Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responsiveness of renin-angiotensin and kallikrein-kinin systems to furosemide challenge has been investigated in forty-six diabetic patients (34 NIDDM/12 IDDM), subdivided into Group I (uncomplicated DM), Group II (DM with hypertension), Group III (DM with nephropathy), Group IV (DM with hypertension and nephropathy) and a control group of 10 healthy volunteers. Plasma renin activity (PRA) was estimated by radioimmunoassay in blood samples drawn before and 10 min after furosemide administration (0.5 mg/kg i.v.). Urinary kallikrein levels were measured by bioassay using estrogenized rat uterus preparation in 4h urine samples collected before and after the diuretic. Urinary Na+ and K+ were also measured. The basal PRA in diabetics was not significantly different from controls, whereas, urinary kallikrein levels were markedly low in all patients. Both PRA and kallikrein levels increased after furosemide in controls while in diabetics this response was severely blunted. In a subset of Group I, a paradoxical fall in PRA and kallikrein levels was noted after furosemide, an effect similar to that observed in patients with nephropathy (Group III). This response in absence of clinical and biochemical parameters of nephropathy indicates early derangement of renal hemodynamic mechanisms heralding the onset of nephropathy.
Acta Diabetol Lat
PMID:Plasma renin activity and urinary kallikrein excretion in response to intravenous furosemide in diabetic patients. 208 34

The aim of the study was to investigate the effects of regularly eating a moderate amount of sucrose (30 g/day) in 12 type 1 (insulin-dependent, IDDM) diabetic outpatients in fair blood glucose and lipid control. Two diets, each lasting two months, were compared in a randomized cross-over study. The former was a high-carbohydrate high-fiber diet for diabetic patients with Italian alimentary habits, the latter had the same composition except that 30 g of sucrose replaced 30 g of complex carbohydrates with high glycemic index (bread). The two diets contained equal amounts of carbohydrates, proteins and lipids; the only difference being the contribution of oligosaccharides to total carbohydrates (22% vs 34%) and cholesterol amount. During the control diet, glycosylated hemoglobin was substantially unchanged in both control and sucrose diet periods (control diet: 6.91 +/- 0.29 (SE) vs 6.80 +/- 0.25%; sucrose diet: 6.75 +/- 0.31 vs 6.91 +/- 0.36%). This was true also for fructosamine (control diet: 3.92 +/- 0.21 vs 3.76 +/- 0.18%; sucrose 3.50 +/- 0.14 vs 3.64 +/- 0.20 mmol/l). Circulating blood lipid levels, body weight and daily insulin dose did not show any significant variations during the study. Moderate amounts of sucrose may be allowed to IDDM patients with Italian alimentary habits without worsening diabetic control.
Acta Diabetol Lat
PMID:Long-term effects of eating sucrose on metabolic control of type 1 (insulin-dependent) diabetic outpatients. 208 38

We randomly administered thyrotropin-releasing hormone (200 micrograms, as an i.v. bolus) or control saline (in isovolumic amount) to 30 male diabetic subjects (23 IDDM, 7 NIDDM) in fair metabolic control (HbA1 9.7 +/- 0.3%, means +/- SEM) and to 12 healthy male controls on two different mornings. While GH in the basal state was similar in IDDM, NIDDM and normal subjects, TRH administration evoked a significant GH release only in a single IDDM individual. The only GH-responder to TRH was a newly-diagnosed (two weeks) IDDM patient, still with a high glycated hemoglobin level (HbA1 11.1%), despite normal plasma glucose levels. Saline infusion did not affect GH concentrations either in normals or in diabetics. Exaggerated GH responses to TRH are uncommon in diabetic patients in good metabolic conditions.
Acta Diabetol Lat
PMID:Inappropriate growth-hormone (GH) response to thyrotropin-releasing hormone (TRH) occurs infrequently in well-regulated diabetes mellitus. 211 57

