Contrary to popular belief there is actually a lot of doubt that dietary cholesterol has any direct affect on serum levels. There is no real consensus on the pathogenesis of metabolic syndrome but Patrice D Cani sheds some interesting and revolutionary insight http://diabetes.diabetesjournals.org/content/56/7/1761 From this and other papers the best understanding I could gather is that contrary to maintream dogma, metabolic syndrome is not a nutritional disorder directly but an acute phase response mechanism to infection. In regards to diet, high-fat diets selectively feed inflammatory gut-microbiota leading to over growth, disregulation of intestinal tight junction proteins, and the absorption of endotoxins (immunostimulatory bacterial cell-wall components) across the cell wall. This stimulates a systemic inflammatory response analogous to a low grade sepsis. As with true sepsis dramatic metabolic changes occur to attempt to fight the infection. Leptin is secreted which inhibits hunger. It is believed that this is an attempt to starve off the pathogen (hence why you often have no appetite when you run a fever). However, during the chronic phases leptin resistance occurs to counteract starvation. Leptin resistance is then a likely contributor for eating disorders and obesity. Insulin resistance, cholesterol synthesis and VLDL synthesis are also upregulated during endotoxin challenge. Insulin resistance likely serves as a mechanism to preserve glucose during stress response for reductive biosynthesis and redox maintenance. This allows the body to heal damaged tissues, proliferate immune cells, secrete peroxides against infection, and maintain glutathione function against oxidative stress. The roles of cholesterol and VLDL are less understood. However, it is known that lipoproteins associate with endotoxin binding proteins and therefor serve a dual purpose of distributing lipids and detoxifying lipophilic endotoxins. Hence why lipoproteins embed in the vascular tissue due to its susceptibility to damage by inflammation and infectious microorganisms. Why HDL decreases and LDL increases is not exactly known. Lipoprotein remodeling and HDL/LDL association have been shown to transfer endotoxins in vitro. So there is the possibility that these alterations in lipoprotein profile reflect functional behaviors aimed at channeling immunogenic materials back to the liver.
So in short it's not so much that obesity causes lipoprotein alterations. There is the fact that adipose tissue excretes inflammatory signals and there may be a secondary affect on metabolism as a result, but both obesity and lipoprotein alterations occur as downstream effects of inflammatory cascades.
