Functional lipids and the prevention of the metabolic syndrome

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Author : Teruyoshi Yanagita and Koji Nagao
Keyword : lipids, function, metabolic syndrome, hypertension, adiponectine
DOI :
Issue : Asia Pac J Clin Nutr 2008;17(S1):189-191
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Abstract

The metabolic syndrome is increasingly prevalent in worldwide. The quality and quantity of dietary lipids could be important modulators associated with the cardiovascular morbidity and mortality. At present, functional lipids such as conjugated linoleic acid (CLA) and phospholipids have attracted considerable at- tention because of their beneficial biological effects in attenuating metabolic syndrome. Supplementation of CLA reduces abdominal white adipose tissues, serum triacylglycerol (TAG) level, and liver TAG level in obese Otsuka Long-Evans Tokushima Fatty OLETF rats. These effects were attributed to enhanced fatty acid beta-oxidation and suppressed fatty acid synthesis in the liver. In addition, CLA enhanced en- ergy expenditure in these rats. Anti-hypertensive properties of CLA have also been demonstrated. In obese/diabetic OLETF and Zucker rats, feeding of CLA prevented the development of obesity-induced hypertension. This was associated with an altered production of physiologically active adipocytokines, such as adiponectin, leptin and angiotensinogen. In addition, CLA could alleviate the development of insu- lin resistance and fatty liver. Dietary phospholipids have physiological functions that are different to die- tary TAG. We recently reported that phosphatidylcholine (PC) alleviated orotic acid-induced fatty-liver through the suppression of hepatic lipogenesis in rats, and omega3-PC from salmon roe prevented the de- velopment of obesity-related diseases through the suppression of lipogenic gene expressions and the en- hancement of lypolytic gene expressions in the liver of obese rats. However, reports which studying the nutritional functions of minor phospholipids, such as phosphatidylinositol (PI), are scarce. Our study indi- cated that dietary PI lowered lipids in the plasma and liver by suppressing hepatic TAG synthesis.

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