Relationship between Serum 1,5-anhydroglucitol, as an Indicator of Postprandial Glycemic Control, and Serum Uric Acid, Considering the Renal Threshold for Glucosuria in the Elderly

Postprandial hyperglycemia is an independent risk factor for cardiovascular disease-related morbidity and mortality, not only in diabetes mellitus (DM) but also in impaired glucose tolerance. Postprandial glycemic levels have been difficult to monitor, but recently 1,5-anhydroglucitol (1,5-AG) levels have proven to be beneficial for this purpose. In humans, 1,5-AG, a 1-deoxy-glucopyranose, is a major and abundant polyol, of which 90% is derived from ingested food, and little is produced from glycogen in the liver. Nearly all 1,5-AG is reabsorbed in normoglycemia, but the reabsorption rate decreases in proportion to the degree of hyperglycemia above the renal threshold for glucosuria, which is 160 to 180 mg dL. Glucosuria appears if the level of blood glucose rises above this level. The renal reabsorption of 1,5-AG is competitively inhibited by glucosuria. The 1,5-AG level appears to be well suited for monitoring glucose homeostasis in subjects with near-normoglycemia or with postprandial hyperglycemia without fasting hyperglycemia. However, few studies have shown a relationship, which remains controversial, between the serum 1,5-AG level and the age or sex of nondiabetic subjects. Therefore, we investigated the effects of sex and age on serum 1,5-AG levels in nondiabetic subjects. This study has demonstrated that the serum 1,5-AG concentration tends to decrease with age and is significantly correlated with age in both males and females. Moreover, the serum 1,5-AG concentration tends to be higher in males than in females, but this sex difference decreases with age. The 1,5-AG level is less sensitive for identifying postprandial hyperglycemia in elderly women with near-normoglycemia, partly because they have a higher renal threshold for glucose. Lifestyle changes in recent years have led to concerns about not only postprandial hyperglycemia, but also hyperuricemia. Serum levels of UA are related to urethritis and to several more serious conditions, such as kidney disease, hypertension, DM, metabolic syndrome, and cardiovascular disease. Furthermore, increased serum UA levels after menopause suggest that estrogen promotes UA excretion in the kidneys. A previous study has shown that estradiol suppresses levels of urate transporter 1 (URAT1), a urate reabsorptive transporter, in the mouse kidney. In the relationship between the levels of uric acid and glucose metabolism, a previous study has found that both serum UA levels and the frequency of hyperuricemia increase with moderately increasing levels of HbA1c (6.0%―6.9%) and then decrease as levels of HbA1c increase further, due to the uricosuric effect of glucosuria.