Bär A, Lina B A, de Groot D M, de Bie B, Appel M J
Bioresco AG, Hauptstrasse 63, Binningen, 4102, Switzerland.
Regul Toxicol Pharmacol. 1999 Apr;29(2 Pt 2):S11-28. doi: 10.1006/rtph.1998.1266.
D-tagatose is an incompletely absorbed ketohexose (stereoisomer of D-fructose) which has potential as an energy-reduced alternative sweetener. In an earlier 90-day toxicity study, rats fed diets with 10, 15 and 20% D-tagatose exhibited increased liver weights, but no histopathological alterations. To determine whether there might be any toxicological relevance to this effect, three studies were conducted in male, adult Sprague-Dawley rats. In the first study, four groups received Purina diet (group A), Purina diet with 20% D-tagatose (group B), SDS diet (group C), or SDS diet with 20% D-tagatose (group D). For groups A and B, the 28-day treatment period was followed by a 14-day recovery period (Purina diet). Food remained available to all animals until the time of sacrifice. Groups of 10 rats were killed on days 14 (groups A and B), 28 (groups A-D), and 42 (groups A and B). Body weights, as well as weights of wet and lyophilized livers, were determined. The lyophilized livers collected on day 28 from groups A and B were analyzed for protein, total lipid, glycogen, DNA, and residual moisture. By day 14, relative wet liver weights had increased by 23% in group B. On day 28, the increase was 38% in group B and 44% in group D. At the end of the recovery period, the increase had diminished to 14% in group B. On day 28, liver glycogen content (in %) was significantly increased, and liver protein, lipid, and DNA contents were significantly decreased in group B compared to group A. Total amounts per liver of protein, total lipid, glycogen, and DNA were significantly increased. In the second study, four groups of 20 rats each received SDS diet with 0, 5, 10, and 20% D-tagatose for 29-31 days. The food was available until the time of sacrifice. At termination, plasma was obtained from 10 rats/group for clinicochemical analyses. Five rats/group were subjected to whole-body perfusion, followed by processing of livers for qualitative and quantitative electron microscopic examination. Livers of 6 rats/group were analyzed for acyl-CoA oxidase and laurate 12-hydroxylase (cytochrome P450 4A1) activity, DNA synthesis (Ki-67 index), and number of nuclei per unit area of tissue. Liver weights were significantly increased in linear relation to the D-tagatose intake. Plasma transaminases (but not glutamyl transferase and alkaline phosphatase) were increased in the high-dose group. Except for glycogen accumulation, no ultrastructural changes were seen on electron microscopic examination of livers of the control and high-dose groups. Morphometric analysis confirmed the increase of glycogen and the absence of alterations of endoplasmatic reticulum, mitochondria, and Golgi apparatus. The Ki-67 index did not differ between the groups. A dose-related decrease of the number of nuclei per unit area signified some hepatocellular hypertrophy. Acyl-CoA oxidase and CYP4A1 activity were significantly increased in the mid- and high-dose groups, but these increases were small and not accompanied by electron-microscopic evidence of peroxisome proliferation. In the third study, four groups received SDS diet (groups A and C) or SDS diet with 5% D-tagatose (groups B and D). All animals were killed on day 28. Groups A and B were fasted for 24 h before sacrifice; groups C and D had food available until sacrifice. Liver weights and liver composition were measured as in Study 1. Relative wet and dry liver weights were increased in response to the treatment in rats killed under the fed condition, but not in rats killed under the fasted condition. The livers of the treated rats (group D) had an increased glycogen content in comparison to the controls (group C). Taken together, these results demonstrate that D-tagatose at dietary levels of 5-20% increases liver glycogen deposition and relative liver weights in nonfasting rats. In fasted rats the 5% dose level is the no-effect level. (ABSTRACT TRUNCATED)
D-塔格糖是一种吸收不完全的酮己糖(D-果糖的立体异构体),有潜力作为一种低能量的替代甜味剂。在早期一项为期90天的毒性研究中,喂食含10%、15%和20%D-塔格糖饲料的大鼠肝脏重量增加,但无组织病理学改变。为确定这种效应是否具有任何毒理学相关性,对成年雄性斯普拉格-道利大鼠进行了三项研究。在第一项研究中,四组大鼠分别接受普瑞纳饲料(A组)、含20%D-塔格糖的普瑞纳饲料(B组)、SDS饲料(C组)或含20%D-塔格糖的SDS饲料(D组)。对于A组和B组,28天的治疗期后接着是14天的恢复期(普瑞纳饲料)。在处死前所有动物均可自由进食。分别在第14天(A组和B组)、第28天(A - D组)和第42天(A组和B组)处死10只大鼠的组。测定体重以及湿肝和冻干肝的重量。对第28天从A组和B组收集的冻干肝进行蛋白质、总脂质、糖原、DNA和残留水分分析。到第14天时,B组相对湿肝重量增加了23%。在第28天,B组增加了38%,D组增加了44%。在恢复期结束时,B组增加幅度降至14%。在第28天,与A组相比,B组肝脏糖原含量(百分比)显著增加,而肝脏蛋白质、脂质和DNA含量显著降低。每只肝脏的蛋白质、总脂质、糖原和DNA总量显著增加。在第二项研究中,四组每组20只大鼠分别接受含0%、5%、10%和20%D-塔格糖的SDS饲料,持续29 - 31天。在处死前动物可自由进食。处死时,从每组10只大鼠获取血浆进行临床化学分析。每组5只大鼠进行全身灌注,随后对肝脏进行定性和定量电子显微镜检查。对每组6只大鼠的肝脏分析酰基辅酶A氧化酶和月桂酸12-羟化酶(细胞色素P450 4A1)活性、DNA合成(Ki-67指数)以及单位组织面积的细胞核数量。肝脏重量随D-塔格糖摄入量呈线性显著增加。高剂量组血浆转氨酶(但谷氨酰转移酶和碱性磷酸酶未升高)升高。除糖原积累外,对照组和高剂量组肝脏的电子显微镜检查未发现超微结构变化。形态计量分析证实糖原增加且内质网、线粒体和高尔基体无改变。各组间Ki-67指数无差异。单位面积细胞核数量的剂量相关减少表明存在一些肝细胞肥大。中剂量组和高剂量组酰基辅酶A氧化酶和CYP4A1活性显著增加,但这些增加幅度较小且无电子显微镜证据表明过氧化物酶体增殖。在第三项研究中,四组大鼠接受SDS饲料(A组和C组)或含5%D-塔格糖的SDS饲料(B组和D组)。所有动物在第28天处死。A组和B组在处死前禁食24小时;C组和D组在处死前可自由进食。如研究1中那样测量肝脏重量和肝脏组成。在喂食状态下处死的大鼠中,处理后相对湿肝和干肝重量增加,但在禁食状态下处死的大鼠中未增加。与对照组(C组)相比,处理组大鼠(D组)肝脏糖原含量增加。综上所述,这些结果表明,在非禁食大鼠中,饮食中5% - 20%的D-塔格糖会增加肝脏糖原沉积和相对肝脏重量。在禁食大鼠中,5%剂量水平为无效应水平。(摘要截断)
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