Dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk
Abstract Metabolic alterations are related to tumorigenesis and other age-related diseases that are accelerated by “Westernized” diets. In fact, hypercaloric nutrition is associated with an increased incidence of cancers and faster aging. Conversely, lifespan-extending strategies, such as caloric re...
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Nature Portfolio
2025-01-01
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| Series: | Communications Biology |
| Online Access: | https://doi.org/10.1038/s42003-025-07451-y |
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| author | José Xavier do Nascimento Júnior Júlia da Conceição Gomes Ricardo Imbroisi Filho Helber de Maia Valença Jéssica Ristow Branco Amanda Bandeira Araújo Amanda de Oliveira Esteves Moreira Letícia Diniz Crepaldi Larissa Pereira Paixão Alan C. Ochioni Thainá M. Demaria João Gabriel Bernardo Leandro Livia Marques Casanova Mauro Sola-Penna Patricia Zancan |
| author_facet | José Xavier do Nascimento Júnior Júlia da Conceição Gomes Ricardo Imbroisi Filho Helber de Maia Valença Jéssica Ristow Branco Amanda Bandeira Araújo Amanda de Oliveira Esteves Moreira Letícia Diniz Crepaldi Larissa Pereira Paixão Alan C. Ochioni Thainá M. Demaria João Gabriel Bernardo Leandro Livia Marques Casanova Mauro Sola-Penna Patricia Zancan |
| author_sort | José Xavier do Nascimento Júnior |
| collection | DOAJ |
| description | Abstract Metabolic alterations are related to tumorigenesis and other age-related diseases that are accelerated by “Westernized” diets. In fact, hypercaloric nutrition is associated with an increased incidence of cancers and faster aging. Conversely, lifespan-extending strategies, such as caloric restriction, impose beneficial effects on both processes. Here, we investigated the metabolic consequences of hypercaloric-induced aging on tumor growth in female mice. Our findings indicate that a high-fat high-sucrose diet increases tumor growth mainly due to the boosted oxidation of glucose and fatty acids. Consequently, through an increased expression of lactate, IGFBP3, and PTHLH, tumors modulate liver and white adipose tissue metabolism. In the liver, the induced tumor increases fibrosis and accelerates the senescence process, despite the lower systemic pro-inflammatory state. Importantly, the induced tumor induces the wasting and browning of white adipose tissue, thereby reversing diet-induced insulin resistance. Finally, we suggest that tumor growth alters liver-adipose tissue crosstalk that upregulates Fgf21, induces senescence, and negatively modulates lipids and carbohydrates metabolism even in caloric-restricted-fed mice. |
| format | Article |
| id | doaj-art-47fa09ee20bb4544841c2c454afb0e3a |
| institution | Kabale University |
| issn | 2399-3642 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Communications Biology |
| spelling | doaj-art-47fa09ee20bb4544841c2c454afb0e3a2025-01-12T12:35:44ZengNature PortfolioCommunications Biology2399-36422025-01-018111610.1038/s42003-025-07451-yDietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalkJosé Xavier do Nascimento Júnior0Júlia da Conceição Gomes1Ricardo Imbroisi Filho2Helber de Maia Valença3Jéssica Ristow Branco4Amanda Bandeira Araújo5Amanda de Oliveira Esteves Moreira6Letícia Diniz Crepaldi7Larissa Pereira Paixão8Alan C. Ochioni9Thainá M. Demaria10João Gabriel Bernardo Leandro11Livia Marques Casanova12Mauro Sola-Penna13Patricia Zancan14The MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroThe MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de JaneiroAbstract Metabolic alterations are related to tumorigenesis and other age-related diseases that are accelerated by “Westernized” diets. In fact, hypercaloric nutrition is associated with an increased incidence of cancers and faster aging. Conversely, lifespan-extending strategies, such as caloric restriction, impose beneficial effects on both processes. Here, we investigated the metabolic consequences of hypercaloric-induced aging on tumor growth in female mice. Our findings indicate that a high-fat high-sucrose diet increases tumor growth mainly due to the boosted oxidation of glucose and fatty acids. Consequently, through an increased expression of lactate, IGFBP3, and PTHLH, tumors modulate liver and white adipose tissue metabolism. In the liver, the induced tumor increases fibrosis and accelerates the senescence process, despite the lower systemic pro-inflammatory state. Importantly, the induced tumor induces the wasting and browning of white adipose tissue, thereby reversing diet-induced insulin resistance. Finally, we suggest that tumor growth alters liver-adipose tissue crosstalk that upregulates Fgf21, induces senescence, and negatively modulates lipids and carbohydrates metabolism even in caloric-restricted-fed mice.https://doi.org/10.1038/s42003-025-07451-y |
| spellingShingle | José Xavier do Nascimento Júnior Júlia da Conceição Gomes Ricardo Imbroisi Filho Helber de Maia Valença Jéssica Ristow Branco Amanda Bandeira Araújo Amanda de Oliveira Esteves Moreira Letícia Diniz Crepaldi Larissa Pereira Paixão Alan C. Ochioni Thainá M. Demaria João Gabriel Bernardo Leandro Livia Marques Casanova Mauro Sola-Penna Patricia Zancan Dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk Communications Biology |
| title | Dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk |
| title_full | Dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk |
| title_fullStr | Dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk |
| title_full_unstemmed | Dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk |
| title_short | Dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk |
| title_sort | dietary caloric input and tumor growth accelerate senescence and modulate liver and adipose tissue crosstalk |
| url | https://doi.org/10.1038/s42003-025-07451-y |
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