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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 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

The influence of sulfonylurea drugs in enhancing the effect of endogenous insulin is well documented. Furthermore, combination therapy with sulfonylurea and insulin is effective in the treatment of type II diabetes mellitus. Therefore, to assess the efficacy of this type of combination therapy in type I diabetes, we conducted a double-blind clinical trial with tolazamide and insulin in 15 subjects with type I diabetes. The diagnosis of type I diabetes was confirmed by previous episodes of diabetic ketoacidosis and undetectable C-peptide levels in serum samples from blood drawn from patients two hours after breakfast. During the study protocol, placebo or tolazamide was randomly added to insulin and the combination therapy was continued for three months. In the placebo group, levels of fasting plasma glucose (FPG) and hemoglobin A1c (HbA1c) did not alter significantly at the end of the study period. However, in the tolazamide group, levels of FPG and HbA1c markedly improved after administration of tolazamide (FPG levels before therapy, 10.8 +/- 0.9 mmol/L [mean +/- SEM]; after therapy, 6.7 +/- 0.4 mmol/L; HbA1c levels before therapy, 10.9% +/- 0.6%; after therapy, 9.6% +/- 0.5%). Therefore, adjuvant therapy with tolazamide and insulin may be beneficial in achieving adequate metabolic control in type I diabetes mellitus.
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PMID:Improved metabolic control in insulin-dependent diabetes mellitus with insulin and tolazamide. 304 37

In most studies the distribution of peripheral lymphocyte subsets at diagnosis of type 1 diabetes has been found to be altered. Lymphocyte subpopulations were therefore studied during longitudinal changes in the glycaemic control of 11 type 1 diabetics to investigate whether poor metabolic status affects these results. To avoid any influence of the etiopathogenetic mechanisms, the patients studied had a disease duration of 10 +/- 2 (SEM) years and all but one had no residual beta-cell function. The patients were selected randomly amongst those with a long record of poor glycaemic control and at the first examination they had a mean fasting blood glucose of 15 +/- 1 mmol/l and a mean glucosuria of 67 +/- 11 g/24 h. They were then hospitalized and strictly regulated using pump treatment, resulting in a massive reduction in glucosuria (0 +/- 0 g/24 h) and fasting blood glucose (6 +/- 1 mmol/l) at a second examination a week later. Five of the patients were tested for a third time 35 +/- 4 days later and were still in very good glycaemic control. Peripheral lymphocytes were labelled with monoclonal antibodies and examined by flow cytometry (FACS). Neither CD3+ (pan) T-lymphocytes, CD4+ (helper) T-cells, CD8+ (suppressor/cytotoxic) T-cells, the relation between CD4+ and CD8+ T-cells, nor the total amount of lymphocytes, changed significantly between the first, second, and third examination. None of the results were significantly different from those of healthy controls. There was no correlation between any of the immunological and metabolic parameters. It is concluded that metabolic influence on the distribution of lymphocyte subsets is unlikely.
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PMID:Metabolic state does not influence lymphocyte subsets in type 1 diabetic patients. 307 40

Left ventricular function was evaluated noninvasively before and three months after starting insulin treatment in nine patients (mean age 61.8 years, range 51-68 years) with non-insulin dependent diabetes showing an impaired insulin secretion capacity. After starting insulin treatment, fasting blood glucose decreased from 12.9 +/- 0.5 mmol/l (mean +/- SEM) to 9.8 +/- 1.2 mmol/l (p = 0.03), but the decrease of glycosylated haemoglobin Alc was not significant (9.0 +/- 0.4% vs. 8.3 +/- 0.6%). On systolic time intervals, PEP/LVET ratio improved from 0.44 +/- 0.03 to 0.37 +/- 0.02 (p = 0.03). On M-mode echocardiography, E-F slope became steeper (89 +/- 6 mm/sec vs. 103 +/- 8 mm/sec; p = 0.01) but no significant changes were observed in other variables reflecting diastolic or systolic function. On equilibrium radionuclide angiocardiography, the left ventricular ejection fraction at rest was similar before and after starting insulin treatment (48.6 +/- 3.2% vs. 49.2 +/- 2.8%) but during peak exercise the left ventricular ejection fraction improved significantly (51.0 +/- 5.3% vs. 59.9 +/- 4.7%; p = 0.02). The change of PEP/LVET ratio correlated significantly with the changes of blood glucose and glycosylated haemoglobin Alc levels, but the correlation between these metabolic variables and the change of left ventricular ejection fraction during exercise did not reach statistical significance. In conclusion, the left ventricular function improved concomitantly with improved metabolic control after starting insulin treatment in middle-aged patients with non-insulin-dependent diabetes having an impairment in insulin secretion capacity. This finding suggests that metabolic factors are involved in the left ventricular dysfunction observed in diabetes.
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PMID:Improvement of left ventricular function after starting insulin treatment in patients with non-insulin-dependent diabetes. 307 42

