Abstract
Metabolic syndrome is a condition characterized by the presence of insulin resistance and the presence of two of the following risk factors: obesity, hyperlipidemia (hypertriglyceridemia, decreased high-density lipoprotein cholesterol), hypertension, or microalbuminuria. The multifactorial nature of metabolic syndrome makes it difficult to create an adequate experimental model that would best represent the entire spectrum of the pathophysiology of this condition. This review aims to summarize current literature data on the pathophysiological mechanisms of metabolic syndrome in the context of the development of insulin resistance, obesity, dyslipidemia, impaired glucose tolerance, and inflammation. The article also summarizes modern approaches to the induction of metabolic syndrome in rodents, among which dietary manipulation, genetic modifications, and the use of pharmaceuticals are the most common. As genetic models of metabolic syndrome, rodents with leptin or leptin receptor deficiency are most often used, in particular leptin-deficient mice (ob/ob), leptin receptor-deficient mice (db/db), Zucker obese rats (ZF), diabetic rats lines Zucker with obesity (ZDF) and others. Pharmaceutical drugs that can be used to induce metabolic syndrome include endogenous glucocorticoids and antipsychotic drugs. Several dietary manipulations are used to induce metabolic syndrome in laboratory animals. In particular, one type of diet or a combination of diets can be used, such as diets high in fructose, sucrose and fat, or a diet characterized by a high content of both fructose and fat or sucrose and fat. Manipulations with the composition of products consumed by experimental animals make it possible to simulate the development of metabolic syndrome, since the diet affects the metabolism of the entire body, and has a regulatory effect on hormones, glucose and lipid metabolism pathways.
Published Version
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