UMLS:C0432222 - FACTA Search

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Query: UMLS:C0432222 (SEM)
47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the effects of age and duration and treatment of insulin-dependent diabetes (IDDM) on residual beta-cell function, we measured the fasting and Sustacal-stimulated serum C-peptide levels in 610 conventionally treated IDDM patients (age, 13-39 yr; duration of diabetes, 1-15 yr) during eligibility screening for the Diabetes Control and Complications Trial (DCCT). Fasting and stimulated C-peptide values were closely correlated (r = 0.83; P less than 0.001), and both declined with increasing duration of disease. However, among patients who had been diabetic for more than 5 yr, 11% (33 of 296) of adults compared with 0 of 75 adolescents (P less than 0.001) retained substantial insulin secretory capacity. Patients with stimulated C-peptide levels greater than 0.2 pmol/mL had a significantly lower mean fasting plasma glucose level [177 +/- 6 (+/- SEM) vs. 222 +/- 6 mg/dL; P less than 0.001), a smaller rise in glucose after Sustacal administration (151 +/- 5 vs. 184 +/- 3 mg/dL; P less than 0.001), and lower hemoglobin A1C (8.4 +/- 0.2% vs. 9.3 +/- 0.1%; P less than 0.001) than the patients with a stimulated C-peptide level of 0.05 pmol/mL or less, even though the C-peptide secretors were receiving less insulin (0.52 +/- 0.02 vs. 0.78 +/- 0.02 U/kg X day; P less than 0.001). To determine the effects of treatment of beta-cell function, 33 patients with stimulated C-peptide values between 0.2 and 0.5 pmol/mL at entry in the DCCT were restudied 1 yr after randomization to standard treatment (n = 15) or an experimental (n = 18) treatment designed to achieve and maintain near-normal glucose levels. Although C-peptide levels declined in both groups, experimental treatment was associated with slightly less of a decline in stimulated C-peptide values compared to Standard treatment. The results of C-peptide measurements in this large and well defined population of IDDM patients demonstrate that residual beta-cell function continues for a longer period of time in adults compared to adolescents with IDDM. This endogenous insulin secretion contributes significantly to metabolic control and may be prolonged by intensive insulin treatment regimens.
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PMID:Effects of age, duration and treatment of insulin-dependent diabetes mellitus on residual beta-cell function: observations during eligibility testing for the Diabetes Control and Complications Trial (DCCT). The DCCT Research Group. 288 29

Hormonal and glycemic changes in 22 rhesus monkeys were characterized during the first days after treatment with streptozotocin (STZ) (45 to 55 mg/kg, administered intravenously [IV]). Almost half (10/22) of the monkeys developed insulin-dependent diabetes mellitus (STZ-IDDM) within five days following injection. Four of the remaining monkeys did not become insulin dependent for at least 6 months after STZ treatment, during which time they were considered non-insulin-dependent, and eight monkeys never required exogenous insulin. In the STZ-IDDM group, plasma immunoreactive c-peptide (IRC-P) levels fell by three hours after STZ from a mean +/- SEM of 252 +/- 82 to 101 +/- 45 pg/mL, as glucose and immunoreactive glucagon (IRG) levels increased from 65 +/- 3 and 120 +/- 37, respectively, to 336 +/- 43 mg/dL and 234 +/- 52 pg/mL, respectively. Between six and 30 hours after treatment, IRC-P increased to a peak of 1,561 +/- 360 pg/mL before falling permanently to less than 60 pg/mL by 66 hours. During this period, glucose and IRG responded in a reciprocal fashion by falling and then increasing to levels above 300 mg/dL and 300 pg/mL, respectively, by 66 hours. In the non-insulin-dependent diabetes mellitus (STZ-NIDDM) group, no clear reciprocal relationship between IRC-P and glucose and IRG was obtained. In nine additional monkeys subjected to total pancreatectomy (Px), IRC-P and IRG levels fell immediately and permanently by greater than 90% and 75%, respectively. Levels of immunoreactive somatostatin increased steadily over the initial 96 hours following STZ, but did so both STZ-IDDM and Px monkey groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical changes in rhesus monkey during the first days after streptozotocin administration are indicative of selective beta cell destruction. 296 84

