Modifications in lipoprotein lipase levels lead to elevated triglycerides and reduced high density lipoprotein (HDL), both of which are risk factors for coronary artery disease (CAD). Hence, we examined the influence of the -93T/G, D9N, N291S, and S447X polymorphisms in the lipoprotein lipase (LPL) gene on CAD risk and lipid levels in Croatian patients with and without angiographically confirmed CAD. The N291S polymorphism was significantly associated with CAD (OR = 0.36; 95% CI = 0.13, 0.99; p = 0.048). This association was only moderately affected by adjusting for various lipids (OR = 0.36; 95% CI = 0.12, 1.08; p = 0.068). HDL2-cholesterol and apolipoprotein A-I levels were significantly higher in non-carriers of the -93T/G and D9N polymorphisms in the CAD group (p = 0.017 and 0.028, respectively). The N291S genetic variant did not show any significant difference between carriers and non-carriers in either group studied for any of the lipids. Lower triglyceride and higher HDL2-cholesterol levels in the control group were associated with carriers of the S447X mutation (p = 0.043 and 0.056, respectively). LPL gene polymorphisms might be involved in predisposition to CAD and determination of lipid profiles.
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http://dx.doi.org/10.1515/CCLM.2003.082 | DOI Listing |
J Am Heart Assoc
January 2025
Center for Non-Communicable Disease Management Beijing Children's Hospital, Capital Medical University, National Center for Children's Health Beijing China.
Background: The differential impact of serum lipids and their targets for lipid modification on cardiometabolic disease risk is debated. This study used Mendelian randomization to investigate the causal relationships and underlying mechanisms.
Methods: Genetic variants related to lipid profiles and targets for lipid modification were sourced from the Global Lipids Genetics Consortium.
J Community Hosp Intern Med Perspect
January 2025
Department of Medicine, Division of General Internal Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Acute pancreatitis is a frequent cause of hospital admission, managed with intravenous (IV) fluids, analgesia, and oral feeding when tolerated. In patients with hypertriglyceridemia-induced pancreatitis, insulin and other therapies may be necessary for disease resolution. We present a case of a patient with severe acute pancreatitis and euglycemic diabetic ketoacidosis (DKA) with known lipase maturation factor 1 (LMF1) gene mutations, which can impact insulin efficacy on triglyceride metabolism through altered lipoprotein lipase activity, successfully treated with intravenous insulin.
View Article and Find Full Text PDFSci Rep
January 2025
Division of Pancreatic Surgery, Department of General Surgery, Qilu Hospital, Shandong University, Jinan, 250012, China.
Previous studies have found that dyslipidemia is a risk factor for pancreatic cancer (PC), and that lipid-lowering drugs may reduce the risk of PC. However, it is not clear whether dyslipidemia causes PC. The Mendelian randomization (MR) study aimed to investigate the causal role of lipid traits in pancreatic cancer and to assess the potential impact of lipid-lowering drug targets on pancreatic cancer.
View Article and Find Full Text PDFLancet Neurol
February 2025
Department of Neurology, International University of Health and Welfare, Narita, Japan.
Background: Evidence from preclinical studies suggests that IL-6 signalling has the potential to modulate immunopathogenic mechanisms upstream of autoantibody effector mechanisms in patients with generalised myasthenia gravis. We aimed to assess the safety and efficacy of satralizumab, a humanised monoclonal antibody targeting the IL-6 receptor, in patients with generalised myasthenia gravis.
Methods: LUMINESCE was a randomised, double-blind, placebo-controlled, multicentre, phase 3 study at 105 sites, including hospitals and clinics, globally.
Genes (Basel)
January 2025
Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, 4288A-1151 Richmond Street North, London, ON N6A 5B7, Canada.
Biallelic rare pathogenic loss-of-function (LOF) variants in lipoprotein lipase () cause familial chylomicronemia syndrome (FCS). Heterozygosity for these same variants is associated with a highly variable plasma triglyceride (TG) phenotype ranging from normal to severe hypertriglyceridemia (HTG), with longitudinal variation in phenotype severity seen often in a given carrier. Here, we provide an updated overview of genetic variation in in the context of HTG, with a focus on disease-causing and/or disease-associated variants.
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