Dupas Julie, Feray Annie, Goanvec Christelle, Guernec Anthony, Samson Nolwenn, Bougaran Pauline, Guerrero François, Mansourati Jacques
EA 4324-Optimisation des Régulations Physiologiques, Institut Brestois Santé Agro Matières, Université de Bretagne Occidentale, 6 avenue Victor Le Gorgeu, 29238 Brest Cedex 3, France.
UFR Sciences du Sport et de l'Education, 20 avenue Victor Le Gorgeu, 29238 Brest Cedex 3, France.
Biomed Res Int. 2017;2017:2494067. doi: 10.1155/2017/2494067. Epub 2017 Apr 11.
Increased sugar consumption, especially fructose, is strongly related to the development of type 2 diabetes (T2D) and metabolic syndrome. The aim of this study was to evaluate long term effects of fructose supplementation on Wistar rats. Three-week-old male rats were randomly divided into 2 groups: control (C; = 14) and fructose fed (FF; = 18), with a fructose enriched drink (20-25% w/v fructose in water) for 21 weeks. Systolic blood pressure, fasting glycemia, and bodyweight were regularly measured. Glucose tolerance was evaluated three times using an oral glucose tolerance test. Insulin levels were measured concomitantly and insulin resistance markers were evaluated (HOMA 2-IR, Insulin Sensitivity Index for glycemia (ISI-gly)). Lipids profile was evaluated on plasma. This fructose supplementation resulted in the early induction of hypertension without renal failure (stable theoretical creatinine clearance) and in the progressive development of fasting hyperglycemia and insulin resistance (higher HOMA 2-IR, lower ISI-gly) without modification of glucose tolerance. FF rats presented dyslipidemia (higher plasma triglycerides) and early sign of liver malfunction (higher liver weight). Although abdominal fat weight was increased in FF rats, no significant overweight was found. In Wistar rats, 21 weeks of fructose supplementation induced a metabolic syndrome (hypertension, insulin resistance, and dyslipidemia) but not T2D.
糖摄入量增加,尤其是果糖,与2型糖尿病(T2D)和代谢综合征的发生密切相关。本研究的目的是评估补充果糖对Wistar大鼠的长期影响。将三周龄雄性大鼠随机分为两组:对照组(C;n = 14)和果糖喂养组(FF;n = 18),用富含果糖的饮料(水中含20 - 25% w/v果糖)喂养21周。定期测量收缩压、空腹血糖和体重。使用口服葡萄糖耐量试验三次评估葡萄糖耐量。同时测量胰岛素水平并评估胰岛素抵抗标志物(HOMA 2-IR,血糖胰岛素敏感性指数(ISI-gly))。评估血浆脂质谱。这种果糖补充导致早期无肾衰竭(稳定的理论肌酐清除率)的高血压诱导以及空腹高血糖和胰岛素抵抗的逐渐发展(更高的HOMA 2-IR,更低的ISI-gly),而葡萄糖耐量无改变。FF大鼠出现血脂异常(更高的血浆甘油三酯)和肝功能异常的早期迹象(更高的肝脏重量)。尽管FF大鼠腹部脂肪重量增加,但未发现明显超重。在Wistar大鼠中,21周的果糖补充诱导了代谢综合征(高血压、胰岛素抵抗和血脂异常)但未诱导T2D。