Subcutaneous oxygen tension (tissue PO2) was measured by a polarographic method in the legs of insulin-dependent diabetics (IDDM) and controls. Current flow was measured continuously using a five-stage protocol: baseline; 4 min of complete arterial occlusion; during recovery from ischemia; baseline approximately re-established; induction of hyperemia by local application of heat. Eleven patients with IDDM of 4-32 years of duration, without peripheral arterial disease, were studied and compared with 10 controls. The mean baseline subcutaneous PO2 in diabetics was less than controls; however, the difference was not statistically significant. At the end of arterial occlusion the mean decrease in tissue PO2 was less (P less than 0.025) in diabetics (4.7 +/- 0.9 mm Hg, SEM) compared to controls (10.2 +/- 1.6 mm Hg). With induction of hyperemia the increase in tissue PO2 was lower (P less than 0.001) in diabetics (7.4 +/- 0.4 mm Hg) than in controls (18.6 +/- 1.7 mm Hg). The observed differences provide for the first time direct evidence of altered tissue PO2 responses in diabetes.
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PMID:Altered tissue oxygen tension responsiveness in diabetes. 374 59

The determination of serum C-peptide has been found to be a sensitive indicator of endogenous insulin secretion, and serves to define diabetic patients who require insulin therapy i.e., insulin-dependent (Type I, IDDM) and those non-insulin dependent (Type II, NIDDM). The aim of our study is to establish the types of diabetes mellitus with C-peptide measurement in a group of diabetic subjects on different modes of therapy. Eighty-eight diabetic patients (60 males, 28 females) were studied. Thirty-four were on insulin (age 40 +/- 2 years; means +/- SEM), 35 on oral agents (54 +/- 1 years), and 19 on diet alone (46 +/- 3 years). Twenty healthy subjects (10 males, 10 females) serve as normal controls (37 +/- 3 years). Blood samples for serum C-peptide and blood glucose estimations were obtained after an overnight fast and one hour after a 75 grams oral glucose load. Fasting C-peptide levels obtained for the various groups were: 0.62 +/- 0.07 (nmol/L, means +/- SEM) (normal), 0.16 +/- 0.02 (insulin), 0.79 +/- 0.06 (oral), 2.15 +/- 0.15 (diet). The C-peptide values after oral glucose were 1.80 +/- 0.20 (normal), 0.23 +/- 0.05 (insulin), 1.72 +/- 0.02 (oral), 2.15 +/- 0.15 (diet). Both the fasting and post-glucose C-peptide concentrations were significantly lower (p less than 0.001) in the insulin group compared to the normals, whereas values for the diet and oral groups were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin secretory capacity in Singapore diabetic subjects. 389 77

In order to evaluate the effects of moderate alcohol intake on intermediate metabolites, five normal subjects and five euglycemic insulin-dependent diabetics (IDDM) were administered two different isocaloric diets; in one diet 35% of the caloric intake consisted of red wine. The insulin-dependent diabetics were connected to an artificial endocrine pancreas (AEP), and glucose levels were continuously monitored. Blood lactate, pyruvate, acetoacetate (AcAc), 3-hydroxybutyrate (3-OHB), glycerol, free fatty acids (FFA), and alanine levels were measured over a 15-hour period from 9 AM to 12 PM. The results showed that alcohol intake did not significantly influence the glucose profiles in either group (111 +/- 4 mg/100 ml versus 110 +/- 4 mg/100 ml for IDDM; 72 +/- 2 mg/100 ml versus 82 +/- 3 mg/100 ml for controls, 15-hour mean +/- SEM), but in both groups it induced a marked increased in the levels of lactate (1.115 +/- 0.067 mM/liter with alcohol versus 0.706 +/- 0.031 mM/liter without alcohol for IDDM; 0.847 +/- 0.052 mM/liter with alcohol versus 0.666 +/- 0.035 mM/liter without alcohol for controls), in the lactate/pyruvate ratio (24.04 +/- 2.12 with alcohol versus 11.42 +/- 0.20 without alcohol for IDDM; 20.84 +/- 2.16 with alcohol versus 11.62 +/- 0.27 without alcohol for controls), in the levels of 3-OHB (0.081 +/- 0.007 mM/liter with alcohol versus 0.046 +/- 0.003 mM/liter without alcohol for IDDM; 0.067 +/- 0.007 mM/liter with alcohol versus 0.025 +/- 0.002 mM/liter without alcohol for controls) and in the 3-OHB/AcAc ratio (1.452 +/- 0.153 with alcohol versus 0.599 +/- 0.036 without alcohol for IDDM; 1.723 +/- 0.198 with alcohol versus 0.439 +/- 0.040 without alcohol for controls) because of a more reduced redox state. Alcohol intake during meals depressed alanine concentration, while glycerol levels showed a transient increase. Reduced blood FFA concentrations after alcohol intake were observed only in controls. This study demonstrates that moderate alcohol intake with meals also affects intermediate metabolites despite euglycemia. These effects were similar both in normal subjects and in IDDM, even if the harmful effects of alcohol may be enhanced by poor metabolic control in the latter.
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PMID:Metabolic effects of moderate alcohol intake with meals in insulin-dependent diabetics controlled by artificial endocrine pancreas (AEP) and in normal subjects. 634 61

