Oliveira Daiane Teixeira de, Fernandes Isabela da Costa, Sousa Graziele Galdino de, Santos Talita Adriana Pereira Dos, Paiva Nívia Carolina Nogueira de, Carneiro Cláudia Martins, Evangelista Elísio Alberto, Barboza Natália Rocha, Guerra-Sá Renata
Programa de Pós-graduação em Ciências Farmacêuticas, Escola de Farmácia, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brasil.
Núcleo de Pesquisas em Ciências Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brasil.
Arch Endocrinol Metab. 2020 Feb;64(1):71-81. doi: 10.20945/2359-3997000000199. Epub 2020 Mar 13.
Objective Provide a comprehensive view of the events surrounding the sugar consumption, under conditions of energy equivalence; through the analysis of behavioral aspects of intake, and of biochemical, metabolic and physiological parameters, as well as the effect of this nutrient on the plasticity of adipose tissue. Materials and methods Newly weaned male Wistar rats were classified in two groups and subjected to the following normocaloric diets: standard chow diet or to high-sugar diet (HSD) ad libitum for 18 weeks. Results The animals submitted to the HSD were associated with a lower caloric intake during the 18 weeks of experimentation. However, the HSD induced a significant increase in body weight, white adipose tissue weight, adiposity index, Lee index, and the levels of triglycerides and very low-density lipoprotein in the serum. In addition, it induced glucose intolerance, insulin resistance and compensatory increase of insulin secretion by pancreatic β-cells. Also increased heart rate and induced hyperplasia, and hypertrophy of retroperitoneal visceral adipose tissue. In the liver, the HSD was associated with increased hepatic lipid content (i.e., triglycerides and cholesterol) and hepatomegaly. Conclusion The post-weaning consumption of HSD induces an adaptive response in metabolism; however, such an event is not enough to reverse the homeostatic imbalance triggered by the chronic consumption of this macronutrient, leading to the development of metabolic syndrome, irrespective of caloric intake. These findings corroborate recent evidence indicating that sugar is a direct contributor to metabolic diseases independent of a positive energy balance. Arch Endocrinol Metab. 2020;64(1):71-81.
目的 在能量等效的条件下，通过分析糖摄入的行为方面、生化、代谢和生理参数，以及这种营养素对脂肪组织可塑性的影响，全面了解围绕糖消耗的相关事件。材料与方法 将刚断奶的雄性Wistar大鼠分为两组，给予以下等热量饮食：标准饲料或随意进食高糖饮食（HSD）18周。结果 在18周的实验期间，接受HSD的动物热量摄入较低。然而，HSD导致体重、白色脂肪组织重量、肥胖指数、李氏指数以及血清甘油三酯和极低密度脂蛋白水平显著增加。此外，它还导致葡萄糖耐量异常、胰岛素抵抗以及胰腺β细胞胰岛素分泌的代偿性增加。还使心率加快，并导致腹膜后内脏脂肪组织增生和肥大。在肝脏中，HSD与肝脏脂质含量（即甘油三酯和胆固醇）增加以及肝脏肿大有关。结论 断奶后食用HSD会引发代谢方面的适应性反应；然而，这一事件不足以逆转由长期食用这种宏量营养素引发的体内平衡失衡，从而导致代谢综合征的发展，无论热量摄入如何。这些发现证实了最近的证据，表明糖是代谢疾病的直接促成因素，与正能量平衡无关。《内分泌与代谢档案》。2020年；64(1):71 - 81。
