TOXRUN-Toxicology Research Unit, University Institute of Health Sciences, CESPU, CRL, 4585-116, Gandra, Portugal.
Center of Health Technology and Services Research (CINTESIS), Faculty of Medicine of University of Porto, Rua Dr. Plácido da Costa, 4200-450, Porto, Portugal.
Histochem Cell Biol. 2022 Jun;157(6):657-669. doi: 10.1007/s00418-022-02092-2. Epub 2022 Mar 28.
Early-life consumption of high-fat and sugar-rich foods is recognized as a major contributor for the onset of metabolic dysfunction and its related disorders, including diabetes and nonalcoholic fatty liver disease. The lifelong impact of early unhealthy eating habits that start at younger ages remains unclear. Therefore, to better understand the effects of diet, it is essential to evaluate the structural and functional changes induced in metabolic organs and potential mechanisms underlying those changes. To investigate the long-term effects of eating habits, young male rats were exposed to high-sugar and high-energy diets. After 14 weeks, body composition was assessed, and histopathological changes were analyzed in the liver and adipose tissue. Serum biochemical parameters were also determined. Expression of inflammatory markers in the liver was evaluated by immunohistochemistry. Our results revealed that serum levels of glucose, creatinine, aspartate transaminase (AST), alanine transaminase (ALT), and lipid profile were increased in rats red high-sugar and high-energy diets. Histopathological alterations were observed, including abnormal hepatocyte organization and lipid droplet accumulation in the liver, and abnormal structure of adipocytes. In both unhealthy diet groups, hepatic expression of Toll-like receptor 4 (TLR4), cyclooxygenase 2 (COX-2), and E-selectin were increased, as well as a biomarker of oxidative stress. Together, our data demonstrated that unhealthy diets induced functional and structural changes in the metabolic organs, suggesting that proinflammatory and oxidative stress mechanisms trigger the hepatic alterations and metabolic dysfunction.
早期摄入高脂肪和高糖食物被认为是代谢功能障碍及其相关疾病（包括糖尿病和非酒精性脂肪肝疾病）的主要诱因。目前，人们对于年轻时不健康饮食习惯所带来的终身影响还不清楚。因此，为了更好地了解饮食的影响，评估代谢器官的结构和功能变化以及这些变化的潜在机制是至关重要的。为了研究饮食习惯的长期影响，研究人员让年轻雄性大鼠摄入高糖和高能量饮食。14 周后，评估了它们的身体成分，并分析了肝脏和脂肪组织的组织病理学变化。还测定了血清生化参数。通过免疫组织化学评估了肝脏中炎症标志物的表达。研究结果表明，高糖和高能量饮食组大鼠的血清葡萄糖、肌酐、天门冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）和血脂水平升高。还观察到组织病理学改变，包括肝脏中肝细胞组织异常和脂质滴积累，以及脂肪细胞结构异常。在不健康饮食组中，肝脏中 Toll 样受体 4（TLR4）、环氧化酶 2（COX-2）和 E-选择素的表达增加，以及氧化应激的生物标志物也增加。总之，我们的数据表明，不健康的饮食会引起代谢器官的功能和结构变化，提示炎症和氧化应激机制引发了肝脏改变和代谢功能障碍。
