Objectives: Type 2 diabetic Mellitus (T2DM) is the most common systemic and endocrine disease in humans, and diabetic nephropathy is one of the most serious complications of this disorder. The polymorphisms in the apolipoprotein A5 (ApoA5) gene are strongly related to hypertriglyceridemia and are considered a predisposing factor for diabetic nephropathy. The current study proposed to examine the association of APOA5-S19W polymorphism with serum lipids levels in patients with type 2 diabetic nephropathy in Mazandaran province.
Methods: This case-control study was designed to determine the association of APOA5-S19W polymorphism with plasma lipid profile in 161 T2DM patients with nephropathy (DN+), without nephropathy (DN-), and in 58 healthy individuals. Lipid profile values were measured using Pars Azmoun commercial kits. S19W variant, one of the polymorphisms of the APOA5 gene, was determined by PCR-restriction fragment length polymorphism (PCR-RFLP) and Taq1 restriction enzyme.
Results: In comparison between the three groups, DN+ had a higher mean TG than DN- and the control group (p<0.001). The incidence of the G allele in DN+ was not significant compared to groups of DN-. Comparing the relationship between the mean of biochemical variables with CC and CG genotypes showed that the mean level of TG in people with CC genotype was increased compared to people with CG genotype in diabetic patients. However, this increase was not significant (p=0.19).
Conclusions: There was no association between SNP APOA5 S19W and serum lipids in diabetic patients with and without nephropathy.
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http://dx.doi.org/10.1515/hmbci-2022-0056 | DOI Listing |
Clin Investig Arterioscler
December 2024
Unidad de Lípidos y Riesgo Cardiovascular, Servicio de Medicina Interna, Complejo Hospitalario Universitario de A Coruña, A Coruña, España. Electronic address:
The development of massive sequencing techniques and guidelines for assessing the pathogenicity of variants are allowing us the identification of new cases of familial chylomicronemia syndrome (FCS) mostly in the LPL gene, less frequently in GPIHBP1 and APOA5, and with even fewer cases in LMF1 and APOC2. From the included studies, it can be deduced that, in cases with multifactorial chylomicronemia syndrome (MCS), both loss-of-function variants and common variants in canonical genes for FCH contribute to the manifestation of this other form of chylomicronemia. Other common and rare variants in other triglyceride metabolism genes have been identified in MCS patients, although their real impact on the development of severe hypertriglyceridemia is unknown.
View Article and Find Full Text PDFCirc J
December 2024
Institute of Epidemiology and Preventive Medicine, National Taiwan University.
Toxics
October 2024
Department of Forestry and Natural Resources, Purdue University, West Lafayette, IN 47907, USA.
Per- and polyfluoroalkyl substances (PFAS) may interact with peroxisome proliferator activated receptors (PPARs) and alter lipid homeostasis. Using , we investigated the effect of PFAS on (a) lipid homeostasis and whether this correlated to changes in body and hepatic condition; (b) the expression of hepatic genes regulated by PPAR; and (c) the hepatic lipidome. We chronically exposed tadpoles to 0.
View Article and Find Full Text PDFAm J Hum Genet
November 2024
Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Electronic address:
J Clin Lipidol
August 2024
School of Medicine, Universidad de los Andes, Bogotá, Colombia (Drs Puerto-Baracaldo, Amaya-Montoya, Nieves-Barreto, Gaete and Mendivil); Endocrinology Section, Department of Internal Medicine, Fundación Santa Fe de Bogotá, Bogotá, Colombia (Dr Mendivil). Electronic address:
Background: The genetic substrate of severe hypertriglyceridemia (sHTG) in Latin America is insufficiently understood.
Objective: To identify genetic variants in genes related to triglyceride (TG) metabolism among adults with sHTG from Colombia.
Methods: In individuals with plasma TG≥880 mg/dL at least once in their lifetime, we amplified and sequenced all exons and intron/exon boundaries of the genes LPL, APOC2, APOA5, GPIHBP1 and LMF1.
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