Animal Models of Human Metabolic Syndrome Literature Review

被引:0
作者
Bersenyi Andras [1 ]
Fodor Kinga [1 ]
Korsos Gabriella [1 ]
Fekete Sandor Gyorgy [1 ]
机构
[1] Allatorvostud Egyet, Allattenyesztesi Takarmanyozastani & Lab Tud Int, Lab Tud & Allatvedelmi Osztaly, Istvan U 2, H-1078 Budapest, Hungary
关键词
INSULIN-RESISTANCE; GUT MICROBIOTA; OBESITY; FAT; GENE; MOUSE; DYSFUNCTION; PREVALENCE; PHENOTYPES; REGULATORS;
D O I
暂无
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
The metabolic syndrome (MetS) is a suite of metabolic complications and its prevalence among the world's population is about 20 to 40%. The authors introduced the animal models for the study of MetS aetiology and pathophysiology. In the case of MetS, experimental animals as well as humans may develop cluster lesions. Rodents, especially mice, are the most common animal models. The polygenic models may , be better suited than monogenic ones for studying its genetic underpinnings because most of the metabolic complications are the result of many interacting genes of individually small effect. Therefore, strain background must be considered for assessing phenotypic consequences of gene effects that may confound results. The candidate gene approaches aim at understanding the physiological processes necessary for energy balance, storage and nutrition partitioning. The maternal developmental environment has been shown to affect not only foetal and early postnatal growth, but also adult susceptibility to Me:S, because the epigenetic modifications may increase the risk for MetS. Animal models attempt to understand the link between the obesity and the insulin resistance, which is an important risk factor for developing type-2 diabetes and/or cardiovascular diseases. These can shed light on why some obese individuals develop metabolic complications while others do not. Conversely, why some lean individuals develop multiple MetS components in the absence of obesity. Moreover, the animal models aim at preventing the different disadvantageous pathophysiological processes and have advanced the right prevention and therapies for MetS. However, the bioinformatic tools facilitate design stains that most appropriately mimic the clinical reality of MetS.
引用
收藏
页码:165 / 176
页数:12
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