The objective of this study was to determine the effects of feeding on the excretory nitrogen (N) metabolism of the giant mudskipper, Periophthalmodon schlosseri, with special emphasis on the role of urea synthesis in ammonia detoxification. The ammonia and urea excretion rates of P. schlosseri increased 1.70- and 1.92-fold, respectively, within the first 3 h after feeding on guppies. Simultaneously, there were significant decreases in ammonia levels in the plasma and the brain, and in urea contents in the muscle and liver, of P. schlosseri at 3 h post-feeding. Thus, it can be concluded that P. schlosseri was capable of unloading ammonia originally present in some of its tissues in anticipation of ammonia released from the catabolism of excess amino acids after feeding. Subsequently, there were significant increases in urea content in the muscle, liver and plasma (1.39-, 2.17- and 1.62-fold, respectively) at 6 h post-feeding, and the rate of urea synthesis apparently increased 5.8-fold between 3 h and 6 h. Increased urea synthesis might have occurred in the liver of P. schlosseri because the greatest increase in urea content was observed therein. The excess urea accumulated in the body at 6 h was completely excreted between 6 and 12 h, and the percentage of waste-N excreted as urea-N increased significantly to 26% during this period, but never exceeded 50%, the criterion for ureotely, meaning that P. schlosseri remained ammonotelic after feeding. By 24 h, 62.7% of the N ingested by P. schlosseri was excreted, out of which 22.6% was excreted as urea-N. This is the first report on the involvement of increased urea synthesis and excretion in defense against ammonia toxicity in the giant mudskipper, and our results suggest that an ample supply of energy resources, e.g. after feeding, is a prerequisite for the induction of urea synthesis. Together, increases in nitrogenous excretion and urea synthesis after feeding effectively prevented a postprandial surge of ammonia in the plasma of P. schlosseri as reported previously for other fish species. Consequently, contrary to previous reports, there were significant decreases in the ammonia content of the brain of P. schlosseri throughout the 24 h period post-feeding, accompanied by a significant decrease in brain glutamine content between 12 h and 24 h.
AIMS: The aim of this study is to compare the efficacy of low glycaemic index (GI) vs. conventional carbohydrate exchange (CCE) dietary advice on glycaemic control and metabolic parameters in patients with type 2 diabetes.
METHODS: A total of 104 patients with type 2 diabetes were randomly assigned to either a low GI (GI) or CCE dietary advice over a 12-week period. The primary end-point was glycaemic control as assessed by glycated haemoglobin A1c (HbA1c), fructosamine level and plasma glucose. The secondary end-points were anthropometric measurements and metabolic parameters that include blood pressure, lipid profile and insulin levels. The oral antidiabetic medications remained unchanged throughout the duration of the study.
RESULTS: A low-GI diet was associated with significant changes in the fructosamine level (DeltaGI = -0.20 +/- 0.03; DeltaCCE = -0.08 +/- 0.03 mmol/l, p < 0.01) and waist circumference (DeltaGI group = -1.88 +/- 0.30 cm; DeltaCCE group: -0.36 +/- 0.4 cm, p < 0.05) at week 4. At week 12, the changes in fasting glucose (DeltaGI = -0.03 +/- 0.3; DeltaCCE = 0.7 +/- 0.3 mmol/l; p < 0.05) and waist circumference (DeltaGI = -2.35 +/- 0.47 cm; DeltaCCE group = -0.66 +/- 0.46 cm; p < 0.05) in the GI group was significantly lower than the CCE group. With the low-GI diet, the changes in postprandial glycaemia at time 0, 60, 150 and 180 min after consuming the standard test meal was lower than with the CCE diet (p < 0.05). No significant differences were found between the groups for the remaining parameters that were measured.
CONCLUSIONS: Use of a low-GI diet resulted in significant changes of serum fructosamine level, plasma glucose and waist circumference in Asian patients with type 2 diabetes over a 12-week period compared with those following a CCE diet. The effect on HbA1c and other metabolic parameters was not significantly different between the two study groups but the improvement within the GI group was more pronounced and of clinical benefit.