An exogenous insulin administration-modified, frequently sampled iv glucose tolerance test (FSIGT) for application in insulin-dependent diabetic patients (IDDM) to allow for estimation of insulin sensitivity (SI) and glucose effectiveness (SG) with Bergman's minimal model of glucose kinetics was investigated. An insulin infusion protocol (either 4 or 8 mU/min.kg from 20-25 min) was compared to the standard tolbutamide-modified (300 mg at 20 min) FSIGT in normal control subjects. SI and SG were not different for the insulin infusion- and tolbutamide-modified protocols [SI, 2.8 +/- 0.4, 3.6 +/- 0.6, and 2.5 +/- 0.5 X 10(4) min1/(microU/mL), respectively]. SI and SG were quantified in insulin-requiring newly diagnosed IDDM and in noninsulin-requiring IDDM in clinical remission with the exogenous insulin administration protocol. Both SI and SG were reduced in newly diagnosed IDDM compared to normal controls (by 64% and 40%, respectively). SI was normalized in IDDM in clinical remission despite a continued poor insulin secretory response to both glucose and tolbutamide. Although SI was normal in patients in clinical remission, SG remained reduced (by 65%) compared to that in normal controls. In conclusion, our results demonstrate that modification of the FSIGT with the exogenous administration of insulin allows for estimation of insulin sensitivity and glucose effectiveness in IDDM patients. Comparison to the standard protocol in normal subjects suggests that this results in valid measurements of insulin sensitivity and glucose effectiveness. Results of the application of this protocol in IDDM were consistent with previous observations that insulin sensitivity is reduced in poorly controlled IDDM and normalized in well controlled patients. Glucose effectiveness was found to be reduced in all IDDM subjects regardless of the degree of control.
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PMID:A modified protocol for estimation of insulin sensitivity with the minimal model of glucose kinetics in patients with insulin-dependent diabetes. 218 84

The effect of islet surface antibodies (ICSA) on in vitro insulin release was studied. Isolated rat islets were incubated in the presence of immunoglobulin preparations from patients with insulin-dependent and non-insulin-dependent diabetes mellitus (IDDM, NIDDM) and healthy subjects, and stimulated with D-glucose, L-arginine or tolbutamide. After incubation, the amount of insulin release from the rat islets was determined. The immunoglobulin preparations from 5 newly diagnosed IDDM patients who were positive for ICSA, and from 5 age-matched healthy subjects were examined. Even in the absence of complement or lymphocytes, immunoglobulin fractions positive for ICSA significantly inhibited low and high concentrations of glucose-stimulated insulin release compared with normal control (P less than 0.02), but had little influence on insulin release after stimulation with tolbutamide. Arginine-stimulated insulin release was almost the same in ICSA-positive immunoglobulin fractions and the control. Immunoglobulin fractions negative for ICSA either from four patients with recently diagnosed IDDM or from four newly diagnosed NIDDM patients had only negligible effect on insulin release after stimulation with glucose. These results suggest that ICSA in IDDM patients, even in the absence of complement or lymphocytes, may preferentially interfere with the mechanisms of glucose-stimulated insulin release in the pancreatic B cells.
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PMID:Islet cell surface antibodies preferentially inhibit glucose-stimulated insulin release in vitro. 219 Jul 82

An impaired pancreatic polypeptide response (PP) after hypoglycemia has been described in type I diabetic patients with overt autonomic neuropathy. Some authors have suggested that PP release might be useful as sensitive indicator of autonomic neuropathy. The meal test is safer and simpler than the insulin infusion test as PP stimulus. The aim of this study was to compare PP response to insulin infusion and protein meal test and to correlate these responses to the presence of measurable neuropathic disturbances. We thus studied 13 IDDM children and adolescents and 6 normal children. In diabetics the PP response to both tests was not different from that of the control subjects, but PP response to insulin infusion was inversely correlated to the duration of illness and was significantly lower in subjects with pathological heart rate response when compared to the control group. PP responses to the two stimuli were not correlated. We suggest that reduced PP response to hypoglycemia is an early sign of autonomic neuropathy as well as impairment of beat-to-beat variation when impaired PP response to meal test is still not evident.
Acta Diabetol Lat
PMID:Pancreatic polypeptide secretion after insulin infusion and protein meal in juvenile type 1 diabetic subjects. 219 47

The effects of individual teaching imparted during routine diabetologic counselling on the knowledge concerning diabetes and metabolic control, were assessed in 42 outpatients (28 IDDM; 14 NIDDM), attending the diabetic clinic (study group, SG). We evaluated the outcome of a multiple-choice questionnaire and fasting blood glucose (FBG), 24-h urine glucose (UG), mean regulation index (MRI) and glycated hemoglobin (HbA1), before and 60 days after providing information about diet (D), physical exercise (E) and hypoglycemic drugs (HD) or insulin therapy (IT). Results were compared with those obtained in a group of 57 age- and sex-matched patients (36 IDDM; 21 NIDDM) who did not receive individual teaching (control group, CG). Knowledge concerning diabetes at the second evaluation was significantly higher (p less than 0.001) in SG than in CG for D and IT, although an improvement was observed in all items. SG patients showed a significant improvement of knowledge (p less than 0.05) for D, a not significant improvement for HD and IT and no change for E. No change was observed for HbA1, MRI and UG, while a significant decrease (p less than 0.05) was observed for FBG in SG. At the second evaluation, FBG of SG patients was significantly lower (p less than 0.05) than that of CG patients. Our results go to show that individual teaching can improve the level of knowledge of patients without affecting metabolic control. Individual teaching during routine diabetologic counselling represents in our opinion an effective and economic educational model.
Acta Diabetol Lat
PMID:Individual teaching as a first-step intervention for the education of diabetic subjects. 261 28

