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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 leucocyte migration inhibition test (LMT) using the agarose plate method introduced by Clausen is simple and highly reproducible. Using human pancreas extract and beef insulin as antigen, LMT was performed on ten patients with insulin dependent diabetes, twenty patients with insulin independent diabetes, and twelve healthy controls. The migration index was expressed as a percentage of migration calculated from the following formula. Migration index (MI) = average areas of migration in test suspension/average areas of migration in control suspension. Using human pancreas extract, the mean migration index for the insulin dependent diabetics (87.6 +/- 11.1) was significantly lower than in the normal subjects (99.3 +/- 6.3) (p less than 0.05). Using beef insulin as antigen for the insulin dependent diabetics and insulin independent diabetics, the mean migration indices (+/- SD) were 95.8 +/- 14.9 and 98.7 +/- 12.3 respectively. The corresponding values for the control group were 98.9 +/- 7.8. Cellular hypersensitivity to human pancreas extract was shown in the leucocyte migration inhibition test with insulin dependent diabetics, but a negative result was obtained with beef insulin.
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PMID:[Leucocyte migration inhibition test in diabetes mellitus (author's transl)]. 91 18

In 25 diabetics and 8 controls the insulin hypoglycemia test was performed with subsequent determination of growth hormone secretion by the radioimmunoassay method. The rise of the growth hormone level began earlier and persisted longer in diabetics as compared with controls. Juvenile diabetes was associated with a rapid secretory response of the hormone while in maturity-type diabetes the release of growth hormone in response to stimulation was excessive but delayed. A somewhat lower secretory response was found in diabetes lasting over 5 years as compared with short-lasting diabetes. The observed phenomena were not related to the absolute blood glucose level. Although the phenomenon of growth hormone hypersecretion remains yet to be explained, it seems, however, to be secondary to carbohydrate metabolism disturbance and insulin disorders.
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PMID:Secretion of growth hormone in the insulin test in various forms of diabetes. 95 43

HLA-A and B antigens were determined in 112 patients with insulin-dependent juvenile onset diabetes mellitus, who could be subdivided into "non" and "high responder" to insulin. The data revealed a trend of an association of these diabetes subgroups with only one of the diabetes-associated antigens HLA-B8 and HLA-BW15 and indicated the existence of at least two different genetic constellations for susceptibility to juvenile diabetes mellitus. One form with a strong immune-response to insulin seemed to be associated with HLA-BW 15 and the other form without humoral immunoreactivity to insulin seemed to be associated with the presence of HLA-B8 and the absence of HLA-B7.
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PMID:HLA antigens and immunoresponsiveness to insulin in insulin-dependent diabetes mellitus. 96 73

Intravenous glucose tolerance test(taking the age dependent variabilities of the glucose assimilation into consideration) was performed in 68 blood relations (30 siblings, 19 parents, 19 children) of 19 patients with juvenile onset diabetes mellitus (JODM). In 29,4% of the first degree relatives (in 20% of the siblings, in 42% of the parents and in 31,6% of the children) an abnormal glucose tolerance was found. Four of the siblings presented with insulin dependent JODM. Glucose intolerance was detected more often (42%) in siblings and parents of patients with later onset (after age 25) JODM than in siblings and parents of JODM-patients with onset before age 25 (20%).
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PMID:[Age-corrected analysis of glucose tolerance in blood relations of patients with juvenile onset diabetes mellitus]. 102 Mar 80

Adipose tissue cellularity was determined by a microscopic method in 18 men suffering from insulin dependent, juvenile diabetes mellitus for several years. These results were set in relation to the degree of clinical control estimated from the average urinary glucose output or fasting blood glucose during the year preceding the investigation. Furthermore, the results were compared with controls of comparable age and of the same sex. Both young and middleaged diabetic men had smaller fat cells than non-diabetic men. Fat cell size was correlated to the degree of clinical control, small fat cells indicating a poor control. It was suggested that fat cell size might be included as a measure of the long-term metabolic control in patients with insulin dependent diabetes mellitus.
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PMID:Adipose tissue cellularity in relation to metabolism in juvenile onset diabetes mellitus. 109 82

Seventy-three patients with juvenile diabetes mellitus for a mean duration of 42.9 years were retrospectively studied on a multidisciplinary basis. Only three of this group of patients were socially disabled as a result of their long-standing illness. Of all the complications, insulin-induced hypoglycemia was most common. Although diabetic retinopathy was clinically evident in about 75 per cent of patients, only 50 per cent of these seventy-three patients had a significant visual impairment. Nephropathy was apparent in 59 per cent of patients, and neuropathy was demonstrable in half of them. Significant peripheral vascular system impairment was present in 40 per cent and major cardiac complication in 20 percent.
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PMID:Juvenile diabetes mellitus after forty years. 114 May 12

