). Mutant mice homozygous for Clock exibit an altered diurnal feeding rhythm, developing metabolic syndrome with hyperlipidemia [11], and a reduced amount of time spent asleep both in entrained and free-running conditions [12]. So, disruption of the circadian rhythm leads to metabolic and sle
%U http://www.biomedcentral.com/1471-2350/11/150