A method employing hamster insulinoma cells (In-111 RI) as targets of islet cell cytoplasmic antibodies (ICA) with indirect immunofluorescence assay, was compared with the original method using fixed pancreaticcomponente of human O group blood of the sera positive to the fixed human pancreatic component, somereactions were considered as non-specific immunofluorescent reactions to In-111 RI cells. Occasional false-positive reactions were also made due to the presence of autoantibodies against cytoplasmic components (anti nuclear antibody etc). When we examined a stamp slide of In-111 RI cells with immunofluorescence, we could distinguish the specific reactions of ICA to the cytoplasm of In-111 RI cells, in comparison withcontrol antigenic cells (CCRF-CEM). ICA titre was deternined by analysing the final dilution teter showingpositive immunofluorescence. Compared to the original method, this new assay system was much morespecific to islet cells and enabled us to distinguish non-specific cytoplasmic reactions easily. Insulin antibodiesin the serum did not give false-positive results in assay. Using this assay, 20% of IDDM patients wereICA-positive, and this value was much higher than in NIDDM patients and controls.

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To assess the effects of acarbose on glycemic control in IDDM, we administered 100 mg of acarbose or aplacebo just before each meal to 8 patients with IDDM in a crossover trial, under feedback control with Biostator ® for 2 consecutive days. The insulin requirements 3 hours after breakfast, lunch and supperrespectively, with acarbose administration, were lower than those with placebo intake (post-breakfast: 14.8±1.5 U/3 hrs vs 18.9±1.8, post-lunch 9.4±1.1 vs 12.9±1.2 (p<0.01), post-supper 11.1±1.2 vs 14.3±1.0 (p<0.05)). The period of time taken from the beginning of each meal to the point of maximum postprandialblood glucose level with acarbose administration was longer than that with placebo intake (post-breakfast145±27 min vs 68±7 (p<0.05), post-lunch 133±27 vs 72±18 (p<0.05), post-supper 136±22vs93±13). Weconclude that acarbose reduced insulin requirements through the action of delaying the point of maximumpostprandial blood glucose level.

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We determined the serum fructosamine (FRA), HbA₁c, and fasting plasma glucose (FPG) levels in 80 insulin-dependent diabetes mellitus patients (IDDM) aged from 3 to 27 years, and compared with those in 34 non-diabetic subjects of the same age.
The venous blood was collected at a single hospital visit, and FRA was measured using the Fructosamine Test (Roche).
1) FRA levels in children from 1 to 10 years old were low in both the non-diabetic and diabetic groups.
2) There was a significant correlation between FRA and HbA₁c levels (r=0.79) but there was less correlation between FRA and FPG levels (r=0.29). There was no correlation between FRA or HbA₁c and the weekly mean FPG levels of SMBG measured during the 4 weeks before, in 13 IDDM patients.
3) In the 13 IDDM patients undergoing SMBG testing for 4 weeks, FRA level was 3.99±0.69 mmol/l (M±SD) and HbA₁c level was 8.9±1.1%. In the another 10 IDDM patients who had maintained good glycemic control during the previous 3 months, FRA level was 3.65±0.50 mmol/l and HbA₁c was 7.8±1.0%.
The fluctuating plasma glucose in IDDM has a weak correlation with FRA, while FRA and HbA₁c have a strong correlation with each other. Therefore, fructosamine measurement may be useful as an indicator of glycemic control in diabetic children.

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In order to clarify if vasopressin (VP) plays a role in the pathophysiology of hyperosmolar nonketoticdiabetic coma (HNDC) VP infusion was administered to diabetic rats, and the plasma levels of glucose (PG), ketone bodies, FFA, and glucagon were determined. High-dose VP infusion (1.2 U/kg/h) causedgradual elevation of PG and glucagon levels, while ketone bodies were decreased transiently at 30 min Low-dose VP infusion (0.06 U/kg/h) caused no change in PG levels, and the rise of ketone bodies noted duringsaline infusion was gradual. Under the suppression of glucagon secretion by combined infusion of VP andsomatostatin (100μg/kg/h), PG increased by 25% with high-dose VP, and ketone bodies decreased by 30%both with high-and low-dose VP, throughout the infusion. VP seems to reduce FFA levels, but a dissociationof FFA and ketone bodies was observed, suggesting that major anti-ketogenic effects were occurring in theliver. These findings indicate that the VP which is often elevated in HDNC has an anti-ketogenic effectprobably due to hepatic action.

