Agheli N, Kabir M, Berni-Canani S, Petitjean E, Boussairi A, Luo J, Bornet F, Slama G, Rizkalla S W
Department of Diabetes and INSERM U341, Hôtel-Dieu Hospital, 75004 Paris, France.
J Nutr. 1998 Aug;128(8):1283-8. doi: 10.1093/jn/128.8.1283.
The aim of this study was to evaluate the chronic effects of a short-chain fructo-oligosaccharide (FOS)-containing diet on plasma lipids and the activity of fatty acid synthase (FAS) in insulin-resistant rats. Normal male Sprague-Dawley rats, 5 wk old, were randomly assigned to two groups and fed either a sucrose-rich diet (S, 575 g sucrose /kg diet and 140 g lipids/kg diet) or a sucrose-rich diet supplemented with 10 g/100 g short-chain fructo-oligosaccharides (S/FOS). A third reference group (R) was fed a standard nonpurified diet (g/kg, 575 g starch, 50 g fat). After 3 wk the sucrose-fed rats (compared with the R group) were characterized by the following: 1) higher insulin responses after a glucose challenge (P < 0.05); 2) heavier liver (P < 0.001) and retroperitoneal adipose tissue (P < 0.01); 3) hypertriglyceridemia (P < 0.0001) and higher plasma free fatty acids (P < 0.0001); and 4) higher fatty acid synthase activity in the liver but a low activity in the adipose tissue (P < 0.001). The addition of FOS to the diet resulted in 11% lower liver weight than in the S group (P < 0.05) and tended to result in lower adipose tissue weight (P < 0.11). Plasma triglycerides and plasma free fatty acids were lower in S/FOS- than in S-fed rats (P < 0.05). Chylomicrons + VLDL, and intermediate density lipoprotein (IDL) concentrations did not differ between groups, nor was plasma cholesterol influenced by diet. Hepatic FAS activity was lower in S/FOS-fed rats than in the S-fed rats (P < 0.05). In adipose tissue, however, this activity tended to be greater in rats fed S/FOS than in rats fed the S diet (P < 0.07). In conclusion, in a rat model of diet-induced (57.5% sucrose and 14% lipids) insulin resistance, the addition of short-chain FOS prevented some lipid disorders, lowered fatty acid synthase activity in the liver and tended to raise this activity in the adipose tissue. Short-chain FOS, in addition to being a nondigestible sweetener with good bulking capacity, might be useful in the treatment of insulin resistance and hyperlipidemia.
本研究旨在评估含短链低聚果糖(FOS)饮食对胰岛素抵抗大鼠血浆脂质及脂肪酸合酶(FAS)活性的慢性影响。将5周龄的正常雄性斯普拉格 - 道利大鼠随机分为两组,分别给予富含蔗糖的饮食(S组,575克蔗糖/千克饮食和140克脂质/千克饮食)或补充10克/100克短链低聚果糖的富含蔗糖饮食(S/FOS组)。第三组作为参照组(R组),给予标准非纯化饮食(克/千克,575克淀粉,50克脂肪)。3周后,蔗糖喂养的大鼠(与R组相比)表现出以下特征:1)葡萄糖激发后胰岛素反应更高(P < 0.05);2)肝脏更重(P < 0.001)和腹膜后脂肪组织更重(P < 0.01);3)高甘油三酯血症(P < 0.0001)和血浆游离脂肪酸水平更高(P < 0.0001);4)肝脏中脂肪酸合酶活性更高,但脂肪组织中活性较低(P < 0.001)。在饮食中添加FOS使肝脏重量比S组低11%(P < 0.05),且有使脂肪组织重量降低的趋势(P < 0.11)。S/FOS组大鼠的血浆甘油三酯和血浆游离脂肪酸水平低于S组大鼠(P < 0.05)。乳糜微粒+极低密度脂蛋白(VLDL)和中间密度脂蛋白(IDL)浓度在各组间无差异,饮食也未影响血浆胆固醇水平。S/FOS组大鼠肝脏中的FAS活性低于S组大鼠(P < 0.05)。然而,在脂肪组织中,S/FOS组大鼠的该活性有高于S组大鼠的趋势(P < 0.07)。总之,在饮食诱导的(57.5%蔗糖和14%脂质)胰岛素抵抗大鼠模型中,添加短链FOS可预防一些脂质紊乱,降低肝脏中脂肪酸合酶活性,并使脂肪组织中的该活性有升高趋势。短链FOS除了是一种具有良好填充能力的不可消化甜味剂外,可能对胰岛素抵抗和高脂血症的治疗有用。