PKR1 null mutant mice (PKR1^−/−) exhibit obesity at the later age.

<p>A) Body weight (g), and WAT and pancreas (pancr) weight (g), and food intake (g/24 h) at the age of 40 weeks (*p<0.05, n = 6). B) Representative illustration of abdominal obesity in PKR1^−/− mice. C) Representative illustration of semi-thin sections of adipocyte tissue derived from PKR1^−/− and WT mice. D) Histograms show cell number and diameter differences between these two groups of mice. E) Representative illustration of Ki67 positive cells (green) and dapi positive total cells (blue) in adipose tissue of PKR1^−/− and WT mice. Quantification of Ki67⁺ cell numbers in the high power field (HPF, ×40 objective) (*p<0.05, n = 20 HPF). Flow cytometery for Ki67 positive nuclei in the cells that were prepared from PKR1^−/− and WT type abdominal (epididymal and visceral) WATs tissue after removal of adipocytes. F) Representative illustration and quantification of pref-1⁺/Ki67⁺ positive cells (orange) and dapi positive total cells (blue) in adipose tissue of PKR1^−/− and wild type mice (*p<0.05, n = 20 HPF, ×40 objective). G) qPCR analyses of transcript levels of adipogenic genes of PKR1^−/− mice over WT mice (fold increase). H) Representative illustration of electron microscopic analyses of adipose tissues derived from PKR1^−/− and WT mice demonstrating cytoplasmic lipid droplets (lp) and swollen mitochondria (mtc). Nc: nucleus, bv: blood vessel. I) Illustration and histogram shows the PECAM-1 staining and capillary formation are similar between the adipose tissues of PKR1^−/− and WT mice (p<0.05, n = 20 HPF, ×40 objective). J) Illustration and histogram shows the succinyl dehydrogenase (SDH) staining changes between the adipose tissues of PKR1^−/− and WT mice (*p<0.05, n = 20 HPF, ×40 objective). K) Western blots analyses reveal a high level of HIF-1α levels in PKR1^−/− mice (*p<0.05, n = 3).