AI Article Synopsis
- Metabolic syndrome includes various health issues that elevate the chances of heart disease and diabetes, and is linked to increased levels of the enzyme 11β-HSD1 in fat tissue.
- Research with genetically modified mice showed that those expressing the reverse tetracycline-transactivator (rtTA) experienced all symptoms of metabolic syndrome, like obesity, insulin resistance, high cholesterol, and hypertension.
- Gene studies indicated significant changes in processes related to lipid metabolism and inflammation, leading to the conclusion that rtTA expression in fat tissue is a driving factor for metabolic syndrome in these mice.
Article Abstract
Metabolic syndrome is a combination of medical disorders that increases the risk of developing cardiovascular disease and diabetes. Constitutive overexpression of 11β-HSD1 in adipose tissue in mice leads to metabolic syndrome. In the process of generating transgenic mice overexpressing 11β-HSD1 in an inducible manner, we found a metabolic syndrome phenotype in control, transgenic mice, expressing the reverse tetracycline-transactivator (rtTA) in adipose tissue. The control mice exhibited all four sequelae of metabolic syndrome (visceral obesity, insulin resistance, dyslipidemia, and hypertension), a pro-inflammatory state and marked hepatic steatosis. Gene expression profiling of the adipose tissue, muscle and liver of these mice revealed changes in expression of genes involved in lipid metabolism, insulin resistance, and inflammation. Transient transfection of rtTA, but not tTS, into 3T3-L1 cells resulted in lipid accumulation. We conclude that expression of rtTA in adipose tissue causes metabolic syndrome in mice.
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| http://dx.doi.org/10.1007/s11248-011-9562-2 | DOI Listing |
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