Palomino-Schatzlein, M. (Martina)

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    Metabolic footprint of aging and obesity in red blood cells
    (2021) Pineda-Lucena, A. (Antonio); Lamas-Domingo, R. (Rubén); Palomino-Schatzlein, M. (Martina); Domingo-Ortí, I. (Inés); Hernández, C. (Cristina); Ciudin, A. (Andreea); Herance, J.R. (José Raúl)
    Aging is a physiological process whose underlying mechanisms are still largely unknown. The study of the biochemical transformations associated with aging is crucial for understanding this process and could translate into an improvement of the quality of life of the aging population. Red blood cells (RBCs) are the most abundant cells in humans and are involved in essential functions that could undergo different alterations with age. The present study analyzed the metabolic alterations experienced by RBCs during aging, as well as the influence of obesity and gender in this process. To this end, the metabolic profile of 83 samples from healthy and obese patients was obtained by Nuclear Magnetic Resonance spectroscopy. Multivariate statistical analysis revealed differences between Age-1 (<= 45) and Age-2 ( 45) subgroups, as well as between BMI-1 (<30) and BMI2 (>= 30) subgroups, while no differences were associated with gender. A general decrease in the levels of amino acids was detected with age, in addition to metabolic alterations of glycolysis, the pentose phosphate pathway, nucleotide metabolism, glutathione metabolism and the Luebering-Rapoport shunt. Obesity also had an impact on the metabolomics profile of RBCs; sometimes mimicking the alterations induced by aging, while, in other cases, its influence was the opposite, suggesting these changes could counteract the adaptation of the organism to senescence.
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    Body-fat sensor triggers ribosome maturation in the steroidogenic gland to initiate sexual maturation in Drosophila
    (2021) Carranza-Valencia, J. (Juan); Morante, J. (Javier); Hartog, E. (Emily) de; Pineda-Lucena, A. (Antonio); Palomino-Schatzlein, M. (Martina); Juárez-Carreño, S. (Sergio); Romero, A. (Aitana); Ballesta-Illán, E. (Esther); Ferres-Marco, D. (Dolors); Vallejo, D.M. (Diana Marcela); Ramón-Canellas, P. (Pol); Domínguez-Castellano, M. (María); Santoro, R. (Roberto); Payette-Peterson, H. (Hannah)
    Fat stores are critical for reproductive success and may govern maturation initiation. Here, we report that signaling and sensing fat sufficiency for sexual maturation commitment requires the lipid carrier apolipophorin in fat cells and Sema1a in the neuroendocrine prothoracic gland (PG). Larvae lacking apolpp or Sema1a fail to initiate maturation despite accruing sufficient fat stores, and they continue gaining weight until death. Mechanistically, sensing peripheral body-fat levels via the apolipophorin/Sema1a axis regulates endocytosis, endoplasmic reticulum remodeling, and ribosomal maturation for the acquisition of the PG cells' high biosynthetic and secretory capacity. Downstream of apolipophorin/Sema1a, leptin-like upd2 triggers the cessation of feeding and initiates sexual maturation. Human Leptin in the insect PG substitutes for upd2, preventing obesity and triggering maturation downstream of Sema1a. These data show how peripheral fat levels regulate the control of the maturation decision-making process via remodeling of endomembranes and ribosomal biogenesis in gland cells.
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    Mild muscle mitochondrial fusion distress extends drosophila lifespan through an early and systemic metabolome reorganization
    (2021) Roca, M. (Marta); Pineda-Lucena, A. (Antonio); Palomino-Schatzlein, M. (Martina); López-del-Amo, V. (Víctor); Lahoz, A. (Agustín); Galindo, M.I. (Máximo Ibo); Tapia, A. (Andrea)
    In a global aging population, it is important to understand the factors affecting systemic aging and lifespan. Mitohormesis, an adaptive response caused by different insults affecting the mitochondrial network, triggers a response from the nuclear genome inducing several pathways that promote longevity and metabolic health. Understanding the role of mitochondrial function during the aging process could help biomarker identification and the development of novel strategies for healthy aging. Herein, we interfered the muscle expression of the Drosophila genes Marf and Opa1, two genes that encode for proteins promoting mitochondrial fusion, orthologues of human MFN2 and OPA1. Silencing of Marf and Opa1 in muscle increases lifespan, improves locomotor capacities in the long term, and maintains muscular integrity. A metabolomic analysis revealed that muscle down-regulation of Marf and Opa1 promotes a non-autonomous systemic metabolome reorganization, mainly affecting metabolites involved in the energetic homeostasis: carbohydrates, lipids and aminoacids. Interestingly, the differences are consistently more evident in younger flies, implying that there may exist an anticipative adaptation mediating the protective changes at the older age. We demonstrate that mild mitochondrial muscle disturbance plays an important role in Drosophila fitness and reveals metabolic connections between tissues. This study opens new avenues to explore the link of mitochondrial dynamics and inter-organ communication, as well as their relationship with muscle-related pathologies, or in which muscle aging is a risk factor for their appearance. Our results suggest that early intervention in muscle may prevent sarcopenia and promote healthy aging.