To give new insight to alterations of cardiac lipid metabolism accompanied by a fructose-rich diet (FRD), rats of both sexes were exposed to 10 % fructose in drinking water during 9 weeks. The protein level and subcellular localization of the main regulators of cardiac lipid metabolism, such as lipin 1, peroxisome proliferator-activated receptor α (PPARα), peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α), carnitine palmitoyltransferase I (CPTI), and CD36 were studied. Caloric intake in fructose-fed rats (FFR) of both sexes was increased. Circulating triacylglyceroles (TAG) and non-esterified fatty acids were increased in male FFR, while females increased visceral adiposity and blood TAG. Total expression of lipin 1 in cardiac cell lysate and its cytosolic and microsomal level were increased in the hearts of male FFR. PPARα and PGC-1α content were decreased in the nuclear extract. In addition, cardiac deposition of TAG in male FFR was elevated, as well as inhibitory phosphorylation of insulin receptor substrate 1 (IRS-1). In contrast, in female FFR, lipin 1 level was increased in nuclear extract only, while overall CPTI expression and phosphorylation of IRS-1 at serine 307 were decreased. The results of our study suggest that fructose diet causes gender-dependent alterations in cardiac lipid metabolism. Potentially detrimental effects of FRD seem to be limited to male rats. Most of the observed changes might be a consequence of elevated expression and altered localization of lipin 1. Increased inhibitory phosphorylation of IRS-1 is possible link between cardiac lipid metabolism and insulin resistance in FFR.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s11745-014-3909-4 | DOI Listing |
Am J Physiol Heart Circ Physiol
January 2025
Department of Biochemistry and Molecular Biology, Dalhousie University, Dalhousie Medicine New Brunswick, 355 Campus Ring Road, Saint John, New Brunswick, E2L 4L5, Canada.
Lipid phosphate phosphatase 3 (LPP3) is a membrane-bound enzyme that hydrolyzes lipid phosphates including the bioactive lipid, lysophosphatidic acid (LPA). Elevated circulating LPA production and cellular LPA signaling are implicated in obesity-induced metabolic and cardiac dysfunction. Deletion of LPP3 in the cardiomyocyte increases circulating LPA levels and causes heart failure and mitochondrial dysfunction in mice.
View Article and Find Full Text PDFJ Cell Mol Med
January 2025
School of Forensic Medicine, Guizhou Medical University, Guiyang, China.
Deubiquitinating enzymes (DUBs) are integral regulators of protein stability. Among these, Ubiquitin-specific protease 18 (USP18) has emerged as a potential therapeutic target for heart failure. However, its precise role in atherosclerosis remains to be comprehensively understood.
View Article and Find Full Text PDFCurr Cardiol Rep
January 2025
Third Department of Medicine, General University Hospital and First Faculty of Medicine, Charles University, 121 08, Prague, Czech Republic.
Purpose Of Review: In recent years, the terms "metabolic associated fatty liver disease-MAFLD" and "metabolic dysfunction-associated steatotic liver disease-MASLD" were introduced to improve the encapsulation of metabolic dysregulation in this patient population, as well as to avoid the negative/stigmatizing terms "non-alcoholic" and "fatty".
Recent Findings: There is evidence suggesting links between MASLD and coronary heart disease (CHD), heart failure (HF), atrial fibrillation (AF), stroke, peripheral artery disease (PAD) and chronic kidney disease (CKD), although the data for HF, AF, stroke and PAD are scarcer. Physicians should consider the associations between MASLD and CV diseases in their daily practice.
Multimed Man Cardiothorac Surg
January 2025
• Department of Cardiac Sciences, King Abdulaziz Medical City, Ministry of National Guard Health Affairs, Jeddah, Saudi Arabia • King Abdullah International Medical Research Center, Ministry of National Guard Health Affairs, Jeddah, Saudi Arabia • College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Ministry of National Guard Health Affairs, Jeddah, Saudi Arabia.
Prostaglandin E1 is a potent vasodilator that prevents the ductus arteriosus from closing. Its use in neonates with cyanotic heart defects has revolutionized the management of children with cyanotic heart defects. Although the use of prostaglandin E1 is a temporary solution, the establishment of dependable pulmonary blood flow is of paramount importance.
View Article and Find Full Text PDFJ Eval Clin Pract
February 2025
Department of Vascular Medicine, University Medical Center Utrecht, Utrecht, the Netherlands.
Rationale: Established coronary artery disease (CAD) patients are at increased risk for recurrence of cardiovascular events and mortality due to non-attainment of recommended risk factor control targets.
Objective: We aimed to evaluate the attainment of treatment targets for risk factor control among CAD patients as recommended in the Indonesian CVD prevention guidelines.
Methods: Patients were consecutively recruited from the Makassar Cardiac Center at Wahidin Sudirohusodo Hospital, Indonesia.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!