Title: Endotoxin-Induced Changes in Very-Low-Density Lipoprotein and Myocardial Utilisation of Triacylglycerol from Abnormal VLDL in the Rat
Abstract: Lipids are major energetic substrates in oxidative tissues; they are calorifically efficient but poorly water soluble and transport in plasma requires hydrophilic packaging. Non-esterified fatty acids (NEFA) are carried complexed to albumin but toxicity limits their concentration and hence quantitative availability; triacylglycerols (TAG) are the favoured storage form of lipid and can be transported in large amounts as lipid-protein assemblies (“lipoproteins”)—chylomicrons, synthesised in the gastrointestinal tract and very-low-density lipoprotein (VLDL), synthesised in liver from endogenous lipid and de novo lipogenesis. The protein components of both these lipoproteins (“apoproteins”) serve a variety of functions including structural support (apoB) and receptor recognition (apoE). Apoprotein-CII (apo-CII) is an activator of the enzyme responsible for TAG hydrolysis, lipoprotein lipase (EC 3.1.1.34; LPL). LPL activity is considered rate-limiting for circulating TAG utilisation and is tissue-specific depending on tissue activity. During systemic sepsis, plasma [TAG] is increased; this is due to increased plasma VLDL, a result of both increased hepatic lipogenesis and VLDL secretion, and of decreased adipose tissue LPL activity limiting peripheral uptake. These effects are mediated by pathogen-derived endotoxin stimulating host immune cells to release inflammatory mediators (cytokines). The function of the excess VLDL-TAG produced during
Publication Year: 2006
Publication Date: 2006-01-16
Language: en
Type: article
Indexed In: ['crossref', 'pubmed']
Access and Citation
AI Researcher Chatbot
Get quick answers to your questions about the article from our AI researcher chatbot