Estimation of available energy of dietary fibres by indirect calorimetry in rats.

BACKGROUND: Knowledge of energetic availability of dietary fibres is important for human nutrition. But up to now results are often different and depend on the methods used. Estimation of metabolisable energy of dietary fibres (mainly by balance technique) is a time-consuming procedure and needs special technical effort. AIM OF THE STUDY: Validation of the experimental design for short-term studies by using indirect calorimetry with feeding below maintenance requirement to evaluate the energetic availability of dietary fibres and their influence on absorption velocity of carbohydrates (CHO). METHODS: Energy expenditure and CHO oxidation (including short-chain fatty acids as fermentation products) were estimated in Wistar rats over 23 h after being fed a basal diet for the first day (300 KJ/kg0.75, 20% protein, 3% fat, 77% CHO) followed by supplementation with either microcrystalline cellulose, the soluble rye fibre arabinoxylan, apple pectin, amylomaize starch (with 48% of resistant starch) or gelatinised wheat starch (200 KJ/kg0.75 each) as control for the following days. Energetic availability was determined by comparing the increase of CHO oxidation after addition of gelatinised wheat starch with that of the dietary fibres tested. RESULTS: In comparison to wheat starch (100%), the following energetic availability of the dietary fibres was found: microcrystalline cellulose 14%, arabinoxylan 33%, pectin 39%, amylomaize starch 62%. The time-course of CHO oxidation indicated that microcrystalline cellulose enhances, whereas the soluble rye fibre slows down the velocity of CHO absorption due to the different consistency of the intestinal contents modified by the kind and properties of the used dietary fibres. After intake of arabinoxylan or pectin, CHO oxidation remained at a higher level during the experimental period elucidating an increased activity of fermentation to short-chain fatty acids. CONCLUSIONS: Short-term experiments in rats using indirect calorimetry are a suitable method for comparative estimation of the energetic availability of dietary fibres. Results are partly in agreement with values estimated by long-term in vivo methods.

Changes in energy metabolism and metabolite patterns of obese rats after application of dexfenfluramine.

Serotonergic neuronal networks are important for food intake and body weight regulation. Dexfenfluramine (dF), a serotonin releaser and reuptake inhibitor, was used to investigate changes in food intake, body weight development, energy expenditure, respiratory quotient, and substrate oxidation rates for 12 days. Rats, which had been made obese by early postnatal overfeeding, received an energy-controlled mash diet and water ad lib and were intraperitoneally injected daily with either saline, 5 or 10 mg dF/kg. Compared to controls, food intake, body weight development, and energy expenditure were decreased in a dose-dependent manner, especially during the first 6 days. Lipid oxidation was increased while oxidation of carbohydrates was decreased. Pair-feeding experiments over 2 days revealed that this was not solely a result of diminished food intake but also an additional metabolic effect of dF, different from its anorectic effect. At the end of these experiments, plasma glucose and liver glycogen were unchanged after dF, but plasma free fatty acids were significantly decreased. Insulin-sensitivity was probably improved, indicated by decreased insulin levels and increases in muscle glycogen contents and activities of muscle pyruvate kinase. Liver-glutamine and contents of valine, leucine, and isoleucine in the muscle were significantly decreased after dF-treatment, the latter indicating a diminished proteolysis. The plasma tryptophan/large neutral amino acids ratio of the dF-rats was unchanged but that of the paired-fed rats was changed, despite similar changes in food intake. It is concluded that both increased oxidation of endogenous fat and reduced food intake could mediate the body weight reducing effect of dF.

Energy expenditure and substrate oxidation rates of obese rats during a 12-day treatment with dexfenfluramine.

Serotoninergic neuronal networks are included in regulation and modification of eating behavior and energy metabolism. Dexfenfluramine (dF), a serotonin releaser and reuptake inhibitor, was used to investigate changes in food intake, body weight development, energy expenditure, respiratory quotient, and substrate oxidation rates for 12 days. Rats which had been made obese by postnatal overfeeding received an energy-controlled mash diet and water ad libitum and were intraperitoneally injected with either saline or 5 or 10 mg dF/kg. As compared with controls, food intake and energy expenditure were significantly decreased in a dose-dependent manner, especially during the first 6 days. Lipid oxidation was increased, while the oxidation of carbohydrates was decreased. The body weight was only slightly reduced after 2 days of dF treatment. After 4 days, dF-treated rats resumed body weight, but as compared with controls both dF groups exhibited lower body weights at the end of the experiment. After 12 days the plasma glucose concentration was unchanged, whereas plasma free fatty acids were significantly decreased. Plasma insulin levels were unchanged after dF, but 10 mg dF/kg led to increased muscle and, especially liver glycogen contents, indicating an improved nonoxidative glucose disposal. Muscle pyruvate kinase was slightly but not significantly increased after dF treatment but that of the liver was significantly decreased, indicating a reduced glycolytic activity of the liver. Whereas the renal N excretion was rather decreased, the plasma concentrations of urea, citrulline, arginine, and ornithine were increased, and the liver contents of glutamine and arginine were decreased. Possibly, there is a shift of ammonia removal from glutamine synthesis to production of urea. The sum of all large neutral amino acids in muscle was significantly decreased after dF treatment, indicating a diminished proteolysis. Pair-feeding experiments over 2 days revealed that this was not solely a result of diminished food intake, but also an additional metabolic effect of dF, different from its anorectic effect. It is concluded that both increased oxidation of endogenous fat and reduced food intake could mediate the body weight reducing effect of dF.

Energy metabolism and metabolite patterns of rats after application of dexfenfluramine.

Serotoninergic neuronal networks are important for food intake and body weight regulation. However, the mechanisms by which some metabolic pathways are influenced are rather unclear. Dexfenfluramine (DF), a serotonin releaser and re-uptake inhibitor, was used to investigate changes in food intake, body weight development, energy expenditure, respiratory quotient and substrate oxidation rates for 12 days. Normal rats, receiving an energy-controlled mash diet and water ad libitum were intraperitoneally injected daily with either saline, 1, 2.5, 5 or 10 mg DF/kg. Compared to controls, food intake, body weight development and energy expenditure were decreased in a dose-dependent manner, especially during the first six days. Lipid oxidation was increased while oxidation of carbohydrates was decreased. Pair-feeding experiments over three days revealed that this was a clear pharmacological effect and not simply a result of diminished food intake. At the end of these experiments, plasma glucose and liver and muscle glycogen were unchanged after DF, but isoleucine, leucine and lysine were significantly decreased in plasma and liver. Therefore, the plasma tryptophan/large neutral amino acids ratio was slightly increased. Protein oxidation was unchanged after DF. It is concluded that a prompt decline in energy expenditure with increased fat oxidation rates could mediate the body weight reducing effect of DF.

Postprandial thermogenesis of rats with glutamate induced obesity in relation to energy intake.

Postprandial thermogenesis was estimated in 4-month-old male rats with glutamate induced obesity after being fed with 300, 450 and 600 kJ/kg0.75 of a pellet diet, respectively by indirect calorimetry in computer-controlled open circuit metabolic cages over 8 h. After an intake of 600 kJ/kg0.75 (above the maintenance energy requirement) postprandial thermogenesis was significantly reduced in the obese animals to about 40% of control rats (12.0 versus 31.5 kJ/kg0.75 x 8h). It is concluded that the glutamate obese rat can be accepted as an animal model with impaired facultative thermogenesis, mainly caused by a reduction of sympathetic adrenergic activity.