In the yeast Saccharomyces cerevisiae, the molecular species profile of the major membrane glycerophospholipid phosphatidylcholine (PC) is determined by the molecular species-selectivity of the biosynthesis routes and by acyl chain remodeling. Overexpression of the glycerol-3-phosphate acyltransferase Sct1p was recently shown to induce a strong increase in the cellular content of palmitate (C16:0). Using stable isotope labeling and mass spectrometry, the present study shows that wild type yeast overexpressing Sct1p incorporates excess C16:0 into PC via the methylation of PE, the CDP-choline route, and post-synthetic acyl chain remodeling. Overexpression of Sct1p increased the extent of remodeling of PE-derived PC, providing a novel tool to perform mechanistic studies on PC acyl chain exchange. The exchange of acyl chains occurred at both the sn-1 and sn-2 positions of the glycerol backbone of PC, and required the phospholipase B Plb1p for optimal efficiency. Sct1p-catalyzed acyl chain exchange, the acyl-CoA binding protein Acb1p, the Plb1p homologue Plb2p, and the glycerophospholipid:triacylglycerol transacylase Lro1p were not required for PC remodeling. The results indicate that PC serves as a buffer for excess cellular C16:0.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.bbalip.2013.03.002 | DOI Listing |
Front Biosci (Landmark Ed)
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University of Hospital Würzburg, 97080 Würzburg, Germany.
Background: The inheritance of the short allele, encoding the serotonin transporter (SERT) in humans, increases susceptibility to neuropsychiatric and metabolic disorders, with aging and female sex further exacerbating these conditions. Both central and peripheral mechanisms of the compromised serotonin (5-HT) system play crucial roles in this context. Previous studies on SERT-deficient (Sert) mice, which model human SERT deficiency, have demonstrated emotional and metabolic disturbances, exacerbated by exposure to a high-fat Western diet (WD).
View Article and Find Full Text PDFNutrients
January 2025
Department of Food & Nutrition, Kyung Hee University, Seoul 02447, Republic of Korea.
Background/objectives: The pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH) is closely associated with increased oxidative stress and lipid peroxidation. Coenzyme Q (CoQ) and selenium (Se) are well-established antioxidants with protective effects against oxidative damage. This study aimed to investigate the effects of CoQ and Se in ameliorating MASH induced by a methionine choline-deficient (MCD) diet in mice.
View Article and Find Full Text PDFFoods
January 2025
Laboratório de Indústria e Inspeção de Carnes e Derivados, Universidade Federal da Bahia, Salvador 40170-115, Brazil.
Five types of frankfurters were formulated: a control without tamarind (T0) and four samples using 5% tamarind pulp paste (PT5), seeds (ST5), peel (CT5), and a blend of all of them (PSCT5), replacing the same portion of meat. The inclusion of tamarind components led to a reduction in the moisture and protein content of the reformulated frankfurters. In terms of mineral composition, CT5 showed the highest ( < 0.
View Article and Find Full Text PDFAnn Clin Lab Sci
November 2024
Emergency Department, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, Zhejiang, China
Objective: Myocardial injury is a prevalent complication of sepsis. This study aims to shed light on the role of Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) in regulating Fatty Acid Synthase (FASN) to identify the intrinsic molecular mechanisms of sepsis-induced myocardial injury.
Method: H9c2 cells were treated with Lipopolysaccharide (LPS) to model sepsis-induced cardiomyocyte injury and were subsequently divided into seven groups: Control, LPS, LPS+sh-NC, LPS+sh-ACSL4, LPS+sh-ACSL4+Erastin, LPS+sh-ACSL4+oe-NC, and LPS+sh-ACSL4+oe-FASN.
Adv Sci (Weinh)
January 2025
Shanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Acute myocardial infarction (AMI) is associated with well-established metabolic risk factors, especially hyperlipidemia and obesity. Myocardial ischemia-reperfusion injury (mIRI) significantly offsets the therapeutic efficacy of revascularization. Previous studies indicated that disrupted lipid homeostasis can lead to lipid peroxidation damage and inflammation, yet the underlying mechanisms remain unclear.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!