Departamento de Ciências Biológicas, Instituto de Ciências Exatas e Biológicas, Universidade Federal de Ouro Preto, Morro do Cruzeiro, Ouro Preto, MG 35 400-000, Brazil.
Lipids Health Dis. 2013 Sep 18;12:136. doi: 10.1186/1476-511X-12-136.
The metabolic syndrome (MS) is characterized by variable coexistence of metabolic and pathophysiological alterations which are important risk factors for developing of type II diabetes and/or cardiovascular diseases. Increased of MS patients in worldwide has stimulated the development of experimental models. However, it is still challenging to find an dietetic model that most closely approximates human MS and, in addition, is not yet fully established the effect of different diets of MS in lipid metabolism in rats of different ages. The aim of this study was to evaluate the effect of different diets of MS in lipid metabolism and ectopic fat deposition and define the most appropriate diet for inducing the characteristic disturbances of the human MS in rats of different ages.
Young (4 weeks old) and adult rats (12 weeks old) were given a high-fat (FAT) or high-fructose diet (FRU) for 13 weeks and biochemical, physiological, histological and biometric parameters were evaluated.
In young rats, the FAT diet induced increased mean blood pressure (MAP) and heart rate (HR), body weight after 6 to 10 weeks, and in the 13th week, increased the liver, mesenteric, retroperitoneal and epididymal fat weights, fasting glucose, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and reduced HDL cholesterol; and also induced non-alcoholic fatty liver disease (NAFLD) and renal inflammatory infiltrates. In adult rats, the FRU diet induced transient elevations of MAP and HR in the 6th week, and, at 13 weeks, increased fasting glucose, triglycerides, total cholesterol, AST and ALT; increased liver, kidneys and retroperitoneal fat weights; and induced macrovesicular and microvesicular NAFLD, the presence of fat cells in the kidney, glomerular sclerosis, and liver and kidney inflammation. Additionally, the FAT and FRU diets induced, respectively, increases in liver glycogen in adults and young rats.
Our data show that FRU diet in adult rats causes biggest change on metabolism of serum lipids and lipid accumulation in liver and kidney, while the FAT diet in young rats induces elevation of MAP and HR and higher increased visceral lipid stores, constituting the best nutritional interventions to induce MS in rats.
代谢综合征(MS)的特征是代谢和病理生理改变的不同共存,这些改变是发生 2 型糖尿病和/或心血管疾病的重要危险因素。全球代谢综合征患者的增加刺激了实验模型的发展。然而,找到一种最接近人类 MS 的饮食模型仍然具有挑战性,此外,不同饮食对不同年龄大鼠脂代谢的影响尚未完全确定。本研究旨在评估不同 MS 饮食对脂代谢和异位脂肪沉积的影响,并确定最适合诱导不同年龄大鼠人类 MS 特征性紊乱的饮食。
年轻(4 周龄)和成年(12 周龄)大鼠分别给予高脂肪(FAT)或高果糖(FRU)饮食 13 周,评估生化、生理、组织学和生物计量学参数。
在年轻大鼠中,FAT 饮食诱导平均血压(MAP)和心率(HR)升高,体重在 6 至 10 周后增加,在第 13 周时增加肝脏、肠系膜、腹膜后和附睾脂肪重量,空腹血糖、丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)降低,高密度脂蛋白胆固醇降低;还诱导非酒精性脂肪肝(NAFLD)和肾脏炎症浸润。在成年大鼠中,FRU 饮食在第 6 周诱导 MAP 和 HR 短暂升高,在第 13 周时,空腹血糖、甘油三酯、总胆固醇、AST 和 ALT 升高;肝脏、肾脏和腹膜后脂肪重量增加;诱导大泡性和微泡性 NAFLD、肾脏脂肪细胞、肾小球硬化和肝、肾炎症。此外,FAT 和 FRU 饮食分别诱导成年和幼年大鼠肝脏糖原增加。
我们的数据表明,成年大鼠 FRU 饮食引起的血清脂质代谢和肝脏和肾脏脂质堆积变化最大,而幼年大鼠 FAT 饮食引起的 MAP 和 HR 升高以及内脏脂肪储存增加更大,是诱导大鼠 MS 的最佳营养干预措施。