Synthesis of interleukin-2 (IL-2) by lymphocytes from 26 insulin-dependent diabetic subjects (IDDM) was compared with that by lymphocytes from 24 nondiabetic control subjects. The control group produced 1.001 +/- 0.071 U/ml (mean +/- SEM). The IDDM group, containing patients diagnosed between 5 days and 10 yr before testing, produced only 0.59 +/- 0.050 U/ml (P less than 0.002). IL-2 synthesis by 6 non-insulin-dependent diabetic subjects (NIDDM) was not decreased (mean +/- SEM, 1.20 +/- 0.04 U/ml). Moreover, decreased levels of IL-2 production was found with lymphocytes of patients in good control, as well as those in poor control. These data suggest that decreased IL-2 synthesis is specific for IDDM, not explainable solely as a consequence of poor metabolic control, and thus, might be involved in the pathogenesis of the disease.
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PMID:Decreased synthesis of interleukin-2 (IL-2) in insulin-dependent diabetes mellitus. 660 55

Insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1) modulates the metabolic and mitogenic effects of IGFs. Although IGFBP-1 levels are abnormally high in insulin-dependent diabetes (IDDM), relatively little is known in NIDDM; conflicting data have suggested both high and low levels. We investigated whether treatment modifies IGFBP-1 levels in two groups of NIDDM patients. Study 1 examined fasting concentrations in groups of patients with NIDDM, comparable except for treatment type (sulfonylurea, n = 23; once daily insulin, n = 15; sulfonylurea plus once daily insulin, n = 14; multiple insulin injections, n = 9) and 25 nondiabetic subjects. In sulfonylurea-treated patients there were markedly reduced plasma IGFBP-1 concentrations (median, interquartile range in parentheses): control, 61.0 (36-96) micrograms/L; sulfonylureas alone, 31.5 (21-61) micrograms/L (P < 0.01); and sulfonylureas plus insulin, 31.5 (9-53) micrograms/L (P < 0.01). Once daily insulin was associated with values similar to those in the control group [62.0 (27-103) micrograms/L; P = NS], whereas IGFBP-1 levels were higher with multiple insulin injection therapy [156.0 (71-184) micrograms/L; P < 0.05]. Proinsulin levels were higher in sulfonylurea-treated patients, but there was no significant correlation between IGFBP-1 and proinsulin within any individual group. Study 2 examined the effects of treatment on the dynamics of IGFBP-1 levels between 0800-1900 h. In control subjects (n = 8), levels fell from 0800 h (mean +/- SEM, 22.4 +/- 5.2 micrograms/L) to 1000 h (14 +/- 5.2 micrograms/L), followed by a rise, more rapid after food, to a peak at 1240 h (20.6 +/- 3.7 micrograms/L). Levels then declined until 1500 h (10.7 +/- 2.9 micrograms/L), with a further postprandial peak at 1840 h (23.1 +/- 3.2 micrograms/L). Sulfonylurea therapy (n = 6) resulted in a complete loss of this pattern, with a marked fall in IGFBP-1 from 0800 h (22 +/- 2.7 micrograms/L) to less than 7 micrograms/L for the remainder of the study (area under the curve, 1150-1400 h, P < 0.001 vs. control). By contrast, in metformin-treated patients (n = 7), neither IGFBP-1 levels nor postprandial peaks were significantly different from those in the control group. Our findings suggest that in patients with NIDDM, the regulation of IGFBP-1 is markedly influenced by the choice of treatment.
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PMID:Choice of treatment affects plasma levels of insulin-like growth factor-binding protein-1 in noninsulin-dependent diabetes mellitus. 753 8

Although increased plasma fibronectin (PF) levels have been found in diabetic patients with microalbuminuria, there is still controversy about its clinical implication for detecting early diabetic nephropathy. To evaluate the PF concentration as a possible marker for early diabetic nephropathy, three groups of sex-and age-matched patients were studied I) 22 insulin dependent diabetic (IDDM) patients with microalbuminuria (mean age +/- SEM: 23.3 +/- 3.6 years, mean urinary albumin excretion rate (AER) +/- SEM: 47.1 +/- 39.5 micrograms/min); II) 17 IDDM patients with normoalbuminuria (mean age: 23.4 +/- 4.4 years, mean AER: 7.8 +/- 2.1 micrograms/min) and III) 20 healthy control subjects (mean age: 22.6 +/- 4.1 years, mean AER: 6.7 +/- 2.1 micrograms/min). PF and urinary excretion of albumin were measured by an immunoturbidimetric method using commercially available kits (Boehringer Mannheim GMBH FRG, and Miles Lab., UK). The mean PF was significantly higher in the group with microalbuminuria (406.5 +/- 122.9 micrograms/ml) than in the group with normoalbuminuria (295.6 +/- 96.9 micrograms/ml, P < 0.01) or in the control group (299.54 +/- 105.5 micrograms/ml, P < 0.01). A weak positive correlation was found between PF and urinary albumin values (r = 0.35, P < 0.05). There were no significant correlations between PF and the other variables such as age, duration of diabetes, body mass index, arterial blood pressure, fasting blood glucose, fructosamine and HbA1 in the diabetic patients or in the control group. Our results suggest that the PF concentration could be a weak marker for early diabetic nephropathy. We cannot therefore use PF instead of microalbuminuria because there is only a weak correlation between PF and microalbuminuria.
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PMID:Can we use plasma fibronectin levels as a marker for early diabetic nephropathy. 762 76

