The use of an amino acid as a precursor of a bioactive metabolite in combatting an infectious disease: The efficacy of a tryptophan-enriched diet in the treatment of leprosy.

Deoxyfructosylserotonin (DFS), a stable derivative of serotonin, was shown to have an anti-leprosy effect (Mester and Antia). Therefore, a tryptophan-enriched food (NAL) was devised to increase the concentration of free tryptophan as serotonin precursor in blood.32 multibacillary lepromatous leprosy patients were divided in 3 groups receiving: 1) MDT (multi-drug therapy, control - 8 patients), 2) NAL (50 g/day - 13 patients) and 3) NAL + 1/2 MDT (11 patients). The clinical improvement (clinical score) was 24.2% for 1), 19.9% for 2) and 30.4% for 3). The loss of viability of theM. leprae bacilli in the mouse foot-pad test was 66% for 1), 75% for 2) and 70% for 3). The improvement by serodiagnosis (ELISA) was 19.4% for 1), 25.1% for 2) and 23.3% for 3).These preliminary results (6 months) suggest that the NAL-food is efficient against leprosy and apparently not very different from the control MDT in that respect.

Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man.

The metabolic balance method was performed on three men to investigate the fate of large excesses of carbohydrate. Glycogen stores, which were first depleted by diet (3 d, 8.35 +/- 0.27 MJ [1994 +/- 65 kcal] decreasing to 5.70 +/- 1.03 MJ [1361 +/- 247 kcal], 15% protein, 75% fat, 10% carbohydrate) and exercise, were repleted during 7 d carbohydrate overfeeding (11% protein, 3% fat, and 86% carbohydrate) providing 15.25 +/- 1.10 MJ (3642 +/- 263 kcal) on the first day, increasing progressively to 20.64 +/- 1.30 MJ (4930 +/- 311 kcal) on the last day of overfeeding. Glycogen depletion was again accomplished with 2 d of carbohydrate restriction (2.52 MJ/d [602 kcal/d], 85% protein, and 15% fat). Glycogen storage capacity in man is approximately 15 g/kg body weight and can accommodate a gain of approximately 500 g before net lipid synthesis contributes to increasing body fat mass. When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate-oxidation rates and substantial de novo lipid synthesis (150 g lipid/d using approximately 475 g CHO/d) without postabsorptive hyperglycemia.

Energy/protein interrelation in experimental food restriction.

The effects of restriction of energy and/or protein intake were studied in rats during pregnancy and lactation and in adult mice. Three approaches were employed: sucrose stimulus-induced reduction in the intake of an adequate diet given simultaneously; restriction of intake of a complete food by 30% of ad libitum levels and selective protein or energy restriction of a high protein diet and a non-protein diet. Casein or lactalbumin was the protein source. During lactation the rat's natural food intake regulatory mechanism prevailed over the sucrose stimulus. Restricted intake of the complete food and selective restriction of protein or energy, variably influenced gestational and lactational performance and weight of young at weaning. A distinct regulation in the intake of protein and energy during pregnancy and lactation was observed on selective energy or protein restriction. Restricted feeding of the composite diet starting in the second year of life, to mice previously ad libitum fed a lab chow of constant composition, promoted the highest survival rate.

Caffeine and coffee: their influence on metabolic rate and substrate utilization in normal weight and obese individuals.

A series of four trials was carried out to investigate the effects of caffeine and coffee on the metabolic rate and substrate utilization in normal weight and obese individuals. In the first trial 8 mg/kg caffeine was compared with a placebo in normal weight subjects. Metabolic rate increased significantly during the 3 hr after caffeine ingestion. While plasma glucose, insulin, and carbohydrate oxidation did not change significantly, plasma free fatty acid levels rose from 432 +/- 31 to 848 +/- 135 muEq/liter and were accompanied by significant increases in fat oxidation during the last hour of the test. In the second and third trials the effects of coffee providing 4 mg/kg caffeine were studied in control and obese subjects. Metabolic rate increased significantly in both groups; however, significant increases in fat oxidation were only observed in the control group. Plasma free fatty acids did not change in the obese. In the fourth trial, coffee was taken with a 3080 kJ meal. The thermic effect of the meal was significantly greater after coffee than after decaffeinated coffee and again fat oxidation was significantly greater after coffee. In conclusion caffeine/coffee stimulates the metabolic rate in both control and obese individuals; however, this is accompanied by greater oxidation of fat in normal weight subjects.

Biochemical changes in a 100 km run: free amino acids, urea, and creatinine.

Free amino acids, urea, and creatinine were analyzed in venous blood and urine of 11 trained (28--81 years old) male subjects before, immediately after, and 1 day after a 100 km running competition. The urinary excretion per minute of all amino acids was lowered after the contest. The renal clearance of creatinine was reduced from 116 to 60 ml/min and the clearance of most amino acids was reduced to a similar extent. However, for the amino acids with a resting clearance under 1 ml/min (x), a high relative clearance ratio (y in % of x) was seen post-exercise: y = -92.3 (log10 x) +23.1, r = -0.83, showing that their high reabsorption capacity had been impaired. Serum concentrations of most free amino acids, including the branched-chain amino acids and alanine, were reduced to 35--85% of the pre-race values. The sulfur amino acids were elevated either at the end of (cystine, to 180%) or 24 h after (methionine, to 155%) the race. Urea production increased by 44% while creatinine production tended to decrease. The production of 3-methylhistidine remained unchanged. These findings are compatible with a stimulation of gluconegenesis at the expense of the amino acid pool without induction of muscle protein catabolism.