Specialists do not consider any of MS symptoms as a main symptom including abdomi nal obesity, since new data have been reported that abdominal obesity has ethnic related characteristics (for example, the eastern nations), and is not always associated with development of the metabolic syn drome. The development of MS diagnostic criteria is one of the most important tasks, however to consider the diversity of all processes in the human body at the development of this syndrome in one characteris tic is an extremely difficult problem. Currently, in clinical practice several definitions of MS are used [1]. Thus, to develop new MS and DM (diabetes mel litus) models, the necessity of reconstruction of a broad spectrum of pathological processes that occur in humans upon these diseases must be considered.It is known that guinea pigs, owing to certain organism peculiarities, such as blood lipid composi tion and the absence of endogenous vitamin C, are the optimal model for the study of carbohydrate and lipid metabolism disorders [2,3]. When modeling of MS in these animals, there is no extraneous influen ce of enhanced antioxidants secretion and blood atherogenic properties on the development of patho logical processes. Upon prolonged intramuscular administration of protamine sulfate to guinea pigs a number of symptoms, indicating the development of systemic homeostasis disorders, were observed. In particular, carbohydrate metabolism disorder (hyperglycemia and reduction of glycogen store in the liver) and lipid metabolism disorder (increase in choleste rol level) as well as inflammatory processes in the liver and kidneys (increased level of ALT, AST, creatinine and microalbuminuria), disorder of insulin synthesis, degradation of βcells and accu mulation of free radicals were observed [4,5]. The symptoms mentioned above are typical in the devel opment of MS and DM in humans.It is known that oxidative damage to tissues has been implicated in the etiology and pathogene sis of chronic complications in several diseases [6]. It has been shown that the increased production of reactive oxygen species induced by hyperglycemia upon metabolic syndrome and subsequent glucose toxici ty lead to the development of oxidative stress accompanied by a lesion of the pancreatic βcells and hepato cytes [7]. Recent studies have suggested that the development of the pathological conditions, doi: http://dx