title: Relationship between serum 1,5-anhydroglucitol and urinary excretion of N-acetylglucosaminidase and albumin determined at onset of NIDDM with 3-year follow-up.
abstract: OBJECTIVE
  This prospective study was designed to elucidate the relationship between the serum level of 1,5-anhydroglucitol (1,5AG) and the urinary excretion of N-acetylglucosaminidase (NAG) and albumin in patients who were in the early stages of diabetes.
  
  
  METHODS
  A total of 1,062 male nondiabetic subjects with impaired glucose tolerance were monitored for blood glucose level once every 2-3 months, and the values were evaluated. Of these 1,062 subjects, 112 showed a worsening of glycemia during the observation period to the level seen in diabetes. We began to monitor the glycemia and parameters of renal damage in the 112 patients from the onset of diabetes.
  
  
  RESULTS
  The urinary excretion of NAG and albumin were elevated even at the onset of diabetes. The abnormal excretion of NAG and albumin was associated with a change in serum 1,5AG and was quickly reversible when the serum 1,5AG improved. In the 3 years after the onset of diabetes, we obtained at least 18 measurements of one parameter for each patient and calculated the mean. Urinary NAG was found to be significantly correlated with the fasting plasma level of glucose (FPG; r = 0.512, P < 0.0001), the level of HbA1 (r = 0.351, P = 0.001), and the level of 1,5AG (r = -0.790, P < 0.0001). The urinary excretion of albumin was weakly but significantly correlated with levels of FPG (r = 0.383, P < 0.0001) and HbA1 (r = 0.337, P < 0.0001), but it was more strongly correlated with 1,5AG (r = -0.632, P < 0.0001). The level of 1,5AG was significantly correlated with FPG (r = -0.681, P < 0.0001) and HbA1 (r = -0.609, P < 0.0001).
  
  
  CONCLUSIONS
  When the renal damage is not severe, the serum level of 1,5AG appeared to be an indicator of the reversible renal damage caused by hyperglycemia, as well as of the severity of the glycemia itself.
authors.affiliation: Second Department of Internal Medicine, University of Teikyo, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yamanouchi
authors.forename: T
authors.initials: T
authors.lastname: Kawasaki
authors.forename: T
authors.initials: T
authors.lastname: Yoshimura
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: E
authors.initials: E
authors.lastname: Koshibu
authors.forename: N
authors.initials: N
authors.lastname: Ogata
authors.forename: H
authors.initials: H
authors.lastname: Funato
authors.forename: I
authors.initials: I
authors.lastname: Akaoka
authors.forename: H
authors.initials: H
authors.lastname: Miyashita
mesh_terms: D000118:Acetylglucosaminidase / Q000097:blood*; D000328:Adult; D000419:Albuminuria / Q000453:epidemiology; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D001798:Blood Proteins / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003847:Deoxyglucose / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy / Q000652:urine; D003929:Diabetic Neuropathies / Q000097:blood / Q000652:urine; D005500:Follow-Up Studies; D018149:Glucose Intolerance / Q000097:blood* / Q000503:physiopathology / Q000652:urine; D005951:Glucose Tolerance Test; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007536:Isomerism; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012044:Regression Analysis; D013453:Sulfonylurea Compounds / Q000627:therapeutic use; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D001798:Blood Proteins; D008076:Cholesterol, HDL; D007004:Hypoglycemic Agents; D013453:Sulfonylurea Compounds; D014280:Triglycerides; C006584:1,5-anhydroglucitol; D002784:Cholesterol; D003847:Deoxyglucose; D000118:Acetylglucosaminidase