Laboratório de Plasticidade Morfofuncional, Departamento de Biologia Celular, Setor de Ciências Biológicas, Universidade Federal do Paraná, Curitiba 81530-000, Paraná, Brazil.
Laboratório de Biologia Estrutural e Funcional, Centro de Ciências Biológicas e da Saúde, Universidade Estadual do Oeste do Paraná, Cascavel 85819-110, Paraná, Brazil.
Int J Mol Sci. 2023 Mar 1;24(5):4730. doi: 10.3390/ijms24054730.
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.
谷氨酸单钠细胞毒性诱导下丘脑核肥胖模型在文献中被广泛应用。然而,MSG 会引起持续的肌肉变化,而且缺乏研究旨在阐明损伤不可逆转的机制。本研究旨在探讨 MSG 诱导肥胖对 Wistar 大鼠全身和肌肉参数的早期和慢性影响。动物从 PND01 到 PND05(=24)每天接受皮下 MSG(4mg·g b.w.)或盐水(1.25mg·g b.w.)处理。之后,在 PND15,处死 12 只动物以确定血浆和炎症特征,并评估肌肉损伤。在 PND142,处死其余动物,并获得组织学和生化分析样本。我们的结果表明,早期暴露于 MSG 会降低生长速度、增加肥胖程度,并诱导高胰岛素血症和促炎状态。在成年期,观察到:外周胰岛素抵抗、纤维化增加、氧化应激和肌肉质量减少、氧化能力降低、神经肌肉接头减少、纤维化增加和氧化应激。因此,我们可以得出结论,成年期发现的状况以及肌肉特征难以恢复与早期建立的代谢损伤有关。