Single nucleotide polymorphisms in CIDEC gene are associated with metabolic syndrome components risks and antihypertensive drug efficacy

Abstract

The association of single nucleotide polymorphisms rs1053239 and rs2479 of cell death-inducing DFFA-like effector c with the risk of metabolic syndrome and its components, and with the efficacy and cost-effectiveness of antihypertensive drugs was investigated. Totally 1064 subjects with metabolic syndrome and 1099 controls of Chinese Han nationality were recruited. Clinical assessment was conducted with medication records collected at baseline and during 5-year follow-up. Carriers of rs2479 A allele were at higher risk to develop elevated fasting glucose than non-carriers (P = 0.004). A allele at rs2479 were associated with a 5-year aggravation of blood triglyceride (P < 0.001) and diastolic blood pressure (P = 0.003), and C allele at rs1053239 with the exacerbation of systolic (P < 0.001) and diastolic blood pressure (P = 0.001). Moreover, efficacy and cost-effectiveness of angiotensin II-targeted drugs were higher in subjects with rs2479 A allele or rs1053239 C allele. These findings suggest that carriers of rs2479 A allele are predisposed to the development of increased fasting glucose, and the progressive elevation of blood triglyceride. Individuals with A allele at rs2479 or C allele at rs1053239 are more susceptible to a rapid progression of blood pressure, and benefit more from angiotensin II-targeted therapy.

Therapeutic silencing of FSP27 reduces the progression of atherosclerosis in Ldlr–/– mice

“…Our data in previous reports [11,12,20] and herein suggest that hepatic FSP27 activity promotes VLDL-TAG secretion. Importantly, two SNPs in CIDEC are associated to elevated fasting triglyceridemia [32]. We hypothesize that the large reduction in circulating VLDL-TAG in ASO-Fsp27-treated mice is, at least in part, a driver for the atheroprotective phenotype in our study by limiting the availability of remnant particles.…”

CIDEC silencing attenuates diabetic nephropathy via inhibiting apoptosis and promoting autophagy

“…A previous study has shown CIDEC inhibits the expression of ATGL at the transcriptional level by stimulating EGR1, the inhibitory factor for ATGL transcription 16 . CIDEC also inhibits lipid decomposition by preventing the expression, activation and localization of ATGL 27 . The activity of ATGL promoter can be inhibited dose‐dependently by CIDEC in vitro and this ATGL promoter domain contains the combinding region of transcription factor EGR1, which directly combines to the ATGL promoter and prevents its activity 16 .…”

A prognostic score model based on eight metabolism-associated genes predicts the survival of adult females with lung adenocarcinoma

“…CIDEC, a member of the cell death-inducing DNA fragmentation factor-like effector family, could promote lipid droplet formation in adipocytes and mediate adipocyte apoptosis (31). It was reported that the CIDE family regulated lipid metabolism and played an important role in the development of metabolic disorders such as obesity (32), insulin resistance (33) and hepatic steatosis(34)Ming Yu et alAccording to HPA database, CIDEC was a characteristic gene in lung cancer and other cancers. A four-gene signature (involving CIDEC; dickkopf WNT signaling pathway inhibitor 1, DKK1; ubiquitin speci c peptidase 4, USP4; and ZFP3 zinc nger protein, ZFP3) is an independent prognostic marker, which can be used to predict the outcomes of LUAD patients (35).…”