Fig. 1.
Development of mice with adipocyte deficiency of angiotensinogen (AGT). A: schematic representation of the loxP-flanked AGT allele before (a) and after successive recombination with Flp (b) and transgenic fatty acid-binding protein 4 promoter (aP2)-driven Cre expression (c). The disrupted allele is shown in (c), indicating deletion of exon 2 of the AGT gene. B: genotyping of different adipose tissues [retroperitoneal fat (RPF), epididymal fat (EF), subcutaneous fat (Subc), and brown adipose tissue (BAT)] from Agtfl/fl and AgtaP2 mice. Amplicons are 249 bp (Agtfl/fl wild-type) or 362 bp (AgtaP2, disrupted). Since DNA from whole adipose tissue extracts were probed using PCR primers, the presence of an amplicon at 249 bp in AgtaP2, most likely results from the presence of other cell types in adipose tissue. C: AGT mRNA abundance in adipose and nonadipose tissues from Agtfl/fl control and AgtaP2 mice. Data are means ± SE from n = 4–11/group; *P < 0.05 compared with Agtfl/fl.