Biomedical subjects

K Ichiki

Publications and source records attributed to K Ichiki.

At least 55 records · Page 3Linked to original sources

PubMedDate not supplied

Clinofibrate therapy raises high-density lipoprotein levels and lowers atherogenic index in diabetes mellitus patients.

The effects of clinofibrate on serum lipoprotein concentrations, lecithin cholesterol acyl transferase activity and atherogenic index were studied in 10 diabetes mellitus patients. The patients comprised five with well-controlled non-insulin-dependent diabetes, and five with poorly controlled insulin-dependent diabetes; six non-insulin-dependent diabetics acted as placebo controls. No adverse side-effects were reported and there were no significant changes in total cholesterol, triglyceride or high-density lipoprotein 3-cholesterol concentrations following 600 mg/kg clinofibrate treatment for 4 weeks in either insulin-dependent or non-insulin-dependent diabetics. High-density lipoprotein-cholesterol concentrations and lecithin cholesterol acyl transferase activity were significantly (P less than 0.05) increased by clinofibrate treatment in insulin-dependent and non-insulin-dependent diabetics and high-density lipoprotein 2-cholesterol concentrations were significantly (P less than 0.05) increased by clinofibrate in insulin-dependent diabetics. The atherogenic index was significantly (P less than 0.01) reduced in non-insulin-dependent diabetics. It is suggested that the enhanced plasma lecithin cholesterol acyl transferase activity following clinofibrate therapy is the result of increased high-density lipoprotein-cholesterol and high-density lipoprotein 2-cholesterol concentrations and may play a central role in the efficacy of clinofibrate.

Adult↗

PubMedDate not supplied

Influence of prostaglandin E1 on heavy proteinuria in slightly azotaemic diabetics.

Treatment of non-insulin-dependent diabetes mellitus patients with nephropathy of the nephrotic type using 40 micrograms prostaglandin E1 given intravenously twice daily for 4 weeks reduced the urinary protein concentration. Prostaglandin E1 also increased the total serum protein and serum albumin concentrations, and reduced creatinine clearance and plasma renin activity following frusemide loading. Treatment with the prostaglandin did not, however, significantly affect the blood urea nitrogen and the serum creatinine concentration. It is concluded that prostaglandin E1 has overt effects on diabetic nephropathy.

Aged↗

PubMedDate not supplied

Does protease inhibitor inhibit complement activation caused by the immune complex associated with islet cell surface antibody?

Sera containing islet cell surface antibody were obtained from seven children with insulin-dependent diabetes mellitus soon after the onset of disease. After incubation of 51Cr-labelled rat islet cells with islet cell surface antibody, human AB-type serum with or without nafamostat mesylate was added before further incubation. Radioactivity in the supernatant was measured to determine complement-dependent antibody-mediated cytotoxicity. Cytotoxicity in untreated sera [mean (+/- SD) 19.4 +/- 4.0%] was significantly (P less than 0.001) inhibited by ethyleneglycoltetraacetic acid (EGTA) (7.1 +/- 4.9%), ethylenediaminetetraacetic acid (EDTA) (2.5 +/- 0.9%) and nafamostat mesylate (2.8 +/- 1.8%). Cytotoxicity of nafamostat mesylate-treated serum was significantly (P less than 0.05) lower than that of EGTA-treated serum but not significantly different from that of EDTA-treated serum. There was no difference in cytotoxicity between nafamostat mesylate-treated and untreated, inactivated human serum. The results indicate that the protease inhibitor nafamostat mesylate completely inhibited the complement activation of the immune complex associated with islet cell surface antibody by the classical and alternative pathways.

Animals↗

PubMedDate not supplied

Complement activation via the alternative pathway in a patient with insulin-dependent diabetes mellitus.

A 41-year old male with insulin-dependent diabetes mellitus previously unsuccessfully treated with a controlled diet and glibenclamide, and subsequently with increasing insulin doses (5 and 20 IU/day) experienced polyuria, glycosuria and loss of weight. On admittance to hospital serum C3 concentrations were found to be depressed. The insulin dose was further increased to 30 IU/day and the patient was also treated with 20 mg nafamostat mesylate given intravenously twice daily for 6 days. On completion of nafamostat mesylate treatment serum C3 concentrations were increased but after 17 days they started to decrease again.

Adult↗

PubMedDate not supplied

Decreased creatinine clearance which may be observed during prostaglandin E1 therapy: is it reversible with discontinuation of therapy?

