Mazzocco Yanina Luciana, Bergero Gastón, Del Rosso Sebastian, Cejas Gallardo Zoé Magalí, Canalis Alejandra Mariel, Baigorri Ruth Eliana, Mezzano Luciana, Mladin Juan Javier, Díaz-Gerevini Gustavo Tomás, Martínez Benavidez Claudia, Cano Roxana Carolina, Aoki Maria Pilar
Consejo Nacional de Investigaciones Científicas y Técnicas, CONICET, Centro de Investigación en Bioquímica Clínica e Inmunología, CIBICI, Córdoba, Argentina.
Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica, Córdoba, Argentina.
Sci Rep. 2025 Jul 1;15(1):20861. doi: 10.1038/s41598-025-04335-3.
The study of type 2 diabetes mellitus (T2DM) pathophysiology relies mainly on the use of animal models, the most common of which involves the consumption of high-fat diets comprising 60% calories from fat. Although these models reproduce the onset and most complications associated with T2DM, they do not accurately mimic human dietary patterns, as they lack the addition of carbohydrates such as fructose in drinking water. The aim of this study was to develop a mouse model for studying complications related to T2DM. To this end, male C57BL/6 mice were fed a medium-fat diet (34.5% kcal from fat), given 20% fructose in drinking water, and injected with a single low dose of streptozotocin (STZ; 100 mg/kg) (D + T). At week 20, D + T mice exhibited significant weight gain, elevated fasting blood glucose levels, and the development of insulin resistance compared with control mice. Furthermore, the circulating levels of liver enzymes (GPT, GOT, and alkaline phosphatase), total cholesterol, and LDL increased. Multi-organ damage, including reduced pancreatic islet size and number, severe hepatic steatosis, inflammatory infiltration in visceral adipose tissue, and cardiac and renal dysfunction, was also detected. The proposed model replicates T2DM-associated complications in young mice by combining a medium-fat diet with fructose and STZ.
2型糖尿病(T2DM)病理生理学的研究主要依赖于动物模型的使用,其中最常见的是食用高脂肪饮食,这种饮食中60%的热量来自脂肪。尽管这些模型再现了与T2DM相关的发病过程和大多数并发症,但它们不能准确模拟人类的饮食模式,因为它们缺乏在饮用水中添加果糖等碳水化合物。本研究的目的是开发一种用于研究与T2DM相关并发症的小鼠模型。为此,给雄性C57BL/6小鼠喂食中等脂肪饮食(34.5%的热量来自脂肪),在饮用水中给予20%的果糖,并注射单次低剂量链脲佐菌素(STZ;100 mg/kg)(D+T组)。在第20周时,与对照小鼠相比,D+T组小鼠体重显著增加,空腹血糖水平升高,并出现胰岛素抵抗。此外,肝酶(谷丙转氨酶、谷草转氨酶和碱性磷酸酶)、总胆固醇和低密度脂蛋白的循环水平升高。还检测到多器官损伤,包括胰岛大小和数量减少、严重肝脂肪变性、内脏脂肪组织炎症浸润以及心脏和肾脏功能障碍。所提出的模型通过将中等脂肪饮食与果糖和STZ相结合,在年轻小鼠中复制了与T2DM相关的并发症。