Abstract
Obesity is a metabolic abnormality characterized by increased levels of plasma free fatty acids and triglycerides, decreased levels of High-Density Lipoprotein (HDL), and abnormal Low-Density Lipoprotein (LDL) composition. The most significant contributing factor for obesity-related dyslipidemia is likely uncontrolled fatty acid release from adipose tissue, especially visceral adipose tissue, through lipolysis, which causes increased delivery of fatty acids to the liver and synthesis of Very-Low-Density Lipoprotein (VLDL).
Highlights
Obesity is a metabolic abnormality characterized by increased levels of plasma free fatty acids and triglycerides, decreased levels of High-Density Lipoprotein (HDL), and abnormal Low-Density Lipoprotein (LDL) composition [1]
How is pathophysiology of dyslipidemia associated with insulin resistance? Altered metabolism of TG-rich lipoproteins plays a pivotal role in the pathophysiology of dyslipidemia associated with insulin resistance
A discernable decrease was observed in triglyceride, total cholesterol and lowdensity lipoprotein cholesterol
Summary
Obesity is a metabolic abnormality characterized by increased levels of plasma free fatty acids and triglycerides, decreased levels of High-Density Lipoprotein (HDL), and abnormal Low-Density Lipoprotein (LDL) composition [1]. Increased levels of free fatty acids can decrease mRNA expression or activity of Lipoprotein Lipase (LPL) in adipose tissue and skeletal muscle, and increased synthesis of VLDL in the liver can inhibit lipolysis of chylomicrons, which promotes hypertriglyceridemia [2]. Another metabolic abnormality associated to obesity and increased body lipids is insulin resistance. Other research showed steps by which excess lipid depots could contribute to insulin resistance: 10 by altering supply (either in absolute terms or in particular anatomical locations, eg, portal vein to liver) or type of fatty acids, which impact on insulin signaling or glucose metabolism in insulin-responsive tissues; 20 by increasing or decreasing secretion of humoral factors from adipocytes (adipokines) or liver (hepatokines) that enhance (eg, adiponectin, fibroblast growth factor 21) or inhibit (eg, Fetuin A) insulin signaling; 30 by attracting the invasion of cells, which release inflammatory cytokines (TNF) that impact on the insulin-signaling pathway in adjacent or distant tissue; 40 sequestering a favorable factor (25-hydroxyvitamin D [25OHD]) or by conversion of a circulating factor to a form with more adverse metabolic activity
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