Figure 2.

FGF21 promotes brown fat activation and white fat browning, and improves glucose metabolism. After 16 weeks of treatment, interscapular BAT (iBAT) (A) and gonadal WAT (gWAT) (D) were weighed. In iBAT, the lipid content (B) and expression of uncoupling protein-1 (UCP-1) (C) were quantified after haematoxyline & eosin (H&E) staining and UCP-1 immunostaining, respectively. The browning of subcutaneous WAT (sWAT) was determined by H&E staining and UCP-1 immunostaining, and representative pictures are shown (E). The relative expression of genes involved in mitochondrial function (F) and inflammation (G) in sWAT, and the relative mRNA levels of adiponectin in iBAT and sWAT (H) were measured. Fasting plasma adiponectin levels were measured at week 0 and week 16 (I). The intraperitoneal glucose tolerance test (IPGTT) was performed after 6 weeks of the treatment, during which plasma glucose (J) and insulin (K) levels were measured. In addition, the homoeostatic model assessment for insulin resistance (HOMA-IR) was calculated (L). Data are represented as mean ± SEM (A–D, n = 14–16; F–H, n = 8–9; I, n = 10 or 15–16; J–L, n = 7–8). (A–I), data were obtained from the first experiment; (J–L), data were obtained from the second experiment. *P < 0.05; **P < 0.01, ***P < 0.001 (unpaired two-tailed Student’s t-test). Adipoq, adiponectin; CoxIV, mitochondrial cytochrome C oxidase subunit IV; Cox7a1, cytochrome C oxidase polypeptide 7A1; Il1-β, interleukin 1 β; Mfn1/2, mitofusin-1/2; Mttp, microsomal triglyceride transfer protein; Opa1, dynamin-like 120 kDa protein, mitochondrial; Pgc1α, peroxisome proliferator-activated receptor γ coactivator 1-α; Tnfα, tumour necrosis factor α.