Fourteen diabetic patients (13 males, 1 female, 7 IDDM and 7 NIDDM) were tested during wakefulness with a battery of tests examining parasympathetic and sympathetic control of the cardiovascular system. Subsequently sleep recordings including EEG, EOG, submental, left and right anterior tibialis EMGs, ECG, nasal airflow, thoracic and abdominal respirograms, nocturnal penile tumescence, were performed in each subject. The assessment of cardiovascular functions during sleep was based on the following parameters: Rbm, R-wake, apnea index, adequate penile tumescence during phase REM. Parasympathetic and sympathetic control of cardiovascular system were both impaired during wakefulness in only one patient, who also showed a low Rbm index indicative of ascertained autonomic neuropathy. Indices Rbm sufficiently low to be considered an evidence of probable autonomic neuropathy were found in 5 patients (3 IDDM and 2 NIDDM); all but one with normal cardiovascular tests during wakefulness. Five patients showed gross deficiency upon nocturnal penile tumescence monitoring. In comparison with a control group the patients showed a significantly lower overall Rbm index (p less than 0.001). IDDM patients showed an increased plasma GH response to insulin-induced hypoglycemia compared to NIDDM and normal subjects. Increased GH secretion was furthermore confirmed by GH values obtained in blood samples drawn during the first REM stage of the night in IDDM patients. The evaluation of the variables taken into consideration during sleep appears to be crucial for the assessment and prevention of autonomic neuropathies and neuroendocrine dysregulation in diabetic patients.
Acta Diabetol Lat
PMID:Wake and sleep cardiovascular reflex tests and GH profiles in diabetic patients. 261 29

In a previous study, we observed an impairment of the theophylline-induced suppressive system in recent onset IDDM patients, and demonstrated also a correlation with metabolic derangement. The aim of this study was to better investigate the relationship between theophylline sensitivity (ThS) and blood glucose/plasma insulin levels in recent onset IDDM patients subjected to preprogrammed variations by an insulin/glucose clamp with artificial pancreas. Eight patients were studied within 8 weeks from the onset of IDDM. ThS was evaluated as the ability of theophylline to inhibit blastogenic response of peripheral blood lymphocytes (PBL) to Concanavalin A (ConA), after 120 min preincubation of the cells. All patients were connected to an artificial pancreas. Through i.v. continuous insulin infusion (0.02 U/kg/h) and/or i.v. continuous glucose and saline infusion, the following experimental conditions, lasting at least 1h, were obtained: T1: relative euglycemia and normal insulinemia; T2: relative euglycemia and hyperinsulinemia; T3: hyperglycemia and normal insulinemia; T4: hyperglycemia and hyperinsulinemia. ThS was maintained in 6/8 patients at T1 and in 8/8 patients at T4. ThS was lost in 4/8 patients at T2 and T3. These data suggest that the loss of ThS induced by hyperglycemia can be corrected by hyperinsulinemia, and that it is maintained when euglycemia is accompanied by hypoinsulinemia. It is lost when these two parameters lose their interrelationship.
Acta Diabetol Lat
PMID:Impairment of lymphocyte suppressive system in recent onset insulin-dependent diabetes mellitus. Correlation with blood glucose and serum insulin levels. 269 17

Insulin autoantibodies (IAAs) are associated with type I diabetes mellitus (DM) and have been suggested as predictive markers of the disease. Using an ELISA assay, we have studied the prevalence of binding to human insulin in sera from an Arab type I DM population and compared it with the prevalence in the family members (FMs) of the probands, in type II DM patients from the same population, and in Arab control subjects. Significant levels of binding occurred in 11/16 (69%) of type I DM patients and in 21/34 (62%) of their FMs, but in only 5/31 (16%) of type II DM patients and in 1/25 (4%) of control subjects. Within families, there was homogeneity with regard to the level of insulin binding and the mean family levels correlated with those of the proband (r = 0.68, df = 7, p = 0.05). HLA-DR3 or -DR4 antigens occurred in 55/63 (87%) of type I DM patients and in 95/118 (81%) of their FMs. This was significantly higher (p less than 0.001) than in either type II DM patients (39/75, 52%) or in control subjects (34/93, 37%). ICAs were present in significantly more (25/43, 58%) of type I DM patients than their FMs (3/82, 3%) (p less than 0.001). They did not occur in either type II DM patients or in the control group. In conclusion, insulin binding occurred in sera from both type I diabetic patients and their kindred, and hence did not appear to be specifically associated with the development of clinical diabetes.
Acta Diabetol Lat
PMID:Insulin binding substances, autoimmunity and type I diabetes in Kuwaiti patients and their kindred. 278 62


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