A study was carried out in four patients with nephrotic diabetic nephropathy in order to determine if decreased creatinine clearance observed during prostaglandin E1 therapy was reversible on discontinuation of therapy. The patients received 40 micrograms prostaglandin E1 intravenously twice daily for 4 weeks and creatinine clearance and daily excretion of urinary protein were measured immediately before, during and 2 weeks after therapy. Total serum protein and serum albumin were also determined. There was a significant decrease in creatinine clearance during therapy and after therapy clearance increased but not significantly. It is concluded that decreased creatinine clearance during prostaglandin E1 therapy has a partial reversibility on discontinuation of the treatment.

Alprostadil↗

PubMedDate not supplied

Effect of prostaglandin E1 on renal haemodynamics in a patient with diabetic nephropathy.

A 66-year old male with severe hyperglycaemia due to previously uncontrolled diabetes mellitus was also suffering from arteriosclerosis obliterans and diabetic nephropathy. The patient was treated with 16 IU/day insulin zinc suspension. In addition, an intravenous infusion of 80 micrograms/day prostaglandin E1 was given for 28 days in an attempt to improve the arteriosclerosis obliterans and diabetic nephropathy. Treatment resulted in a reduction in fasting blood glucose but no decline in urinary protein. Prostaglandin E1 treatment, however, produced an improvement in renal haemodynamics assessed by renography.

Aged↗

PubMedDate not supplied

Dose-dependent effect of hydroxymethylglutaryl-coenzyme A reductase inhibitor on serum cholesterol with limited dietary restrictions: a case study.

Hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (pravastatin sodium) can selectively inhibit cholesterol biosynthesis in the liver and may lower serum cholesterol concentrations even where there are no particular dietary restrictions. A 72-year old housewife with non-insulin-dependent diabetes mellitus complicated by hyperlipaemia type IIb, who did not follow directions for diet therapy or kinesitherapy, was administered HMG-CoA reductase inhibitor. The initial dose of 10 mg/day HMG-CoA reductase inhibitor was increased by 10 mg/day every 4 weeks to 30 mg/day, maintained at 30 mg/day for 8 weeks and then reduced gradually until discontinuation after a further 27 weeks. Test results showed the changes in low-density lipoprotein cholesterol and apoprotein B to be dose-dependent. The findings represent the first clinical evidence that hypercholesterolaemia can be adequately managed by the use of HMG-CoA reductase inhibitor, even when no specific dietary restrictions are imposed, and may contribute to improvements in the quality of daily life for many patients suffering from hyperlipaemia type IIb.

Aged↗

PubMedDate not supplied

Effect of prostaglandin E1 on the renin-aldosterone system in patients with diabetic nephropathy.

The effect of prostaglandin E1 (PGE1) on the renin-aldosterone system was investigated in hospitalized patients with non-insulin-dependent diabetes mellitus presenting with continuous proteinuria but without nephrotic syndrome. Of the 20 patients studied, 10 had continuous positive proteinuria > or = 200 mg/day and 10 had continuous positive proteinuria < 200 mg/day. Prostaglandin E1 (40 micrograms in 100 ml normal saline) was infused intravenously over 2 h twice daily for 4 weeks. Plasma renin activity (PRA) and the plasma aldosterone concentration (PAC) were determined by radioimmunoassay at 0 and 120 min after a frusemide injection given before the start of PGE1 treatment and during administration of PGE1 in week 4. The patients who had proteinuria < 200 mg/day showed significant decreases in the PRA0 and the ratio of PRA120:PRA0 and a decrease in the PAC120 during prostaglandin PGE1 administration. When the results for the two patient groups were combined, both the PAC120 and the PRA120 were found to be significantly lowered during administration of PGE1. The results indicate that PGE1 may be valuable in the treatment of diabetic nephropathy, since the compound inhibited the increased reactivity of the renin-aldosterone system in patients with non-insulin-dependent diabetes mellitus.

Aged↗

PubMedDate not supplied

Effect of an anxiolytic on lipid profile in non-insulin-dependent diabetes mellitus.

The effects on serum lipid levels of reducing stress were examined in 20 patients with non-insulin-dependent diabetes mellitus. An anxiolytic, fludiazepam, was administered to the patients for 12 weeks and their lipid profiles and State-Trait Anxiety Inventory scores at the beginning and end of treatment were compared. The high-density lipoprotein cholesterol level increased significantly after the administration of anxiolytic, but other aspects of the lipid profile were unchanged. Both trait and state anxiety scores decreased significantly with the administration of anxiolytic. The results indicate that improvement of stress in patients with non-insulin-dependent diabetes mellitus increases high-density lipoprotein levels.

