ABSTRACT
The intake of large amounts of lactulose and other non-digestible oligosaccharides can cause diarrhoea in rats and humans. The purpose of our study was to estimate tendency and scope of changes in caecum development, amount and composition of caecal digesta and activity of caecal microbial enzymes under the influence of lactulose-rich diet evoking or not evoking diarrhoea. Male Wistar rats were fed on 8%-lactulose diet for 4 weeks. Feeding with lactulose induced enlargement of the caecum (digesta and wall) compared to the control group. However, the hypertrophy of the caecal wall in rats with diarrhoea was less than in these without that ailment. Dry matter of caecal digesta was significantly decreased in rats with diarrhoea. Diarrhoea lowered concentrations of enzymatic protein and short-chain fatty acids in the caecum, and the activity of bacterial beta-glucuronidase, alpha- and beta-galactosidase, alpha- and beta-glucosidase in caecal digesta, compared to rats without diarrhoea. The ammonia concentration in the caecum was enhanced by diarrhoea symptoms. Occurrence of diarrhoea significantly deteriorated functioning of the caecal ecosystem what in turn limited potential benefits of diet supplementation with lactulose.
Subject(s)
Cecum/drug effects , Cecum/growth & development , Diarrhea/chemically induced , Lactulose/toxicity , Ammonia/metabolism , Animals , Cecum/metabolism , Cecum/microbiology , Dietary Carbohydrates/toxicity , Fatty Acids, Volatile/metabolism , Glucuronidase/metabolism , Humans , Male , Rats , Rats, WistarABSTRACT
Lactulose has profound health benefits by way of increasing bifidobacterial flora in the intestine of infants thereby protecting them against enteric infection, constipation and systemic encephalopathy. In the present study to assess the sub chronic toxicity of lactulose syrup, the rats were fed on a basal feed supplemented with lactulose syrup at 0.5, 1.0, 2.0 and 5.0% for a period of 21 weeks. Monitoring of food consumption, gain in body weight and physical observations did not reveal any treatment-related toxicity in any of the group of rats. Terminal autopsy also did not reveal any signs of toxicity. Further, no significant alterations in relative organ weight, serum biochemistry and urinalysis were observed up to 1% lactulose supplementation level. The results suggest that supplementation of lactulose in the diet does not produce any toxicity at the doses tested.
Subject(s)
Lactulose/toxicity , Administration, Oral , Animals , Blood Cell Count , Blood Chemical Analysis , Dietary Supplements/toxicity , Dose-Response Relationship, Drug , Lactulose/administration & dosage , Male , Organ Size/drug effects , Rats , Rats, Wistar , Safety , Weight Gain/drug effectsABSTRACT
We sought to determine, in a piglet model, whether severe sugar malabsorption causes colonic injury or inflammation. Twenty-four piglets were randomized to receive either control formula (CON) or CON supplemented with lactulose (LAC) (N = 12 each group). After seven days, inflammation, apoptosis, and crypt cell proliferation were assessed in the proximal colon (cecum). Lactulose feeding caused persistent diarrhea. In both groups, breath H2 concentration was low, suggesting no increased fermentation in the LAC group. Weight gain/volume formula intake was identical in the CON and LAC groups (0.09+/-0.13 and 0.09+/-0.11 g/ml) respectively. Injury to the colon did not occur, but inflammation of the colon (scale 0-5) was greater in LAC (score of 1.5+/-1.38) than in CON (0.42+/-0.79; P<0.05). Cell proliferation at the basal 40% of the crypt was 92% increased in CON (labeling index 22.8+/-9.9 vs. 11.9+/-2.8; P<0.05). We conclude that persistent feeding during severe sugar malabsorption permits weight gain but may cause colitis.
