The transcription initiation codon and the secretory signal recognition peptide sequence, of the fibrinogen-like protein 1 (Fgl1) gene have been replaced with a loxP-flanked neomycin resistance (neo) cassette, abolishing gene expression. FGL1 is expressed in the liver and is involved in hepatocyte proliferation and repair. It has been found overexpressed in hepatocellular carcinomas and following acute liver injury. Homozygotes are viable and fertile. Fgl1-/- mice are 37% heavier than wild type mice at three weeks of age. They are also longer and contain more adipose tissue. These mice have decreased plasma cholesterol, free fatty acid levels, and fasting hyperglycemia with enhanced gluconeogenesis. Adipose tissue morphology is abnormal in Fgl1-/- mice. Brown adipose tissue contains larger lipid droplets and has reduced number of nuclei, while white adipocytes are larger and fewer in number than in wildtype mice.

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Fgl1-/- mice may be useful for studying metabolism and liver regeneration.

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