Tumor necrosis factor beta (TNF-beta) (lymphotoxin) may play an important role in the immune response and pathologic inflammatory diseases. Insulitis is an important early step in the development of insulin-dependent diabetes mellitus. To understand better the role of TNF-beta in the regulation of inflammation and type 1 diabetes, we produced transgenic mice in which the murine TNF-beta gene was regulated by the rat insulin II promoter. The transgene was expressed in the pancreas, kidney, and skin of transgenic mice. The expression of TNF-beta in the pancreas of transgenic mice resulted in a leukocytic inflammatory infiltrate consisting primarily of B220+ IgM+ B cells and CD4+ and CD8+ T cells. The insulitis is reminiscent of the early stages of diabetes, though the mice did not progress to diabetes.
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PMID:Insulitis in transgenic mice expressing tumor necrosis factor beta (lymphotoxin) in the pancreas. 127 67

Flow cytometry with monoclonal antibody Leu-7 (CD57), Leu-11 (CD56) and Leu-19 (CD56) were used to study the content of different subpopulations of natural killer cells (NK-cells) in the blood of type I diabetes mellitus patients before and after insulin treatment and in healthy people. After a course of insulin therapy most patients showed restoration of the total cell number with antigens on their surface characteristic of NK-cells, especially CD56, that indicates the essential role of hypoinsulin in the depression of the NK-system. At the same time a small group of patients was distinguished who did not show such normalization. This may indicate participation of other mechanisms in the formation of natural immunity failure, in particular, the genetic.
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PMID:[The effect of insulin therapy on the level of natural killer cells of different immunological phenotypes (CD16+, CD56+ and CD57+) in the blood of patients with diabetes mellitus type I]. 128 83

The changes in plasma gastrin-releasing peptide (GRP), arginine vasopressin (AVP), neuropeptide Y (NPY), corticotropin releasing hormone (CRH), galanin, ACTH, cortisol, delta sleep-inducing peptide (DSIP), adrenaline, noradrenaline and pancreatic polypeptide (PP) were measured after 5 and 15 minutes of acute insulin-induced moderate hypoglycaemia (2.0 mmol/l) in 10 patients with Type 1 diabetes mellitus with no autonomic neuropathy and in 10 healthy subjects. Plasma catecholamine and PP levels rose in both groups in response to hypoglycemia and the secretory response of ACTH was lower in the diabetic subjects (p < 0.01). GRP concentrations increased during hypoglycaemia (p < 0.01) while a reduction in AVP occurred at the start of hypoglycaemia (p < 0.001). The plasma AVP concentrations were higher in the diabetic group compared with those in the normal group (p < 0.05). The NPY concentrations were higher in the normal subjects (p < 0.05) but no change in the mean level occurred in either group during hypoglycaemia. No group differences or changes in mean plasma concentrations were found for galanin, DSIP and CRH. These observations support the view that regulatory peptides, if involved in glucose homeostasis, may rather have a modulatory effect than a direct action in restoring normoglycaemia.
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PMID:The response of regulatory peptides to moderate hypoglycaemia of short duration in type 1 (insulin-dependent) diabetes mellitus and in normal man. 128 60

Nicotinamide (NCT) has been shown to be effective in preventing the onset of type 1 diabetes mellitus (IDDM) in mice with non-obese diabetic (NOD) and beta cell damage, mediated by the diabetogenic agents including streptozotocin. NCT therapy in man has been shown to have a beneficial effect on the remission phase of IDDM, and its use is safe. In this open pilot trial we therefore studied the effect of oral NCT administration on insulin secretion rate and islet-cell antibody (ICA) titres in IDDM high risk subjects. NCT (25 mg/10 kg bw) was administered in 6/13 high risk patients identified by a family screening programme. Those subjects tested after eight months without treatment showed a decreasing secretion in comparison to onset baseline (56,1 +/- 37.8 versus 35,5 +/- 12.2), whereas the treated subjects showed an increasing insulin secretion after treatment (26 +/- 10 versus 50.2 +/- 26.6), in spite of ICA persistence. Statistical analysis shows an increased insulin secretion in the treated group versus the untreated group (chi 2 = 3.899, P = 0.048). No side-effects were observed. We conclude that NCT may repair beta-cell function in high risk subjects too if damage is not too severe; furthermore, the effect seems not to be mediated by an immune mechanism.
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PMID:Nicotinamide treatment in subjects at high risk of developing IDDM improves insulin secretion. 128 17


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