We determined the effect of beraprost sodium (BPS) on serum levels of TCH, HDL-CH, and TG in patients with non-insulin-dependent diabetes mellitus (NIDDM). The drug was given orally (120μg/day) for 12 weeks to 23 NIDDM patients. Changes in TCH after 12 weeks of treatment were evaluated by Linear multiple regression analysis. There was no significant alteration in the three serum lipids after 12 weeks. The Changes in TCH were significantly correlated with the level of basal TCH (partial r=-0.51826, P<0.025), basal HDL-CH (partial r=0.60082, P<0.005), and changes in HDL-CH (partial r=0.69876, P<0.005) after 12 weeks of treatment. The change in TCH was not significantly correlated with blood glucose control. These results suggest that the serum level of TCH was decreased in patients with a high level of basal TCH and low level of basal HDL-CH during the treatment period. BPS improved serum lipid metabolism in NIDDM patients.

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To determine the clinical significance of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in hemodialysis patients, we measured levels of these peptides before and after hemodialysis, and examined their correlation with clinical and cardiac parameters in diabetic (DM) and non-diabetic (non-DM) groups. The results were as follows:(1) The change in ANP level correlated significantly with the change in body weight, but the change in BNP level did not correlate with it in either group.(2) The BNP level was significantly higher in the DM group than in the non-DM group, and correlated significantly with the QTc interval in the DM group. It is necessary to measure and evaluate not only ANP, which is a parameter of volume overload, but also BNP, which is a parameter of ventricular overload, in diabetic patients on hemodialysis.

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To investigate the metabolic pathway of glycosylated LDL (G-LDL) in macrophages (Mφ), we measured its accumulation and degradation in Mφ by using ¹²⁵I-labelled G-LDL in both control rats (C group) and streptozotosin-induced diabetic rats under a high-glucose conditionfor 5, 10, and 15 weeks (DM-5w group, DM-10w group, DM-15w group). Also we made the same measurements of native LDL (N-LDL). Accumulation and degradation of G-LDL were significantly higher than those of N-LDL in all four groups. In comparing the four groups no differences were observed in accumulation and degradation. Accumulation and degradation of G-LDL showed no difference from those of N-LDL in Mφ in diabetic rats when Mφ were incubated for 3 hours. But those values for G-LDL were significantly higher than those for N-LDL when Mφ were incubated for 6 hours or more.
These results suggest that uptake of G-LDL in Mφ in diabetic rats depends on the incubation time, and is not influenced by the duration of a high-glucose condition.

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For the purpose of establishing a medical examination for diabetes mellitus by mail, we measured the percentage of HbA1c in dry blood samples (DBS) spotted on a sheet of filter paper under various conditions. The level of HbA1c was measured by the latex agglutination reaction (LAR) using the fluid obtained by immersing DBS in a hemolyzing solution. That of Hb was measured by the alkaline hematin reaction using the same fluid. The HbA1c values of fresh venous blood samples (VBS) determined by LAR correlated well with the values determined by HPLC (r=0.978). The HbA1c values in VBS obtained by LAR correlated well with those in DBS (r=0.980). The within-run precision measurement in DBS by LAR yielded coefficients of variation (CV) of 1.88-4.48%. To confirm the stability of HbA1c in DBS, we maintained the samples at-20, 5, 25, and 50°C for several days. The values of CV of all samples were 0.46-5.11% in this assay.
In conclusion, we were able to use DBS to measure the HbA1c levels by LAR under various conditions, to apply them to the medical examination for diabetes mellitus by mail.

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We report a 22-year-old man with NIDDM presenting with hyperosmolar diabetic coma with rhabdomyolysis, acute renal failure and DIC. The patient had a family history of diabetes, and was obese. He was admitted to an other clinic because of general malaise and body weight loss a month after glycosuria was detected in a medical check-up. On the next day, he became hypotensive, oliguric and comatose, and then was referred to our hospital. He had severe hyperglycemia, hypernatremia, elevated levels of serum creatinine and creatine phosphokinase, and a decreased platelet count. Medical treatment including fluid supplementation, intravenous infusion of insulin, dopamine and anti-coagulants led to almost full recovery without significant sequelae. Finally good glycemic control was achieved by diet therapy alone. Rhabdomyolysis is one of the well-recognized complications of hyperosmolar coma in diabetic subjects. We propose that attention should be paid to rhabdomyolysis not only in the elderly but also in younger patients with NIDDM.

