Περίληψη:
Cardiometabolic syndrome (CMS), a disease entity characterized by abdominal obesity, insulin resistance (IR), hypertension, and hyperlipidemia, is a global epidemic with approximately 25% prevalence in adults globally. CMS is associated with increased risk for cardiovascular disease (CVD) and development of diabetes. Due to its multifactorial etiology, the development of several animal models to simulate CMS has contributed significantly to the elucidation of the disease pathophysiology and the design of therapies. In this review we aimed to present the most common mouse models used in the research of CMS. We found that CMS can be induced either by genetic manipulation, leading to dyslipidemia, lipodystrophy, obesity and IR, or obesity and hypertension, or by administration of specific diets and drugs. In the last decade, the ob/ob and db/db mice were the most common obesity and IR models, whereas Ldlr -/-and Apoe -/-were widely used to induce hyperlipidemia. These mice have been used either as a single transgenic or combined with a different background with or without diet treatment. High-fat diet with modifications is the preferred protocol, generally leading to increased body weight, hyperlipidemia, and IR. A plethora of genetically engineered mouse models, diets, drugs, or synthetic compounds that are available have advanced the understanding of CMS. However, each researcher should carefully select the most appropriate model and validate its consistency. It is important to consider the differences between strains of the same animal species, different animals, and most importantly differences to human when translating results. © 2021 Georg Thieme Verlag. All rights reserved.
Συγγραφείς:
Aravani, D.
Kassi, E.
Chatzigeorgiou, A.
Vakrou, S.
Λέξεις-κλειδιά:
high density lipoprotein cholesterol; low density lipoprotein cholesterol; melanocortin 4 receptor; biological marker; insulin; lipid, Apoe gene; body weight; caloric intake; cardiometabolic risk; diet therapy; DNA modification; gene deletion; gene mutation; genotype; hormone deficiency; human; hypercholesterolemia; hyperglycemia; hypertriglyceridemia; insulin resistance; Ldlr gene; mouse; nonhuman; obesity; phenotype; Review; Western diet; animal; blood; disease model; genetics; glucose blood level; hyperlipidemia; insulin resistance; lipid diet; metabolic syndrome X; metabolism; obesity; pathophysiology; transgenic mouse, Animals; Biomarkers; Blood Glucose; Diet, High-Fat; Disease Models, Animal; Hyperlipidemias; Insulin; Insulin Resistance; Lipids; Metabolic Syndrome; Mice; Mice, Transgenic; Obesity
