Fig. 1 | Nature Communications

Fig. 1

From: An inflammatory-CCRK circuitry drives mTORC1-dependent metabolic and immunosuppressive reprogramming in obesity-associated hepatocellular carcinoma

Fig. 1

Dietary obesity-induced CCRK over-expression promotes lipid accumulation, glucose intolerance, and liver damages in male mice. a Schematic diagram of NASH mouse model with different diets (CD chow diet, HFHC high-fat high-carbohydrate) and lentivirus-mediated Ccrk knockdown (CD+shCtrl, n=8; HFHC+shCtrl, n = 15; HFHC+shCcrk, n = 15). b Body weight, c blood triglyceride and non-esterified fatty acid (NEFA) levels in mice were increased by HFHC at 28 weeks, which could be reduced by Ccrk knockdown. d, e CCRK impaired insulin sensitivity in mice. d Intraperitoneal glucose tolerance test (IPGTT) and e intraperitoneal insulin tolerance test (IPITT) were performed on CD-fed and HFHC-fed mice, blood glucose was measured at indicated time points after glucose or insulin injection (left), and area under the curve (AUC) is shown in a bar chart (right). f CCRK protein expression was induced by HFHC in mouse livers, which could be reduced by shRNA-mediated knockdown. Quantification of CCRK protein levels (relative to β-actin) is shown in a bar chart (bottom). g Representative pictures of Oil Red O, ballooning degeneration, and spotty necrosis of liver tissues in different groups (image magnification = ×200 or ×400, scale bar = 20 μm). h, i Quantifications of Oil Red O, ballooning degeneration and j scoring of spotty necrosis showed increased lipid accumulation, ballooning and spotty necrosis in HFHC-fed mice, which were reduced by Ccrk knockdown. Data are presented as mean ± SD. *p < 0.05; **p < 0.01; and ***p < 0.001 as calculated by unpaired two-tailed Student’s t-test (b), one-way ANOVA followed by Bonferroni post-hoc test (cf, h, j), two-way ANOVA followed by Bonferroni post-hoc tests (d, e), and Chi-square test (i)

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