Abnormal vascular reactivity has been implicated in the aetiology of diabetic microvascular disease and we have previously demonstrated enhanced contractility of hand veins to noradrenaline in insulin-dependent diabetic (IDDM) patients with microalbuminuria. We have now assessed the possible contribution of subclinical peripheral nerve dysfunction to exaggerated vascular reactivity in micro-albuminuric patients. Twenty-five IDDM patients (15 with microalbuminuria), none of whom had symptomatic neuropathy, and 10 control subjects were studied. Vasoconstrictor responses were measured in dorsal hand veins using noradrenaline and phenylephrine. Conduction in median, peroneal and sural nerves was assessed using electrophysiology, and autonomic function using standard cardiovascular reflex tests. The noradrenaline dose causing 50% vasoconstriction was significantly lower in the microalbuminuric diabetic subjects compared with normoalbuminuric (3.6(1.7) mean (SEM) ng/min vs 20.1(6.0) ng/min, p = 0.0002) and non-diabetic subjects (35.1(5.0) ng/min; p < 0.0001). However, reactivity to phenylephrine did not differ between the groups. Median nerve motor conduction velocity was significantly slower in microalbuminuric (48.4(1.4) m/s) than in normoalbuminuric (52.7(1.2) m/s, p = 0.04) and non-diabetic subjects (56.7(0.9) m/s, p = 0.0001). In the diabetic group overall, there was a strongly positive linear correlation between vascular response to noradrenaline and conduction velocity in both the median nerve (r = 0.62, p = 0.0009) and peroneal nerve (r = 0.53, p = 0.006). There was no correlation between phenylephrine-induced responses and motor conduction velocity in either nerve, nor were indices of autonomic function correlated with vascular reactivity to either agent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Asymptomatic peripheral nerve dysfunction and vascular reactivity in IDDM patients with and without microalbuminuria. 785 85

We studied a group of 50 adolescents, average age 16 years, with diagnosed IDDM present for about seven years. Twenty-five had microalbuminuria (MA) averaging 111.0 +/- 34.0 (SEM) micrograms/min albumin excretion rate versus 6.7 +/- 7.4 micrograms/min in the 25 without MA. In other respects, such as sex ratio, age, body mass index, duration of IDDM, hemoglobin A1c, and normotensive systolic, diastolic and mean blood pressures (BP), these subgroups were closely matched. We compared them with a control group of 39 normotensive adolescents, of whom 18 were carefully matched siblings of the IDDM subjects with MA and 21 were similarly matched siblings of the IDDM non-MA subjects. Plasma renin concentration was determined by a direct radioimmunoassay method (Sanofi-Pasteur) and found to be virtually the same in the control and IDDM adolescents as a whole. There was also no real difference between the MA and non-MA subgroups. In contrast, plasma prorenin was significantly higher in the combined IDDM group (197.5 +/- 9.3 vs. control, 134.0 +/- 7.9 pg/ml, P < 0.0001). It was also higher in the MA subgroup than in the non-MA subgroup (226.4 +/- 13.6 vs. 168.5 +/- 10.1 pg/ml, P < 0.001). Interestingly, the 18 control siblings matching the MA subgroup had higher plasma prorenin than the 21 control siblings matching the non-MA subgroup (P < 0.001), suggesting a familial predisposition that precedes detectable diabetes and nephropathy. Our findings confirm and extend reports by other workers that elevated plasma prorenin is associated with incipient nephropathy, manifested by MA. The exclusive renal origin of this prorenin, its role in plasma, and the mechanism responsible for its elevation in IDDM with MA, are yet to be demonstrated, as is the general applicability of these findings to different populations of diabetics, with a higher incidence and severity of complications.
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PMID:Plasma prorenin as an early marker of nephropathy in diabetic (IDDM) adolescents. 786 11

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