The lipid-lowering effect of pantethine, a new drug affecting lipid metabolism, had been evaluated in carbohydrate-induced hyperlipidemic rats. Administration of the drug raised post-heparin lipolytic activities, the change being due to an increase in lipoprotein lipase activity, whereas hepatic lipase activity remained virtually unchanged. Total lipoprotein lipase activity per g of adipose tissue increased in pantethine-treated rats compared with controls. Furthermore, the soluble lipoprotein lipase of fat-pads was fractionated by heparin-Sepharose affinity chromatography. The first active peak, originated from the microsomal fractions, significantly increased after the drug treatment, while the second one, originated from the plasma membranes, remained unchanged. The increase in the microsomal lipoprotein lipase activity may be due to an increase in intracellular synthesis of lipoprotein lipase enzyme proteins. The heterogeneity of lipoprotein lipase of rat adipose tissues was ensured using affinity chromatography on heparin-Sepharose.
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http://dx.doi.org/10.1055/s-2007-1014754 | DOI Listing |
Toxicol In Vitro
January 2025
Environmental Health Science and Research Bureau (EHSRB), Health Canada, 251 Sir Frederick Banting Driveway, Ottawa, Ontario K1A 0K9, Canada; Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada. Electronic address:
Exposure to environmental pollutants with obesogenic activity is being recognised as one of the contributing factors to the obesity epidemic. Bisphenol A (BPA) has been shown to stimulate adipogenesis in both human and mouse preadipocytes, to increase body weight and affect lipid metabolism in animal and epidemiological studies. Regulatory action and public concern has prompted industry to replace BPA with other structurally similar analogues that may have similar effects.
View Article and Find Full Text PDFBBA Adv
December 2024
Gottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Skeletal muscle (SM) is essential for movement, stability, and overall body function, and it readily adapts to changes in energy demand. Myogenesis is energy-intensive and involves complex molecular and cellular events. We recently demonstrated that the absence of lysosomal acid lipase (LAL) significantly impacts the SM phenotype, primarily by disrupting energy homeostasis and reducing ATP production.
View Article and Find Full Text PDFJ Lipid Res
January 2025
Finsen Laboratory, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark; Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark. Electronic address:
Movement of lipoprotein lipase (LPL) from myocytes or adipocytes to the capillary lumen is essential for intravascular lipolysis and plasma triglyceride homeostasis-low LPL activity in the capillary lumen causes hypertriglyceridemia. The trans-endothelial transport of LPL depends on ionic interactions with GPIHBP1's intrinsically disordered N-terminal tail, which harbors two acidic clusters at positions 5-12 and 19-30. This polyanionic tail provides a molecular switch that controls LPL detachment from heparan sulfate proteoglycans (HSPGs) by competitive displacement.
View Article and Find Full Text PDFCurr Med Chem
January 2025
Cukurova University, Faculty of Medicine, Division of Endocrinology, Adana, Turkey.
Introduction: Diabetes mellitus is associated with an increased risk of atherosclerosis related to dyslipidemia. Although the terms hyperlipidemia and Diabetes Mellitus [DM] or diabetic dyslipidemia are interrelated to each other, these two conditions have some differences.
Aim: This study aimed to highlight possible mechanisms of hyperlipidemia and/or dyslipidemia in diabetic patients, which can be treated with available and newer hypolipidemic drugs.
Atheroscler Plus
March 2025
Department of Laboratory Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Background And Aims: Familial hypercholesterolemia (FH) and other disorders with similar features are common genetic disorders that remain underdiagnosed and undertreated, due in part to the cost of screening. The aim of this study was to design and implement a whole gene targeted NGS panel for the molecular diagnosis of FH and statin intolerance with an emphasis on high quality variant calling, including copy number analysis.
Methods: A whole gene panel for hybridisation-based short read NGS was designed for the dominant FH-genes low density lipoprotein receptor (), apolipoprotein B (APOB), proproteinconvertas subtilisin/kexin type 9 (PCSK9), apolipoprotein E (APOE) and the recessive FH-genes low density lipoprotein receptor adaptor protein 1 (), ATP binding cassette subfamily member 5/8 (ABCG5/8) and lipase A, lysosomal acid type (), as well as solute carrier organic anion transporter family member 1B1 (), not an FH gene but linked to statin intolerance.
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