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

• DOI: 10.1038/s42003-025-07451-y
• Publication Date: 2025-01-07T09:52:31Z
• Authors: José Xavier do Na...; Júlia da Conceiçã...; Ricardo Imbroisi ...; Helber de Maia Va...; Jéssica Ristow Br...; Amanda Bandeira A...; Amanda de Oliveir...; Letícia Diniz Cre...; Larissa Pereira P...; Alan C. Ochioni; Thainá M. Demaria; João Gabriel Bern...; Livia Marques Cas...; Mauro Sola-Penna; Patricia Zancan
• Keywords: Senescence; IGFBP3; Crosstalk; Caloric theory; FGF21

Metabolic alterations are related to tumorigenesis and other age-related diseases that accelerated by "Westernized" diets. In fact, hypercaloric nutrition is associated with an increased incidence of cancers faster aging. Conversely, lifespan-extending strategies, such as caloric restriction, impose beneficial effects on both processes. Here, we investigated the metabolic consequences hypercaloric-induced aging tumor growth in female mice. Our findings indicate a high-fat high-sucrose diet increases mainly due boosted oxidation glucose fatty acids. Consequently, through expression lactate, IGFBP3, PTHLH, tumors modulate liver white adipose tissue metabolism. liver, induced fibrosis accelerates senescence process, despite lower systemic pro-inflammatory state. Importantly, induces wasting browning tissue, thereby reversing diet-induced insulin resistance. Finally, suggest alters liver-adipose crosstalk upregulates Fgf21, senescence, negatively modulates lipids carbohydrates metabolism even caloric-restricted-fed Physiological responses different dietary regimens process and, consequently, biology tissues, WAT during growth.