This study investigated the efficacy of aerobic exercise training (AET) in the prevention of dyslipidemia, insulin resistance (IR), and atherogenesis induced by severe low-sodium (LS) diet. LDL receptor knockout (LDLR KO) mice were fed a low-sodium (LS) (0.15% NaCl) or normal-sodium (NS; 1.27% NaCl) diet, submitted to AET in a treadmill, 5 times/week, 60 min/day, 15 m/min, for 90 days, or kept sedentary. Blood pressure (BP), plasma total cholesterol (TC) and triglyceride (TG) concentrations, lipoprotein profile, and insulin sensitivity were evaluated at the end of the AET protocol. Lipid infiltration, angiotensin II type 1 receptor (AT1), receptor for advanced glycation end products (RAGE), carboxymethyllysine (CML), and 4-hydroxynonenal (4-HNE) contents as well as gene expression were determined in the brachiocephalic trunk. BP and TC and gene expression were similar among groups. Compared to the NS diet, the LS diet increased vascular lipid infiltration, CML, RAGE, 4-HNE, plasma TG, LDL-cholesterol, and VLDL-TG. Conversely, the LS diet reduced vascular AT1 receptor, insulin sensitivity, HDL-cholesterol, and HDL-TG. AET prevented arterial lipid infiltration; increases in CML, RAGE, and 4-HNE contents; and reduced AT1 levels and improved LS-induced peripheral IR. The current study showed that AET counteracted the deleterious effects of chronic LS diet in an atherogenesis-prone model by ameliorating peripheral IR, lipid infiltration, CML, RAGE, 4-HNE, and AT1 receptor in the intima-media of the brachiocephalic trunk. These events occurred independently of the amelioration of plasma-lipid profile, which was negatively affected by the severe dietary-sodium restriction.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9598599 | PMC |
http://dx.doi.org/10.3390/antiox11102023 | DOI Listing |
J Transl Med
January 2025
Research Unit NeuroBiology of Diabetes, Helmholtz Munich, Ingolstädter Landstraße 1, 85764, Neuherberg, Germany.
Background: Obese subjects undergoing weight loss often fear the Yoyo dieting effect, which involves regaining or even surpassing their initial weight. To date, our understanding of such long-term obesity and weight cycling effects is still limited and often based on only short-term murine weight gain and loss studies. This study aimed to investigate the long-term impacts of weight cycling on glycemic control and metabolic health, focusing on adipose tissue, liver, and hypothalamus.
View Article and Find Full Text PDFJ Complement Integr Med
January 2025
Department of Basic Medical Sciences, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.
Alzheimers Dement
December 2024
Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Background: One of the major outstanding questions in the field of Alzheimer's disease (AD) research is the underlying mechanism by which APOE ε4, the strongest genetic risk factor for AD, contributes to disease pathogenesis. Current therapies targeting amyloid-beta plaques show modest effect in non-APOE4 male AD patients, and greatly increase the risk for amyloid-related imaging abnormalities - edema/effusion (ARIA-E) in APOE ε4 carriers. We made an important discovery that APOE4 neutrophil-microglia interactions drive cognitive impairment in a sex-dependent manner.
View Article and Find Full Text PDFSci Rep
January 2025
College of Pharmacy, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon, 34134, Republic of Korea.
Ferroptosis plays a role in tumorigenesis by affecting lipid peroxidation and metabolic pathways; however, its prognostic or therapeutic relevance in pancreatic adenocarcinoma (PAAD) remains poorly understood. In this study, we developed a prognostic ferroptosis-related gene (FRG)-based risk model using cohorts of The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC), proposing plausible therapeutics. Differentially expressed FRGs between tumors from TCGA-PAAD and normal pancreatic tissues from Genotype-Tissue Expression were analyzed to construct a prognostic risk model using univariate and multivariate Cox regression and LASSO analyses.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Physiology, Spinal Cord and Brain Injury Research Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
Spinal cord injury (SCI) leads to permanent motor and sensory loss that is exacerbated by intraspinal inflammation and persists months to years after injury. After SCI, monocyte-derived macrophages (MDMs) infiltrate the lesion to aid in myelin-rich debris clearance. During debris clearance, MDMs adopt a proinflammatory phenotype that exacerbates neurodegeneration and hinders recovery.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!