An Early and Sustained Inflammatory State Induces Muscle Changes and Establishes Obesogenic Characteristics in Wistar Rats Exposed to the MSG-Induced Obesity Model

The model of obesity induced by monosodium glutamate cytotoxicity on the hypothalamic nuclei is widely used in the literature. However, MSG promotes persistent muscle changes and there is a significant lack of studies that seek to elucidate the mechanisms by which damage refractory to reversal is es...

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Published in:International journal of molecular sciences Vol. 24; no. 5; p. 4730
Main Authors: Zazula, Matheus Felipe, Saraiva, Diego Francis, Theodoro, João Lucas, Maciel, Mônica, Sepulveda, Eliel Vieira Dos Santos, Zanardini de Andrade, Bárbara, Boaretto, Mariana Laís, Maciel, Jhyslayne Ignácia Hoff Nunes, Bronczek, Gabriela Alves, Soares, Gabriela Moreira, Sagae Schneider, Sara Cristina, Bertolini, Gladson Ricardo Flor, Torrejais, Márcia Miranda, Ribeiro, Lucinéia Fátima Chasko, Fernandes, Luiz Claudio, Naliwaiko, Katya
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 01-03-2023
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Summary:The model of obesity induced by monosodium glutamate cytotoxicity on the hypothalamic nuclei is widely used in the literature. However, MSG promotes persistent muscle changes and there is a significant lack of studies that seek to elucidate the mechanisms by which damage refractory to reversal is established. This study aimed to investigate the early and chronic effects of MSG induction of obesity upon systemic and muscular parameters of Wistar rats. The animals were exposed to MSG subcutaneously (4 mg·g b.w.) or saline (1.25 mg·g b.w.) daily from PND01 to PND05 ( = 24). Afterwards, in PND15, 12 animals were euthanized to determine the plasma and inflammatory profile and to assess muscle damage. In PND142, the remaining animals were euthanized, and samples for histological and biochemical analyses were obtained. Our results suggest that early exposure to MSG reduced growth, increased adiposity, and inducted hyperinsulinemia and a pro-inflammatory scenario. In adulthood, the following were observed: peripheral insulin resistance, increased fibrosis, oxidative distress, and a reduction in muscle mass, oxidative capacity, and neuromuscular junctions, increased fibrosis, and oxidative distress. Thus, we can conclude that the condition found in adult life and the difficulty restoring in the muscle profile is related to the metabolic damage established early on.
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ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms24054730