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Titolo:
Effect of D-tagatose on liver weight and glycogen content of rats
Autore:
Bar, A; Lina, BAR; de Groot, DMG; de Bie, B; Appel, MJ;
Indirizzi:
Bioresco AG, CH-4102 Binningen, Switzerland Bioresco AG Binningen Switzerland CH-4102 CH-4102 Binningen, Switzerland TNO, Nutr & Food Res Inst, Div Toxicol, NL-3700 AJ Zeist, Netherlands TNOZeist Netherlands NL-3700 AJ Toxicol, NL-3700 AJ Zeist, Netherlands
Titolo Testata:
REGULATORY TOXICOLOGY AND PHARMACOLOGY
fascicolo: 2, volume: 29, anno: 1999,
parte:, 2 supplemento:, S
pagine: S11 - S28
SICI:
0273-2300(199904)29:2<S11:EODOLW>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEREDITARY FRUCTOSE INTOLERANCE; MICROSOMAL CYTOCHROME-P-452; PEROXISOME PROLIFERATION; PHOSPHATASE-ACTIVITY; CELL-PROLIFERATION; STORAGE DISEASE; HEPATOCYTES; GLUCOKINASE; DEFICIENCY; INDUCTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
71
Recensione:
Indirizzi per estratti:
Indirizzo: Bar, A Bioresco AG, Hauptstr 63, CH-4102 Binningen, Switzerland Bioresco AG Hauptstr 63 Binningen Switzerland CH-4102 Switzerland
Citazione:
A. Bar et al., "Effect of D-tagatose on liver weight and glycogen content of rats", REGUL TOX P, 29(2), 1999, pp. S11-S28

Abstract

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 with20% 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 followedby 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, andDNA 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 glutamyltransferase 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 hepatocellularhypertrophy. 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 SDSdiet 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 hadfood available until sacrifice. Liver weights and liver composition were measured as in Study 1. Relative wet and dry liver weights were increased inresponse 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. At the higher dose levels, the increased glycogen deposition induced minimal hypertrophy and some compensatory growth which reached completion beforethe end of the 28-day treatment period. It is concluded that the liver enlargement seen in response to the consumption of D-tagatose is a physiological response to the treatment-induced increased glycogen deposition. No hepatocellular growth was seen at the 5% dietary level of D-tagatose (corresponding to an intake of 2.6-2.8 g/kg body wt), suggesting that the increase ofliver glycogen at this dose remained within normal limits. (C) 1999 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 15:57:05