No abstract

Anserine is a bioactive dipeptide found in muscles and brains of vertebrates, but little is known about the kinetics of its absorption into blood and the clearance after the ingestion of anserine or anserine-containing diets. This study investigated time-dependent changes in the concentrations of l-histidine-related compounds from deproteinized blood. The concentration of anserine peaked and then decreased to zero, whereas the concentration of pi-methylhistidine gradually increased, at which point anserine was not detected. Thus, ingested anserine is absorbed intact in human blood and is hydrolyzed to pi-methylhistidine and beta-alanine by serum and tissue carnosinases. Moreover, the crossover study suggests that there was no significant difference in absorption under curves of anserine between anserine alone and anserine-containing diet, whereas there was significant difference in the peak concentration of anserine. This is the first study to demonstrate intestinal absorption and blood clearance of anserine.

Abstract. Long-term reduction of serum urate levels is vital in the treatment of gout. However, it is difficult to convince gout-free individuals of the necessity of treatment as few appropriate over-the-counter remedies and dietary supplements are available. Therefore, the present study aimed to investigate the antihyperuricemic efficacy and safety of a tuna extract containing the imidazole compounds to evaluate its potential as a functional food ingredient. A randomized, 4-week, double-blind, placebo-controlled study was conducted. A total of 48 male gout-free subjects with insignificantly high serum uric acid were randomly assigned to low-and high-dose tuna extract groups or a placebo group. The efficacy of the extract was assessed by measuring serum uric acid levels. Furthermore, a safety assessment was performed by physical parameters, hematology, blood biochemistry and urinalysis. The results indicated that the uric acid level was decreased at week 4 during the intervention in the tuna extract groups (low and high dose, -0.23 and -0.34 mg/dl, respectively) compared to the placebo group (-0.07 mg/dl). At week 4 after the intervention, a significant reduction in uric acid levels (-0.41 mg/dl; P<0.05) was observed in the high-dose tuna extract group compared with the placebo group (+0.11 mg/dl). No dose-related adverse events were observed during and following the intervention. Therefore, the present results suggest that oral administration of tuna extract containing the imidazole compounds has hypouricemic activity with no undesirable side effects.

Anserine and L-carnosine are similar dipeptides synthesized by muscles of vertebrates. The functional role of anserine is unknown, although previous studies showed hypoglycemic effects of carnosine through autonomic nerves. Thus, we evaluated the effects of anserine on blood glucose levels and the neural activities. Intraperitoneal administration of specific doses of anserine to hyperglycemic rats reduced hyperglycemia and plasma glucagon concentrations, whereas thioperamide eliminated the effects of anserine. Intraduodenal injection of 0.1 mg anserine to anesthetized rats after laparotomy suppressed sympathetic nerve activity and enhanced activity of the vagal gastric efferent. In addition, oral administration of anserine reduced blood glucose levels during oral glucose tolerance testing in humans. These results suggest the possibility that anserine might be a control factor for the blood glucose, and that histaminergic nerves may be involved in the hypoglycemic effects of anserine.

Abstract. It has been demonstrated that oral administration of N-acetylglucosamine (GlcNAc) alleviates the symptoms of osteoarthritis (OA). The aim of the present study was to elucidate the molecular mechanisms for the chondroprotective action of GlcNAc in OA. Biomarkers for type II collagen degradation and synthesis were evaluated, as were histopathological changes, using a rat anterior cruciate ligament transection (ACLT)-induced OA model. Changes in the expression of genes in the cartilage were assessed via DNA microarray and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results indicated that ACLT induced histopathological changes of articular cartilage, whereas oral administration of GlcNAc (1,000 mg/kg/day for 28 days) significantly suppressed these changes. Additionally, GlcNAc significantly decreased levels of a type II collagen degradation marker in sera compared with that in the ACLT group, although there were no significant changes in the levels of a type II collagen synthesis marker. Furthermore, DNA microarray and reverse transcription-quantitative polymerase chain reaction results demonstrated that GlcNAc treatment downregulated the expression of periostin, which is likely involved in the degradation of cartilage, whereas GlcNAc upregulated the expression of lipocalin 2, which is involved in the regulation of chondrocyte proliferation and differentiation. In conclusion, the results of the present study suggest that GlcNAc is able to suppress the histopathological changes induced by OA and exhibits a chondroprotective action by inhibiting type II collagen degradation in the articular cartilage, possibly via modulation of the expression of inflammatory and chondroprotective molecules, including periostin and lipocalin 2.