Fig. 6: Tumor growth induces browning and reverts insulin resistance in WAT from HFHS-fed mice. | Communications Biology

Fig. 6: Tumor growth induces browning and reverts insulin resistance in WAT from HFHS-fed mice.

From: Dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk

Fig. 6

Lipid metabolism regulation in gWAT lysates was evaluated by western blot in control (tumor-free) and tumor-bearing samples from CR, Chow, or HFHS-fed mice. A Representative immunoblotting of PGC1α, PPARγ, phosphorylated ACLy (S455) and ACC (S79), and ACLy, ACC, and SCD1 protein expressions in gWAT lysates. Actin was used as a loading control. B–D qPCR analysis of B fatty acid synthase (Fasn), C adipose triglyceride lipase (ATGL, Pnpla2), and D Adiponectin (Adipoq) expression. E, F Browning markers expressions: E PR/SET domain 16 (Prdm16) and F uncoupling protein 1 (Ucp1) mRNA expression. To evaluate the insulin signaling pathway, a proportion of the animals received an insulin shot before euthanasia, as described in the Materials and Methods section. G Representatives immunoblot analysis of insulin receptor β (IRβ) expression, phosphorylated PI3K (Y508), AKT (T308 and S473), mTOR (S2448), and p70S6K (T421/S424) in gWAT lysates. Total proteins or β-actin were used as loading control. Western blot densitometries are in S6. H Model of crosstalk between tumor-liver-WAT in HFHS mice. Created in BioRender. Xavier do Nascimento Júnior, J. (2024) BioRender.com/e43f529. Plotted values are mean ± S.E.M. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. For all panels, a two-way ANOVA was performed, followed by Tukey’s post-test. qPCR reactions for each sample were conducted in duplicate and all tissue samples were analyzed.

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