Generation of porcine fibroblasts overexpressing 11β‑HSD1 with adipose tissue‑specific aP2 promoter as a porcine model of metabolic syndrome
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- Published online on: July 17, 2013 https://doi.org/10.3892/mmr.2013.1592
- Pages: 751-756
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Abstract
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.