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A 72-year-old man with non-insulin-dependent diabetes mellitus (NIDDM) of 18 years' duration was admitted to our hospital in January 1997 because of constipation, abdominal pain, and diarrhea. He had a past history of suspected diabetic gastroenteropathy. Abdominal plain X-ray film and CT scanning showed gas-filled cysts in the wall of the small intestine. The cysts disappeared with starvation care on the seventh day after admission. Because of the image findings and clinical course, the patient was diagnosed as having pneumatosis cystoides intestinalis (PCI). The reason for obstruction of the intestine was not revealed by small-intestine fluoroscopy or total colon fiber. Diabetic retinopathy and nephropathy did not change after the occurrence of PCI, but microneurography revealed that the neuropathy was getting worse. Because numbness of the patient increased and neuropathy was worsening, it is likely that diabetic neuropathy had a connection with the occurrence of PCI. Since PCI may occur in a patient with symptoms of suspected diabetic gastroenteropathy, PCI is important for the differential diagnosis of diabetic gastroenteropathy.

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76-year-old woman with a 20-year history of non-insulin-dependent diabetes mellitus was referred to our hospital in 1996 for treatment of a foot impairment. Her past history included a mammary carcinoma. One year before admission, suddenly she had pain and swelling in the left foot but there was no abnormality on her X-ray at that time. On admission to our hospital, an X-ray showed destruction of the talus and MRI showed necrosis of the talus. Though the cause of necrosis was considered to be osteomyelitis or metastasis of the mammary carcinoma, there were neither findings of inflammation in the laboratory data nor other metastatic lesions. Therefore it was diagnosed as aseptic necrosis. Talus aseptic necrosis is known to occur usually following a foot injury, bone fracture or long-term steroid therapy. Since she did not have such a past history, her talus necrosis was considered a neuroarthropathy called “Charcot joint” associated with her severe diabetic neuropathy. Recently it has been clarified by development of imaging methods that the “Charcot joint” consists of not only joint deformity but various changes in the bone and joint. Early radiological examination, especially MRI, should be performed when osteoarthropathy is difficult to treat by medication in diabetic patients.

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There is an idea that hyperglycemia itself in Non-Insulin-Dependent Diabetes Mellitus (NIDDM) is a major pathogenic phenomen that worsens the disorder of glucose metabolism. The basal and additional insulin secretion increases progressively until the fasting plasma glucose (FPG) reaches the peak of 120 mg/dl and postprandial plasma glucose (2hPPG) also reaches its peak of 160 mg/dl. Thereafter, further increases in FPG and 2hPPG levels are associated with the progressive decrease in insulin secretion. This study shows that it is necessary to control plasma glucose levels to lower than the above values.

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The aim of this study was to determine if beta-cell function could be improved in NIDDM patients by treatment with acarbose or metformin. Twenty-four NIDDM patients who had not received any diabetic medication and whose fasting plasma glucose levels were less than 200 mg/dl were divided into two groups. Thirteen were treated with acarbose (150-300 mg/day), the others were treated with metformin (500-1000 mg/day) and all were followed for 12 months. There were no significant differences in the patient profiles before the treatment between the two groups. HbAic levels after the treatment were decreased significantly in both groups. BMI after the treatment in the acarbose-treated group was significantly lower than before the treatment. The area under the curve (AUC) of IRI/AUC of glucose during the 75-g OGTT after the treatment was significantly larger than before the treatment in both groups. Delta IRI/delta glucose from 0 to 30 min after the treatment was significantly higher than before the treatment in the metformin-treated group.
There was no significant change in body fat distribution in either group. In conclusion, improvement of beta-cell function contributes to the reduction in glycemia by acarbose or metformin in NIDDM patients.

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