Adult↗

PubMedDate not supplied

Effects of long-term administration of a combined alpha- and beta-adrenoceptor blocking agent on glucose and lipid metabolisms in patients with non-insulin-dependent diabetes mellitus.

The effects of a combined alpha- and beta-adrenoceptor blocking agent on glucose and lipid metabolism were examined in 27 out-patients with both non-insulin-dependent diabetes mellitus and hypertension. Systolic blood pressure was significantly reduced (P < 0.02), compared with the baseline value, after 1, 2, 3 and 12 months of treatment, and diastolic blood pressure was reduced after 6 and 12 months while the reductions in blood pressure at the other times were not statistically significant. Total cholesterol, and low-density and high-density lipoprotein cholesterol, decreased or showed decreasing trends during treatment, while triglycerides and very low-density lipoprotein cholesterol did not change in response to treatment. The glycosylated haemoglobin level, an indicator of glucose metabolism, did not change throughout treatment compared with its baseline value. The results suggest that a combined alpha- and beta-adrenoceptor blocking agent is less harmful to lipid metabolism and insulin sensitivity than a beta-adrenoceptor blocker would be. Such combined agents may be useful for treating hypertension accompanying diabetes mellitus.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

Improvement of stress reduces glycosylated haemoglobin levels in patients with type 2 diabetes.

The effects of reducing stress on glucose metabolism in diabetics were evaluated in 20 patients with type 2 diabetes (10 of each sex) who were given an anxiolytic (fludiazepam) for 12 weeks. Patients were tested 4 weeks before the start of anxiolytic treatment (A), immediately before the first dose (B), and before the end of the study period (C) using the State-Trait Anxiety Index and glycosylated haemoglobin levels. There were no significant differences between the trait or state anxiety scores or the glycosylated haemoglobin levels at times A and B before treatment. However, for all three measurements, the values at time C, after treatment, showed significant improvements, compared with those at both times A and B (P < 0.05). The improvement in the trait anxiety score was weakly correlated with the decrease in the glycosylated haemoglobin level (r = 0.426, P < 0.01). No correlation was seen between state anxiety scores and glycosylated haemoglobin levels. The results suggest that suppressing anxiety in patients with type 2 diabetes reduces glycosylated haemoglobin levels.

Adult↗

PubMedDate not supplied

Relationship between cardiosympathetic neuropathy and diabetic somatic neuropathy in patients with non-insulin-dependent diabetes mellitus.

The possibility of a relationship between diabetic somatic neuropathy and cardiosympathetic neuropathy was investigated in 103 patients with non-insulin-dependent diabetes mellitus. Cardiosympathetic nerve function was assessed by myocardial scintigraphy. The severity of diabetic somatic neuropathy was determined by measuring the motor conduction velocities of the peroneal and tibial nerves and the sensory conduction velocity of the sural nerve. Analysis of the results did not show any correlations between the measures of cardiosympathetic nerve function and the measures of diabetic somatic neuropathy. The results indicate that diabetic somatic neuropathy and cardiomyosympathetic neuropathy develop independently in patients with non-insulin-dependent diabetes mellitus.

Autonomic Nervous System Diseases↗

PubMedDate not supplied

Effect of an alpha-glucosidase inhibitor combined with sulphonylurea treatment on glucose metabolism in patients with non-insulin-dependent diabetes mellitus.

Ten patients with non-insulin-dependent diabetes mellitus who were being treated with a sulphonylureal compound but whose glucose metabolism needed further improvement were given a combination of their usual sulphonylurea treatment and an alpha-glucosidase inhibitor. Treatment with the alpha-glucosidase inhibitor (0.6 mg/day), in addition to glibenclamide (7.5 mg/day in two patients; 5.0 mg/day in four; 2.5 mg/day in one) or tolbutamide (500 mg/day in three patients) for 4 weeks, improved hyperglycaemia after meals from 237-247 mg/dl to 192 mg/dl, and reduced glycosylated haemoglobin levels from 8.5-8.6% to 7.9% without causing hypoglycaemia.

Blood Glucose↗

PubMedDate not supplied

No effect of an alpha-glucosidase inhibitor on glucose metabolism in patients with non-insulin-dependent diabetes mellitus and low function of pancreatic beta cells.

Twenty patients with non-insulin-dependent diabetes mellitus who had been receiving appropriate dietary treatment for 3 months but whose glucose metabolism needed further improvement were treated with an alpha-glucosidase inhibitor. Treatment with the alpha-glucosidase inhibitor (0.6 mg/day) for 4 weeks, had no significant effect on blood glucose levels 2 h after breakfast or on glycosylated haemoglobin levels.

