**1. Introduction**

Metabolism is the process of making energy and cellular molecules from breaking down the food that made up of proteins, carbohydrates and fats etc. A metabolic disorder occurs when abnormal chemical reactions disrupt this process. When this happens, our body might have too much of some substances or too little of other ones that we need to stay healthy. Metabolic syndrome, a combination of several metabolic risk factors including abdominal obesity, insulin resistance, hypertension, and atherogenic dyslipidemia, is one of the most common health problems in the modern society. Increasingly accumulated evidence from epidemiologic and basic research data, as well as translational, clinical, and intervention studies suggested that metabolic syndrome may be an important etiologic factor for the onset of cancer. In fact cancer has long been indicated as a metabolic disease due to aberrant energy metabolism caused by mitochondrial damage.

In living cells, processes of carbohydrate metabolism, lipid metabolism and energy metabolism are closely related. Metabolic syndrome (MS), such as diabetes, obesity, hyperlipidimia, and hypertension, is, more or less, associated with abnormal lipid metabolism. As a metabolic disease, cancer is caused by impaired energy metabolism due to impaired mitochondrial function, which is linked with abnormal mitochondrial membrane lipids, especially cardiolipin content [1]. Recent studies have indicated that abnormalities in cellular lipid metabolism are involved in both pathogenesis of metabolic syndrome and various cancers [2, 3].

As the major component of membranes and energy resources, cellular lipids, including phospholipids and neutral lipids (mainly triacylglycerols and sterol esters), play a crucial role for both cellular and physiological energy homeostasis. As cellular membrane structure components, phospholipids are important for cellular membrane remodeling and cellular

© 2013 Song et al., licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

proliferation. Disruption of phospholipid homeostasis may lead to carcinogenesis and MS [4, 5]. Triacylglycerol, as an important energy storage form, is closely related to glucose homeostasis and its disregulation is associated with onset of MS such as diabetes, obesity, and cardiovascular diseases [6].

Lipid Metabolism, Metabolic Syndrome, and Cancer 187

As one of the most abundant lipid species and major components of very-low-density lipoprotein (VLDL) and chylomicrons, triacylglycerols (TAG) play an important role in metabolism as energy sources. It can be acquired from de novo synthesis in liver or dietary lipids. Depending on the oil source, TAGs are either the main constituents of vegetable oils (typically more unsaturated) or animal fats (typically more saturated). Animal fat comprises about 40% of the energy intake in the human diet in Western countries, and a high proportion of this is TAG. Fat tissue, liver and intestine are the major places where TAG is synthesized and stored. There is also some intracellular storage of TAG e.g. in the muscle and brain cells. The storage of TAG can be replenished from dietary fat, or by endogenous

synthesis of fat from carbohydrates or proteins, which mainly takes place in the liver.

fundamental component of metabolic disease and insulin resistance [8, 9].

insulin signaling, which is particularly well characterized in muscle [10].

GLUT4 to membrane of muscle and liver cells [13, 14].

*2.1.1. Fatty acids and insulin resistance* 

The overabundance of nutrients such as lipids in obesity and caloric surplus leads to aberrant lipid management and ectopic fat accumulation (i.e., ''lipotoxicity''), which is a

Insulin resistance is the center underlying the different metabolic abnormalities in the metabolic syndrome, in which pathophysiological conditions insulin becomes less effective in lowering blood glucose. Insulin resistance can be induced by various environmental factors, including dietary habits. Muscle, liver and fat are the three major tissues for maintaining blood glucose levels. In the presence of insulin, fat and muscle cells absorb glucose, and the liver regulates glucose levels by reducing its secretion and increasing its storage in the form of glycogen. However, in the condition of insulin resistance, glucose uptake by muscle and fat cells is disrupted, and glycogen synthesis and storage are also reduced in liver cells, resulting in failure of suppressing glucose production and releasing into the blood. Impaired glucose metabolism is associated with molecular alterations of

Insulin also facilitates the uptake and storage of amino acids and fatty acids by converting them to protein and lipid, respectively. Besides the diminished glucose- lowering effects, insulin resistance also causes reduced actions of insulin on lipids and results in decreased uptake of circulating lipids and increased hydrolysis of stored triglycerides and, as a consequence, elevates free fatty acids in the blood plasma. Elevated levels of free fatty acids and triglycerides in the blood and tissues have been reported to contribute to impaired insulin sensitivity in many studies [11, 12]. Increased contents of fatty acids and their metabolites cause phosphorylation of insulin receptor substrate 1 (IRS-1) at serine, which blocks IRS-1 tyrosine phosphorylation and the associated activation of phosphatidylinositol-3' kinase (PI3K) activity, and results in a decreased translocation of the glucose transporter

The conversion of fatty acids to acetyl-CoA, the process known as β-oxidation, mainly occurs in the mitochondria. Defects in mitochondrial fatty acid oxidation and in adipocyte fat metabolism may increase fatty acid content in muscle and liver, which, in turn, cause impaired transport of glucose and defective glycogen synthesis in muscle, and sustained

In this chapter, we focused on the metabolism of phospholipid and triacylglycerol (including fatty acids) and discussed the association of lipid metabolism disorders with pathogenesis of MS and cancer as shown in Figure1. We also discussed the emerging role of omega-3 polyunsaturated fatty acids in preventing lipid disorder associated MS and cancer.

**Figure 1.** Inter-relationship between lipid metabolism, metabolic syndrome and cancer
