Glycolipid Metabolic Disorders, Metainflammation, Oxidative Stress, and Cardiovascular Diseases: Unraveling Pathways.

Simple Summary: Glycolipid metabolic disorders (GLMDs) result from imbalances in glycolipid levels, leading to various health issues, including obesity, diabetes, liver problems, nerve and muscle complications, and cardiovascular and kidney diseases. This study explores the connection between GLMDs, oxidative stress, and chronic inflammation, which exacerbate these conditions. GLMD originates from disruptions in glucose and fat metabolism, often associated with hormone regulation and insulin resistance. These disruptions cause the accumulation of harmful molecules, triggering inflammation in multiple organs. Key molecules, such as advanced glycation end products (AGEs) and sphingosine-1-phosphate (S1P), play significant roles in this process. Understanding these relationships is essential for developing better treatments, reducing illness and mortality rates, lowering healthcare costs, and improving quality of life. Glycolipid metabolic disorders (GLMDs) are various metabolic disorders resulting from dysregulation in glycolipid levels, consequently leading to an increased risk of obesity, diabetes, liver dysfunction, neuromuscular complications, and cardiorenal vascular diseases (CRVDs). In patients with GLMDs, excess caloric intake and a lack of physical activity may contribute to oxidative stress (OxS) and systemic inflammation. This study aimed to review the connection between GLMD, OxS, metainflammation, and the onset of CRVD. GLMD is due to various metabolic disorders causing dysfunction in the synthesis, breakdown, and absorption of glucose and lipids in the body, resulting in excessive ectopic accumulation of these molecules. This is mainly due to neuroendocrine dysregulation, insulin resistance, OxS, and metainflammation. In GLMD, many inflammatory markers and defense cells play a vital role in related tissues and organs, such as blood vessels, pancreatic islets, the liver, muscle, the kidneys, and adipocytes, promoting inflammatory lesions that affect various interconnected organs through their signaling pathways. Advanced glycation end products, ATP-binding cassette transporter 1, Glucagon-like peptide-1, Toll-like receptor-4, and sphingosine-1-phosphate (S1P) play a crucial role in GLMD since they are related to glucolipid metabolism. The consequences of this is system organ damage and increased morbidity and mortality. [ABSTRACT FROM AUTHOR]