Recent studies suggest that angiotensin-converting enzyme inhibitors (ACE-Is) can improve the course of urinary albumin excretion in IDDM patients with microalbuminuria. However, there have been very few studies investigating this effect of ACE-Is in NIDDM patients. To evaluate the effects of ACE Is on the excretion of microalbumin in normotensive and mildly hypertensive NIDDM patients, we followed the albumin index (urinary albumin creatinine ratio; A. I.) using first-void early morning urine specimens for 12 months in 60 patients randomized into two groups matched for clinical data, one the ACE I group (Delapril 30 mg/day), the other the control group.
In the ACE I group, mean A. I. was significantly lower at the 3-and 9-month follow up ; whereas in the control group tended to increase, with a significant increase after 12 months of follow up. A significant negative correlation was observed between HbA_1c, values obtained before treatment and the degree of change in A. I. values during the follow-up period in the ACE-I group. No blood pressure, blood glucose level or serum lipid level changes were observed in either group during the study period.
In conclusion, ACE I had a lowering effect on microalbuminuria in NIDDM patients, independent of changes in systemic blood pressure. The potency of this lowering effect may be lessened by poor glycemic control.

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To investigate the relationship between the coping style of patients with non insulin dependent diabetes mellitus (NIDDM) in stressful situations in their daily life setting and their state of glycemic control, we assessed NIDDM outpatients at Kitakyusyu Municipal Medical Center who had been followed for at least one year. The subjects were divided into two groups, a “good control” group and a “poor control” group, based on their serum glycosylated hemoglobin concentration (HbA₁), and were compared using the Picture-Frustration Study (P F Study). The P F Study is a psychological test using a semi-projective technique to appraise a person's typical mode of reaction in a frustrating setting. The results showed that (1) in the “good control” group a coping style of “accepting one's difficulties as they are” was more frequently used, whereas (2) coping styles of “repressing one's frustration” and “excessive optimism in dealing with one's difficulties” were significant in female patients in the “poor control” group. Based on these findings, the coping style of NIDDM patients with stressors in their daily life may be associated with their state of glycemic control, suggesting that the results of this study can be applied as a useful index for therapeutic intervention in treating NIDDM patients, especially “poor control” patients.

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The proband in this family is 62 years old at present. She was diagnosed as having diabetes mellitus at the age of 48 and was treated by insulin since the age of 55 years. Bilateral hearing loss was first noted in her late 40s and gradually become worse. In this family, nobody except the proband had hearing loss. Electrocardiogram and ultracardiosonography of the proband showed that the walls of the ventricles were mildly hypertrophic. Her daughter, now 28 years old, had IGT and normal hearing ability. The percentages of 3243 mutation (A→G) from the blood sample and fibroblast cells of the proband were 1.0% and 80.0%, respectively. The 16.5% rate of mutation from the blood sample of her daughter was much higher than that of the proband. These data suggest that the daughter, who has a high percentage of this mutation, will havein the future a shortage of insulin due to dysfunction of mitochondria in the pancreatic B cells, cardiomyopathy, and impaired neurological function such as hearing loss.

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A 66-year old man suffered a toe ulcer in March 1992. We diagnosed his illness as diabetic gangrene and treated him on diet therapy, insulin therapy, antibiotics and local therapy. The lesion was cured within 6 weeks. After treatment, his blood glucose level became stable and his hemoglobin A_1c level decreased gradually. Since late August he had remittent fever and a sense of fatigue. His right chest had moist rales. The white cell count was 15800/μl, and CRP was strongly positive. The chest X-ray film showed infiltrates in the right field, diagnosed as bacterial pneumonia. Although we administered broad-spectrum antibiotics, his fever remained unchanged and his chest X-ray film deteriorated. Every sputum culture showed normal flora. Because the condition had improved after changing antibiotics, we regarded his respiratory infection as lung tuberculosis and added anti-tubercle drugs. On the 14th day, he died suddenly of hypovolemic shock after vomiting. The culture of percutaneous lung biopsy specimen proved tubercle bacilli. The abdominal plain film showed dilatation of the stomach on the day of death. The acute dilatation of the stomach may have been due to decreased gastric excretion as a result of diabetic neuropathy in addition to deterioration of lung tuberculosis.

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We report on a family with diabetes mellitus associated with a mitochondrial DNA mutation. The proband (21 yrs, M), his sister (14 yrs) and mother (49 yrs) developed diabetes at the ages of 21, 9 and 35, respectively. At the onset of their disease all 3 patients' fasting plasma glucose levels were elevated to between 250 and 400 mg/dl, and insulin was eventually prescribed. After one and a half months, with improvement in his metabolic abnormalities, the proband could discontinue insulin.
All patients had proteinuria at the onset of diabetes. Retinopathy was not present. In addition, the proband had hypofunction of the parathyroid glands, short stature, decreased intelligence and impaired hearing. The sister had short stature, decreased intelligence, patent ductus arteriosus and minor external anomalies. Her serum concentration of Ca was decreased and P was increased. The GH responses to provocation tests were normal in both the proband and his sister. These clinical abnormalities were not observed in the mother.
A DNA analysis using circulating white blood cells revealed an A to G transition at nucleotide 3243 in the mitochondrial tRNA Leu (UUR) in these 3 patients, with a minimal level of defective DNA in the mother.

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We evaluated the extent of glycation of hair protein (keratin) using a glycation index (A₃₉₀/A₄₁₂) that was calculated from colorations (A₄₁₂, cystine A₃₉₀, glycated protein) of hair that can be quickly obtained by a non invasive procedure and easily stored. The glycation indexes of back hairs from hypercholesterolemic mice with hyperglycemia and diabetic rats were significantly higher 2.3-3.1 fold) than those of normal animals (p<0.05). Their glycation indexes correlated well with levels of glycated protein in hairs (r=0.98, p<0.05) and blood glucose levels (r=0.73, p<0.05). Within run precision (reproducibility, CV) for the assay of glycation index of hair was 6.7-9.4%(n=10).
In conclusion, the proposed glycation index for hair gave reasonable results in animals with normo and hyperglycemia, indicating it to be reliable and diagnostically useful.

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