A longitudinal study was carried out of all patients with newly acquired insulin dependent diabetes during pregnancy (as distinct from non-insulin-dependent gestational diabetes) seen at the Copenhagen Centre for Diabetes and Pregnancy during 1966 to 1980. The series comprised 63 patients with a mean age of 27 (SEM 1) years. At diagnosis the mean fasting blood glucose concentration was 15.6 (1.3) mmol/l and mean maximal insulin dose 49 (3) IU/day. At a prospective follow up examination a mean of 8 (SEM 1) years after diagnosis 46 of 60 patients (77%) were being treated with insulin (35 (2) IU/day) and had a very low mean stimulated plasma C peptide value (0.12 (0.02) nmol/l) suggesting absent or nearly absent beta cell function. The remaining 14 patients (23%), not currently receiving insulin, appeared to be severely glucose intolerant, having a mean fasting blood glucose concentration of 13.4 (1.2) mmol/l. Thus most of these patients developing insulin dependent diabetes during pregnancy had true type I disease. Compared with the age specific incidence of type I diabetes in the background population of women the incidence was at least 70% higher in pregnant than non-pregnant women (p less than 0.001; chi 2 = 11.6; f = 1). This increased incidence occurred in the third trimester when the risk of developing type I diabetes was 3.8 times that of non-pregnant women (p less than 0.000001; chi 2 = 35.6; f = 1). Finally, the risk of developing insulin dependent diabetes during pregnancy was lower when conception occurred in the winter (p less than 0.05; chi 2 = 4.18; f = 1).
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PMID:Increased incidence of true type I diabetes acquired during pregnancy. 310 40

Although glycosuria is important in the control of diabetes in children, few studies clearly show its significance as compared to glycemia. The aim of the present study was therefore to determine the two parameters that control glucose presence in urine, i.e. glucose glomerular filtration rate (GFR) and tubular reabsorption (JrG). GFR was measured by using a 110 min polyfructosan perfusion in 96 diabetic children and adolescents. The results are as follows: 1) In this population there is a significant correlation (p less than 0.01) between the quantity of glucose in urine and mean glycemia during the test; 2) polyfructosan clearance that reflects GFR in diabetic children without renal complication is 2.11 +/- 0.04 ml/s 1.73 m2, or 126 +/- 2.4 ml/min 1.73 m2 (mean +/- SEM); it is higher than in the reference values already published; 3) JrG is correlated with glucose filtered load (p less than 0.01), GFR (p less than 0.01) and sodium reabsorption (p less than 0.01). The ratio JrG/GFR could be substituted for the classical concept of "renal threshold", as it can be easily measured and may help in interpreting glycosuria in some diabetic children. To conclude, in IDD children, the parameters controlling glycosuria may be studied by a simple method. The clinical value of such renal exploration has still to be determined.
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PMID:[Glomerular filtration and tubular reabsorption of glucose in insulin-dependent diabetes in children]. 370 76

Serum C4 concentrations were measured in 102 healthy subjects and 90 subjects with type I diabetes mellitus. A wide range was observed in the group as a whole (0.08-0.67 g/l; mean = 0.26 g/l; SEM = 0.01 g/l). After C4 allotyping it was possible to subgroup 134 of these subjects according to the number of C4 null alleles present. C4 concentrations in the group with two null alleles were lower than in the group without null alleles (mean 0.2 v 0.37 g/l; p less than 0.001). C4 concentrations in the group with one C4 null allele were intermediate and significantly different from those of the group without null alleles (mean 0.24 v 0.37 g/l; p less than 0.001). Appropriate analysis has defined reference ranges for serum C4 concentrations in subjects with two, one, or zero C4 null alleles. Interpretation of low serum C4 concentrations should take account of the number of C4 null alleles present.
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PMID:Reference ranges for serum C4 concentrations in subjects with and without C4 null alleles. 372 9

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


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