Touceda Vanessa, Cacciagiú Leonardo, Moglie Ignacio Barbani, Wiszniewski Morena, Sanchez Valeria, De Lucca Romina C, Vidal Agustina, Finocchietto Paola, Friedman Silvia, González Germán E, Miksztowicz Verónica
Laboratorio de Patología Cardiovascular Experimental e Hipertensión Arterial, Instituto de Investigaciones Biomédicas (UCA-CONICET), Facultad de Medicina, Pontificia Universidad Católica Argentina, Buenos Aires C1107AFF, Argentina.
Unidad de Investigación en Bioquímica Traslacional y Metabolismo (UBiTyM), Cátedra de Bioquímica General y Bucal, Facultad de Odontología, Universidad de Buenos Aires, Buenos Aires C1107AFF, Argentina.
Biology (Basel). 2025 Sep 2;14(9):1171. doi: 10.3390/biology14091171.
High salt (NaCl) intake has been associated with visceral adipose tissue (VAT) dysfunction independently of its impact on blood pressure. Liraglutide (LGT), a GLP-1 agonist, could be a potential therapeutic option. We investigated the impact of a chronic high-salt diet (HSD) on VAT homeostasis and evaluated the potential protective effects of LGT, a GLP-1 receptor agonist. Male C57BL/6 mice were fed a standard diet (Control, C) or 8% NaCl (HSD) for 15 weeks and subsequently treated with LGT or vehicle for 5 weeks. In VAT, histological characteristics, collagen deposition, vascular density, mitochondrial dynamics, oxidative stress, and adipokine expression were evaluated. The HSD significantly decreased body weight, VAT mass, and adipocyte size ( < 0.05). Moreover, it impaired vascular density and induced interstitial fibrosis ( < 0.01). LGT treatment improved vascularization and VEGF expression and reduced fibrosis ( < 0.05 vs. the HSD). The HSD induced oxidative stress and mitochondrial fragmentation, which were attenuated by LGT ( < 0.001). Leptin levels were elevated by the HSD ( < 0.05) and normalized with LGT, while adiponectin levels increased. In conclusion, excessive salt consumption induces structural and metabolic dysfunction in VAT. LGT therapy mitigates several of these adverse effects, supporting its potential as a novel strategy for managing salt-sensitive adipose tissue dysfunction.
高盐（氯化钠）摄入已被证明与内脏脂肪组织（VAT）功能障碍有关，且独立于其对血压的影响。利拉鲁肽（LGT），一种胰高血糖素样肽-1（GLP-1）激动剂，可能是一种潜在的治疗选择。我们研究了慢性高盐饮食（HSD）对VAT稳态的影响，并评估了GLP-1受体激动剂LGT的潜在保护作用。雄性C57BL/6小鼠被喂食标准饮食（对照组，C）或8%氯化钠（HSD）15周，随后用LGT或赋形剂治疗5周。对VAT的组织学特征、胶原蛋白沉积、血管密度、线粒体动力学、氧化应激和脂肪因子表达进行了评估。HSD显著降低了体重、VAT质量和脂肪细胞大小（<0.05）。此外，它损害了血管密度并诱导了间质纤维化（<0.01）。LGT治疗改善了血管生成和血管内皮生长因子（VEGF）表达，并减少了纤维化（与HSD相比，<0.05）。HSD诱导了氧化应激和线粒体碎片化，而LGT减轻了这些变化（<0.001）。HSD使瘦素水平升高（<0.05），LGT使其恢复正常，而脂联素水平升高。总之，过量的盐摄入会导致VAT的结构和代谢功能障碍。LGT治疗减轻了其中的一些不良反应，支持其作为管理盐敏感性脂肪组织功能障碍的新策略的潜力。