Blood Glucose↗

PubMedDate not supplied

Cardiosympathetic neuropathy is independent of cardioparasympathetic neuropathy in patients with non-insulin-dependent diabetes mellitus.

The relationship between cardiosympathetic neuropathy and cardioparasympathetic neuropathy was investigated in 103 patients with non-insulin-dependent diabetes mellitus. Cardioparasympathetic nerve function was assessed by comparing electrocardiographically the expiratory and inspiratory R-R interval ratios, during a period of deep breathing, and the coefficients of variation of the R-R intervals. Cardiosympathetic nerve function was assessed by determining the uptake of [123I]metaiodobenzyl guanidine into the myocardium. The results indicate that there is no significant correlation between cardioparasympathetic and cardiosympathetic nerve function.

Body Mass Index↗

PubMedDate not supplied

How blood pressure in patients with non-insulin-dependent diabetes mellitus is influenced by stress.

The effects of reducing stress on blood pressure were investigated in 20 patients with non-insulin-dependent diabetes mellitus. An anxiolytic, fludiazepam, was administered to the patients for 12 weeks and their blood pressures and State Trait Anxiety Inventory scores at the beginning and end of treatment were compared. Systolic and diastolic blood pressures and trait and state anxiety scores were all significantly reduced during the treatment period. There was also a weak correlation between the extent of the improvement in the same anxiety score and the improvement in diastolic blood pressures.

Adult↗

PubMedDate not supplied

Factors related to stress in patients with non-insulin-dependent diabetes mellitus.

Stress was assessed using State-Trait Anxiety Inventory scores in 40 non-insulin-dependent diabetes mellitus (NIDDM) patients, and the results were compared with those for 40 sex- and age-matched healthy controls. Fludiazepam was administered to the patients for 12 weeks and stress was reassessed. The Manifest Anxiety Scale score correlated with Trait (r = 0.548, P < 0.0001) and State (r = 0.474, P = 0.0001) scores, validating the latter as measurements of stress. Both Trait (43.4 vs 35.8, P < 0.001) and State (41.6 vs 33.8, P < 0.001) scores were significantly higher in NIDDM patients than in healthy controls. Administration of an anxiolytic, fludiazepam (0.25 mg, three times daily, orally) for 12 weeks lowered Trait score (43.5 to 36.9, P < 0.0001), State score (41.6 to 35.8, P < 0.0002), glycosylated haemoglobin (8.4 to 7.3%, P < 0.0001), systolic blood pressure (151.2 to 143.4 mmHg, P < 0.0017) and diastolic blood pressure (84.2 to 77.7 mmHg, P < 0.0018). Multiple regression analysis revealed that the significant explanatory variables for the change in State score during anxiolytic administration were the changes in total cholesterol, high-density lipoprotein cholesterol, triglycerides, apolipoprotein B:A1 and glycosylated haemoglobin (R2 = 0.3224, P < 0.0022). The results indicate that stress is detected at a higher frequency in patients with NIDDM than in healthy controls, and that blood glucose and lipid metabolic factors are significant explanatory variables for this stress. This stress is correlated with glucose metabolism and blood pressure and, moreover, these factors could all be proved concomitantly by the administration of an anxiolytic.

Anxiety↗

PubMedDate not supplied

Is there a correlation between cardiac sympathetic neuropathy or diabetic somatic neuropathy and glycosylated haemoglobin or blood pressure in patients with non-insulin-dependent diabetes mellitus?

The possibility that glycosylated haemoglobin levels and/or blood pressure might correlate with cardiac sympathetic neuropathy and/or diabetic somatic neuropathy was investigated in patients with non-insulin-dependent diabetes mellitus. Sympathetic nerve function was quantified by analysis of [123I]metaiodobenzylguanidine accumulation in the cardiac muscle. Somatic nerve function was assessed by measuring the motor nerve conduction velocities of the peroneal and tibial nerves, and the sensory nerve conduction velocity of the sural nerve. None of the parameters of cardiac sympathetic neuropathy or diabetic somatic neuropathy showed any correlation with blood pressure, nor was there any evidence of a correlation between cardiac sympathetic neuropathy and glycosylated haemoglobin levels; there was, however, a significant correlation between diabetic somatic neuropathy (as indicated by tibial nerve conduction velocity) and glycosylated haemoglobin levels. The results are consistent with the view that different mechanisms are involved in the two types of neuropathies.

3-Iodobenzylguanidine↗