Aim: In a mice study, insulin suppressed apolipoprotein A-V (apoA-V) gene expression in a dose dependent manner. Thus, we investigated the association between apoA-V levels and dyslipidemias in obese children with hyperinsulinemia.
Methods: The subjects were 17 obese children (15 male, 2 female) aged 11.8 ± 2.4 years. Total cholesterol (TC), high-density lipoprotein cholesterol (HDLC), triglyceride (TG), apoA-V and insulin levels were determined.
Results: Obese children with hyperinsulinemia had greater percent overweight, higher TG level, lower HDLC level and lower apoA-V level than those without hyperinsulinemia. In simple regression analysis, apoA-V level correlated negatively with TG (r = -0.613, p = 0.0152) and insulin levels (r = -0.566, p = 0.0279), and positively correlated with HDLC (r = 0.811, p = 0.0002). In stepwise regression analysis, insulin level emerged as the independent determinant of TG level after apoA-V level was taken into account, whereas apoA-V emerged as the independent determinant of HDLC level after adjusting for insulin level.
Conclusions: Insulin may be a potent regulator of serum apoA-V level in obesity, and apoA-V level may partly contribute to the development of obesity-associated dyslipidemia.
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http://dx.doi.org/10.1016/j.orcp.2012.08.192 | DOI Listing |
medRxiv
February 2023
Division of Translational Medicine and Human Genetics, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Background: Plasma triglycerides (TGs) are causally associated with coronary artery disease and acute pancreatitis. Apolipoprotein A-V (apoA-V, gene ) is a liver-secreted protein that is carried on triglyceride-rich lipoproteins and promotes the enzymatic activity of lipoprotein lipase (LPL), thereby reducing TG levels. Little is known about apoA-V structure-function; naturally occurring human variants can provide novel insights.
View Article and Find Full Text PDFJ Atheroscler Thromb
January 2023
Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Primary hyperchylomicronemia is characterized by marked hypertriglyceridemia exceeding 1,000 mg/dL. It is caused by dysfunctional mutations in specific genes, namely those for lipoprotein lipase (LPL), glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 (GPIHBP1), apolipoprotein C2 (ApoC-II), lipase maturation factor 1 (LMF1), or apolipoprotein A5 (ApoA-V). Importantly, antibodies against LPL or GPIHBP1 have also been reported to induce autoimmune hyperchylomicronemia.
View Article and Find Full Text PDFJ Endocr Soc
February 2021
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Context: Lipodystrophy syndromes cause hypertriglyceridemia that improves with leptin treatment using metreleptin. Mechanisms causing hypertriglyceridemia and improvements after metreleptin are incompletely understood.
Objective: Determine relationship of circulating lipoprotein lipase (LPL) modulators with hypertriglyceridemia in healthy controls and in patients with lipodystrophy before and after metreleptin.
FEBS J
August 2020
Laboratory of Biochemical Neuroendocrinology, Clinical Research Institute of Montreal, QC, Canada.
The locus of the human proprotein convertase subtilisin-kexin type-7 (PC7) gene (PCSK7) is on chromosome 11q23.3 close to the gene cluster APOA5/APOA4/APOC3/APOA1, a region implicated in the regulation of lipoprotein metabolism. A GWAS reported the association of PCSK7 SNPs with plasma triglyceride (TG), and exome sequencing of African Americans revealed the association of a low-frequency coding variant of PC7 (R504H; SNP rs142953140) with a ~ 30% TG reduction.
View Article and Find Full Text PDFBiochem Biophys Res Commun
April 2019
Department of Biochemistry and Molecular Biology, University of Nevada, Reno, NV, 89557, USA. Electronic address:
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