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Dear Sir, Protein glycation is assumed to be one of the main reasons for a generation of diabetic complications [1]. This process has been reported to be affected by ascorbic acid [2]. Examinations on healthy volunteers have shown the inhibiting effect of oral ascorbic on protein glycation [3]. We decided to investigate the effect of oral ascorbic acid supplementation on fructosamine and HbAlc levels in Wistar rats with streptozotocin diabetes. Diabetic and non-diabetic rats were divided into control and untreated groups, and groups treated with ascorbic acid added to drinking water (1 g/litre) for 3 months. Blood was sampled from the tail vein of non-fasted animals at the start of the study and 1, 2, and 3 months after the initial administration of ascorbic acid. Blood was assayed for glucose, fructosamine and HbAlc. Supplementation with ascorbic acid did not cause any significant changes in blood glucose levels throughout the study in the diabetic or the non-diabetic rats. Figure I shows that there were no significant changes in either fructosamine or HbAlc levels in non-diabetic rats treated with ascorbic acid. The initial values were 129.5 _+ 13.7 gmol/1 and 1.91 + 0.12 %, respectively, and remained at this level during supplementation. They did not differ from those observed in untreated non-diabetic rats. In contrast, ascorbic acid supplementation affected the HbAlc concentration in diabetic rats. The initial HbAlc concentrations of diabetic rats were 2.06 + 0.09% and 2.21 +0.07% in the treated and untreated group, respectively. HbAI~ levels in diabetic rats rose significantly in both groups but they remained higher in the untreated group [2.74 + 0.06 vs 2.36 + 0.08 % (p < 0.01), 2.96 + 0.07 vs 2.40+0.08% (p <0.001) and 3.51+0.06 vs 2.66+0.06% (p < 0.001) at 1, 2, and 3 months, respectively]. Ascorbic acid administration had a small effect on plasma fructosamine concentration. The statistically significant difference between groups was found at 3 months; 227.4 + 19.5 gmol/1 (treated diabetic) vs 316.3 + 20.5 gmol/1 (untreated diabetic) (p < 0.01). It has been suggested that the fructosamine assay is a measurement of many serum glycated proteins which may be susceptible in different ways to ascorbic acid influence [3]. Similarly, Sinclair et al. [4] did not find significant differences in plasma fructosamine levels in diabetic patients treated with ascorbate for 6 weeks. Our results indicate that ascorbic acid administration decreases the rate of protein glycation, which may be important in prevention of secondary diabetic complications.

SummaryThe solid-phase synthesis and in vitro assays on the glucose-induced insulin secretion from rat pancreatic islets of Langerhans with six new chimeric peptides were performed. All the peptides were built up of the N-terminal galanin (GAL) fragment or its analogues, linked to the C-terminal portion of substance P (SP) analogues or scyliorhinin I (SCY-I) analogues. Two strong antagonists of the inhibitory effect of galanin on the glucose-induced insulin release were found: [cycloleucine4]GAL(1-13)-SP(5-11)-amide and GAL(1-13)-[L-norleucinel~ 10)-amide.

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