TY - JOUR
T1 - Sucrose, glucose and fructose have similar genotoxicity in the rat colon and affect the metabolome
AU - Hansen, M.
AU - Baunsgaard, D.
AU - Autrup, Herman
AU - Vogel, Ulla Birgitte
AU - Møller, Peter
AU - Lindecrona, R.
AU - Wallin, Erik Håkan Richard
AU - Poulsen, Henrik Enghusen
AU - Loft, Steffen
AU - Dragsted, Lars Ove
AU - Hansen, M
AU - Baunsgaard, Dorrit
AU - Autrup, Herman
AU - Vogel, Ulla Birgitte
AU - Møller, P
AU - Lindecrona, R
AU - Wallin, Erik Håkan Richard
AU - Poulsen, H E
AU - Loft, S
AU - Dragsted, L O
N1 - Keywords: Animals; Colon; DNA Damage; Fructose; Glucose; Magnetic Resonance Spectroscopy; Male; Mutagenicity Tests; Mutation; Organ Size; Rats; Sucrose; Sweetening Agents
PY - 2008/2/1
Y1 - 2008/2/1
N2 - We have shown previously that a high sucrose intake increases the background level of somatic mutations and the level of bulky DNA adducts in the colon epithelium of rats. The mechanism may involve either glucose or fructose formed by hydrolysis of sucrose. Male Big Blue rats were fed 30% sucrose, glucose, fructose or potato starch as part of the diet. Mutation rates and bulky DNA adduct levels were determined in colon and liver. The concentration of short-chain fatty acids and pH were determined in caecum, C-peptide was determined in plasma, biomarkers for oxidative damage and proliferation were determined in colon, and a metabonomic analysis was performed in plasma and urine. The sugars increased the mutation rates in colon and the bulky adduct levels in colon and liver to a similar extent. All sugars decrease the caecal concentration of acetic acid and propionic acid. The metabonomic studies indicated disturbed amino acid metabolism and decrease in plasma and urinary acetate as a common feature for all sugars and confirmed triglyceridemic effects of fructose. In conclusion, the genotoxicity may be related to the altered chemical environment in the caecum and thereby also in the colon but we found no related changes in insulin resistance or oxidative stress.
AB - We have shown previously that a high sucrose intake increases the background level of somatic mutations and the level of bulky DNA adducts in the colon epithelium of rats. The mechanism may involve either glucose or fructose formed by hydrolysis of sucrose. Male Big Blue rats were fed 30% sucrose, glucose, fructose or potato starch as part of the diet. Mutation rates and bulky DNA adduct levels were determined in colon and liver. The concentration of short-chain fatty acids and pH were determined in caecum, C-peptide was determined in plasma, biomarkers for oxidative damage and proliferation were determined in colon, and a metabonomic analysis was performed in plasma and urine. The sugars increased the mutation rates in colon and the bulky adduct levels in colon and liver to a similar extent. All sugars decrease the caecal concentration of acetic acid and propionic acid. The metabonomic studies indicated disturbed amino acid metabolism and decrease in plasma and urinary acetate as a common feature for all sugars and confirmed triglyceridemic effects of fructose. In conclusion, the genotoxicity may be related to the altered chemical environment in the caecum and thereby also in the colon but we found no related changes in insulin resistance or oxidative stress.
U2 - 10.1016/j.fct.2007.09.110
DO - 10.1016/j.fct.2007.09.110
M3 - Journal article
C2 - 17988776
VL - 46
SP - 752
EP - 760
JO - Food and Chemical Toxicology
JF - Food and Chemical Toxicology
SN - 0278-6915
IS - 2
ER -