Cardiovascular (CV) disease is the most common cause of morbidity and mortality worldwide, particularly in the presence of the metabolic syndrome (MetS). Classifications and treatment of the MetS have recently been redefined. While the majority of the cardiac components such as hypertension, diabetes mellitus (DM) and dyslipidemia (DLD) are objectively measurable elements, a few disparities among the definitions have to be considered that can variably modify diagnosis, treatment and prevention. Non-cardiac factors such as liver disease (including, but not limited to, alcoholic and non-alcoholic steatosis/hepatitis), renal disease, severe obesity, polycystic ovarian syndrome and obstructive sleep apnea (OSA), may have independent or synergistic relationship with complementary cardiac MetS elements, and these additional risk factors may have an incremental adverse impact on CV outcome. The combination of all these factors potentiates the adverse significance on CV events. MetS not only increases morbidity and mortality but also has economic ramifications for the healthcare system. Prevention of CV disease includes primary and secondary aspects. Besides overall advances to provide optimal care for hypertension, diabetes, and dyslipidemia, early-targeted inventions to diagnose, treat and prevent OSA, and severe obesity, are needed.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2174/1570161114666160722121615 | DOI Listing |
Diabetes Obes Metab
January 2025
Department of Endocrinology, First Hospital of Shanxi Medical University, Taiyuan, China.
Metabolic syndrome-related diseases frequently involve disturbances in skeletal muscle lipid metabolism. The accumulation of lipid metabolites, lipid-induced mitochondrial stress in skeletal muscle cells, as well as the inflammation of adjacent adipose tissue, are associated with the development of insulin resistance and metabolic dysfunction. Consequently, when antidiabetic medications are used to treat various chronic conditions related to hyperglycaemia, the impact on skeletal muscle lipid metabolism should not be overlooked.
View Article and Find Full Text PDFJ Cell Physiol
January 2025
Department of Pharmaceutical Sciences and Center for Blood-Brain Barrier Research, Jerry H. Hodge School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, Texas, USA.
Glucose is a major source of energy for the brain. At the blood-brain barrier (BBB), glucose uptake is facilitated by glucose transporter 1 (GLUT1). GLUT1 Deficiency Syndrome (GLUT1DS), a haploinsufficiency affecting SLC2A1, reduces glucose brain uptake.
View Article and Find Full Text PDFNon-alcoholic fatty liver disease (NAFLD) is a chronic condition characterized by hepatic steatosis in the absence of significant alcohol consumption and is increasingly recognized as the hepatic manifestation of metabolic syndrome (MetS). This review aims to explore the molecular mechanisms underlying the interaction between NAFLD, insulin resistance (IR), and MetS, with a focus on identifying therapeutic targets. A comprehensive review of existing literature on NAFLD, IR, and MetS was conducted.
View Article and Find Full Text PDFJGH Open
January 2025
Division of Research and Development for Minimally Invasive Treatment Cancer Center, Keio University School of Medicine Tokyo Japan.
Background And Aim: It is important for endoscopist to diagnose the lesion redness. In this study, we focused on the redness of duodenal bulb. We objectively analyzed the changes in redness of the duodenal bulb using linked color imaging (LCI) with chromatic indicators.
View Article and Find Full Text PDFActa Pharm Sin B
December 2024
State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Nuclear receptor corepressor (NCoR1) interacts with various nuclear receptors and regulates the anabolism and catabolism of lipids. An imbalance in lipid/energy homeostasis is also an important factor in obesity and metabolic syndrome development. In this study, we found that the deletion of NCoR1 in intestinal epithelial cells (IECs) mainly activated the nuclear receptor PPAR and attenuated metabolic syndrome by stimulating thermogenesis.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!