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Diet‐induced obesity and impaired insulin and glucose tolerance in sterol regulatory element binding protein‐1a knock‐out mice

Sterol regulatory element binding protein‐1 (SREBP‐1) regulates the transcription of key enzymes in fatty acid, triacylglycerol, and cholesterol synthesis. There are two SREBP‐1 isoforms, −1a and −1c. These isoforms, encoded by a single gene, are produced through the use of alternative promoters producing transcripts with unique first exons. Gene trapping targeted to the unique first exon of SREBP‐1a, was used to generate SREBP‐1a−/ − mice. To begin to evaluate the functional role of SREBP‐1a in lipid metabolism, SREBP‐1a−/ − and wild‐type (WT) mice were fed a high fat/ high sucrose diet for 5 mo. Plasma NEFA, total cholesterol, and triacylglycerol did not differ between genotypes. However, SREBP‐1a−/ − mice became obese and weighed 35 % more than WT mice. The increased weight in the SREBP‐1a−/ −mice was due to increased adiposity as demonstrated by 2.5‐ to 4‐fold heavier fat pads. Surprisingly, although the SREBP‐1a−/ −mice weighed more, they ate 30 % less than WT mice. Finally, SREBP‐1a−/ −mice had impaired glucose and insulin tolerance compared to WT mice. This study demonstrates that loss of SREBP‐1a leads to an unexpected tendency towards obesity and defective glucose regulation.