**1. Introduction**

Close to one century ago, Joslin, an American diabetologist, proposed the link between diabetes and obesity [1]. He concluded that "diabetes is largely a penalty of obesity, and the greater the obesity, the more likely is Nature to enforce it". In the 1950s, Vague [2] described that central obesity predisposes not only to diabetes but also to atherosclerosis. In the 1970s, for the first time, Haller [3] used the term "metabolic syndrome" (MetS) for associations of obesity, diabetes mellitus (DM), hyperlipoproteinemia, hyperuricemia, and hepatic steatosis when describing the additive effects of risk factors on atherosclerosis. Phillips developed the concept of metabolic risk factors for myocardial infarction and described a cluster of abnormalities including glucose intolerance, hyperinsulinemia, hyperlipidemia, and hypertension [4,5]. In 1988, Reaven, an American endocrinologist, propounded that insulin resistance (IR) was the cause of glucose intolerance, hyperinsulinaemia, increased very-lowdensity lipoprotein cholesterol (VLDL-C), decreased high-density lipoprotein cholesterol (HDL-C) and hypertension and named the constellation of abnormalities "syndrome X" [6]. Reaven did not include abdominal obesity, which has also been hypothesized as the underlying factor, as part of the condition. In the late 1990s and the early 21st century, MetS was widely recognized as a leading risk factor for cardiovascular morbidity and mortality and variously defined by World Health Organization [7], International Diabetes Federation (IDF [8]), the European Group for the Study of Insulin Resistance [9] and the National Cholesterol Education Program Adult Treatment Panel III [10] based on the reference intervals of its components. Accordingly to these definitions, MetS is thought to represent a combination of cardiometabolic risk determinants, including obesity, glucose intolerance and IR, dyslipidemia (including hypertriglyceridaemia, increased free fatty acids (FFAs) and decreased HDL-C) and hypertension and more recently a growing list of clinical

© 2012 Karimi, 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. © 2012 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.

manifestations like polycystic ovarian syndrome (PCOS), atherosclerosis, proinflammatory state, oxidative stress and non-alcoholic fatty liver disease (NAFLD) has been associated to it.

The MetS is increasingly recognized as a strong predictor of patient risk for developing coronary artery disease. It is associated with an atherogenic dyslipidemia characterized by elevated levels of triglycerides (TGs), reduced levels of HDL-C and a preponderance of small dense low-density lipoprotein (LDL) particles [11]. An atherogenic dyslipidemia is an integral component of MetS, and a major contributor to the cardiovascular risks in patients. These alarming situations increase the priority for developing new methods and technologies to investigate and to fight the MetS and its related comorbidities. Translational physiology offers us specific animal models for investigating these conditions to help support biomedical research efforts towards finding the necessary cures. This chapter summarizes various types of animal models that used as a tool in lipoprotein clinical researches and critically evaluates the physiological fidelity of these animal models to the human condition. The animal models are used to investigate biological or pathobiological phenomena or employed to find therapeutic and/or toxic effects of a xenobiotic or food ingredients. The laboratory animal models are developed and used to study the cause, nature, and cure of human lipoprotein disorders. They may conveniently be categorized in one of the following two groups:

