Fig. 1Flow sheet of microarrays in two different models and validation process. PPAR-γ, peroxisome proliferator-activated receptor-γ; OLETF, Otsuka Long-Evans Tokushima Fatty; LETO, Long-Evans Tokushima Otsuka; RT-PCR, reverse transcription polymerase chain reaction.
Fig. 2Expression of lipocalin-2 in adipose tissue from independent rodent and human samples. (A) Visceral adipose tissues of 24-week-old male Long-Evans Tokushima Otsuka (LETO) rats (black bars) and Otsuka Long-Evans Tokushima Fatty (OLETF) rats (white bars). (B) Visceral adipose tissues of standard chow-fed db/db mice (black bars) and pioglitazone-treated db/db mice (white bars). (C) Visceral adipose tissues of nonobese women (black bars) and obese women (white bars). (D) Subcutaneous adipose tissues of nonobese women (black bars) and obese women (white bars). Gene expression levels were measured by real time reverse transcription polymerase chain reaction. NS, non significant. aP<0.05, bP<0.01.
Fig. 3Spearman correlation coefficient between the level of expression of lipocalin-2 in visceral adipose tissues of humans and (A) body mass index (BMI), (B) white blood cell (WBC) count, (C) serum interleukin-6 (IL-6), and (D) adipocyte fatty acid binding protein (A-FABP) levels. The horizontal axis of each graph indicates the expression ratio of lipocalin-2 versus β-actin in the visceral adipose tissues of humans measured by real time reverse transcription polymerase chain reaction.
Table 1Anthropometric and biochemical variables in rodent models of metabolic syndrome
Table 2KEGG public pathway classification of differentially expressed genes in PPAR-γ agonist-treated db/db mice, as indicated by microarray data
Table 3Biochemical variables of nonobese and obese women