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Metabolic syndrome arises from a combination of disorders that increase the risk of cardiovascular disease and diabetes. In previous studies, it was observed that overexpression of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) induced obesity and the insulin resistance that accompanies metabolic syndrome in rodent adipose tissue. Based on these observations, it was hypothesized that overexpression of 11β-HSD1 may be suitable for the generation of a porcine model of metabolic syndrome. It was evaluated that promoter activities of the porcine adipose fatty acid-binding protein (aP2) gene generates adipose tissue-specific 11β-HSD1 expression. In adipose tissue, the maximum promoter activity (-2,826 to +51 nt) of aP2 was 200-fold higher than that of a promoterless construct. In addition, 11β-HSD1 transcriptional levels were significantly increased following the introduction of the aP2 promoter into 3T3‑L1 adipocytes. These observations indicate that the aP2 promoter may facilitate 11β-HSD1 overexpression in porcine adipose tissue. Transgenic fibroblasts were generated containing 11β-HSD1 cDNA controlled by the aP2 promoter with two screening markers, green fluorescence protein and a neomycin-resistance gene. It was hypothesized that transgenic fibroblasts may be useful for generating a porcine model of metabolic syndrome.

Generation of porcine fibroblasts overexpressing 11β-HSD1 with adipose tissue-specific aP2 promoter as a porcine model of metabolic syndrome