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Insulin sensitivity in glucose metabolism was assessed by a euglycemic clamp technique combined with an isotopic measurement of glucose metabolic rate in spontaneously diabetic GK rats. In normal Wistar rats, steady state plasma insulin (SSPI) was elevated 4-fold by a 120 mU/h dose of insulin. The insulin increased glucose utilization (PGU) in peripheral tissues such as muscle to the 2.4-fold level and suppressed hepatic glucose production (HGP) completely. In GK rats, plasma levels of glucose and insulin were elevated. SSPI was elevated 4-fold by a 120mU/h dose of insulin and steady state plasma glucose level was decreased to within a normal range. The insulin dose-response curve for PGU did not differ from that of Wistar rats, but HGP was not suppressed by the insulin, indicating the presence of insulin resistance in the liver. Hepatic fructose 2, 6-bisphosphate (F2, 6P₂) content was increased by insulin infusion in Wistar rats. However the F2, 6P₂ level in GK rats was lower than that of Wistar rats, and was not changed by the administration of insulin. Thus, the possible implication of abnormal regulation of F2, 6P₂ metabolism by insulin playing a part in the increased HGP level was suggested. Glucose oxidation and lipid synthesis from glucose were stimulated by lower concentrations of insulin in the adipocytes from GK rats than those from Wistar rats. Thus, the sensitivity to insulin in glucose utilization was not decreased in the adipocytes of GK rats in accordance with the in vivo results described above. These results indicate that an increase in HGP based on hepatic insulin resistance contributes to the development of hyperglycemia in GK rats.

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This paper reports a case of non-clostridial gas gangrene of the perineum developing in the vulval and perianal regions. A 57-year-old woman with a 15-year history of untreated diabetes mellitus visited our hospital with hypogastric pain. Swelling and redness extending from the right inguinal region to the right hypogastrium, a tumor of 10cm in diameter, and widespread crepitation over the affected site was observed upon examination. Black necrotic tissue was found to extend from the perianal region to the right major pudendal lip. Roentgenography revealed widespread subcutaneous emphysema in the anterior abdominal wall. She was successfully treated with immediate drainage, debridement and antibiotic administration, together with strict control of the diabetes mellitus. The patient was considered to have developed progressively of extensive necrotizing subcutaneous infection, resulting in gas production. The pathogens involved in this case were E. coli and Bacteroides fragilis, and it is highly likely that the synergistic interaction between these facultative aerobic and anaerobic organisms was enhanced by the diabetes mellitus. This case can be regarded as a typical example of the “synergistic necrotizing cellulitis” described by Stone et al.

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We examined the effects of interleukin-1 (IL-1), a product of macrophages on rat islet insulin secretory function using neonatal rat pancreatic monolayers. Rat IL-1 was derived from Wistar rat peritoneal macrophages stimulated by silica in vitro.
Addition of rat IL-1 containing supernatant to the culture for 4 days inhibited insulin release by 40% to the control levels, and reduced insulin content by 60% at a concentration of 10%(V/V). This effect was dose dependent and reproducible. We also assessed the effects of human rIL-1β on the culture. Dose dependent inhibitory effects on insulin release and content similar to those of rat IL-1 were observed with 0.5 to 5.0u/ml of hrIL-1.
On the other hand, in short incubation studies, hrIL-1stimulated insulin release from the pancreatic monolayers after 2 hrs in the culture.
Morphological studies showed that these actions of IL-1 did not appear to account for pancreatic islet destruction.
These data suggest that IL-1 could play an important role as a potent modulator of insulin secretion, and it could be hypothesized that involved in a pathogenic role in type 1 diabetes mellitus.

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