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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a six year period twelve patients with insulin dependent diabetes and end-stage renal failure received cadaveric kidney grafts. Eleven of the patients have previous to this been hemodialysed, one patient was transplanted before hemodialysis was necessary. The cumulative two year survival was thirty-seven per cent for the patients, and twenty-nine per cent for the kidney grafts. The average time of observation was eleven months, the motality was fifty per cent. The causes of death were acute myocardial infarction in two cases, sepsis in two cases, severe hypoglycemia in one case and unexpected sudden death in one case. The most prominent problems in the treatment of the diabetic patients after the renal transplantation were difficulties in the regulation of the diabetes, rejections, infections, cardiac failure and aggravation in pre-existing hypertension.
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PMID:Renal transplantation in patients with insulin requiring diabetes and renal failure. 78 7

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

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

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

High blood sugar levels in the morning in juvenile type 1 diabetics may be caused by a Somogyi phenomenon (counter-regulation after nocturnal hypoglycaemia) or insulin resistance in the morning hours (dawn phenomenon). To enable differentiation between the two, 1,562 blood sugar profiles (24 h, 3 h, 6 h) were determined in 161 children and juveniles (74 boys, 87 girls; mean age 10.8 [1.0-19.7] years) with type 1 diabetes mellitus. In accordance with the mechanism of the dawn phenomenon there was a close positive correlation between the blood sugar levels in the night and morning (r = +0.696; P less than 0.0001); the mean fasting blood sugar level was about 60 mg/dl above the 3 h value. Low nocturnal blood sugar levels as a possible cause of a high morning blood sugar (greater than 250 mg/dl) was demonstrated in fewer than 1% of profiles. On the other hand, the probability of nocturnal hypoglycaemia rose exponentially in the presence of low morning fasting blood sugar levels. Thus, if the morning level was below 80 mg/dl, the blood sugar levels at 3 h was below 50 mg/dl in 41.2%. This indicates that high morning blood sugar levels result from the dawn phenomenon and require a higher evening dose of slow-release insulin. But if the morning blood sugar values are clearly below 100 mg/dl, the cause may be nocturnal low blood sugar levels and the evening insulin dose should, therefore, be reduced.
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PMID:[The dawn or Somogyi phenomenon? High morning fasting blood sugar values in young type-1 diabetics]. 139 35

We evaluated the effect of previous experimental hypoglycemia on counterregulatory responses to hypoglycemia in 13 IDDM patients. These patients had defects in counterregulatory responses to hypoglycemia compared with 7 nondiabetic control subjects. Plasma EPI and glucagon responses to hypoglycemia in IDDM patients were approximately 60% of levels in nondiabetic subjects (P less than 0.02 and P less than 0.001, respectively). Hepatic glucose output ([3-3H]glucose) was reduced by approximately 60% of normal (P less than 0.005), and the glucose infusion rate required to maintain plasma glucose was correspondingly greater in people with IDDM (P less than 0.001). With a modified glucose clamp (plasma insulin approximately 330 pM), the diabetic subjects underwent two sequential 120-min periods of hypoglycemia (approximately 3.0 mM) with an intervening 60-min euglycemic recovery period. In the IDDM patients, there were 30-50% decreases in plasma GH (P less than 0.005) and cortisol (P less than 0.001) responses during the second hypoglycemic period compared with the first. In addition, glucose output, already defective compared with that in nondiabetic subjects, was further reduced by 33% (P = 0.03) during the second period of experimental hypoglycemia. There was no effect of repeated hypoglycemia on the responses of plasma glucagon, EPI, or NE, though plasma EPI was correlated directly with glucose output (P less than 0.001) and inversely with glucose uptake (P less than 0.05). There was no correlation between the rise in glucose output during hypoglycemia and antecedent glycemic control as measured by HbA1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Further defects in counterregulatory responses induced by recurrent hypoglycemia in IDDM. 139 8

Defective glucose counterregulation commonly seen in intensively treated insulin-dependent diabetes (IDDM) is mediated in part by a failure of compensatory stimulation of hepatic glucose production. Since the response of the liver to insulin-induced hypoglycemia normally involves activation of gluconeogenesis, we measured [14C]alanine conversion to [14C]glucose (a qualitative index of gluconeogenesis) and glucose production (using [3-3H]glucose) in seven intensively treated type I diabetic subjects (hemoglobin-A1, 7.1 +/- 0.4%) during low dose infusion of insulin (0.3 mU/kg.min for 210 min). IDDM patients received insulin overnight to maintain euglycemia before study. Although insulin levels rose to a similar extent as those in normal control subjects (n = 6), the fall in plasma glucose was markedly greater in IDDM (2.5 +/- 0.2 vs. 3.64 +/- 0.2 mM in controls; P < 0.01). The glucagon response was totally lost in IDDM, and epinephrine release was delayed and slightly reduced compared to that in control subjects. In contrast to that in normal subjects, hepatic glucose production in the IDDM subjects remained persistently suppressed by about 60% throughout the study. The conversion of alanine and lactate to glucose remained virtually unchanged in the IDDM, whereas in controls it increased 2-fold above baseline during the last hour of the study. Our data suggest that the failure of gluconeogenesis to increase during hypoglycemia is an important factor contributing to the defective hepatic response observed in the intensively treated type I diabetic subjects.
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PMID:Impaired stimulation of gluconeogenesis during prolonged hypoglycemia in intensively treated insulin-dependent diabetic subjects. 140 Aug 74

The acute and chronic effects of hypoglycemia on cognitive and psychomotor performance are reviewed. Studies involving pediatric and adult subjects, both with and without diabetes were evaluated. The preponderance of studies suggest that hypoglycemia can be an unintended yet frequent result of treatment of patients with IDDM. Significant cognitive and psychomotor deficits were reported even with mild episodes of hypoglycemia. Early age of diabetes onset and frequent episodes of hypoglycemia were found to be highly related to significant deficits in intellectual and academic performance. Patients evidencing performance deficits did not always report symptoms of hypoglycemia. Recovery of cognitive functioning lagged restoration of euglycemia but typically returned to baseline levels of performance. Recommendations for improved patient care are provided.
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PMID:Acute and chronic effects of hypoglycemia on cognitive and psychomotor performance. 140 20

IDDM and eating disorders are common conditions in young women. Whether a specific association exists between these two disorders remains controversial. Some studies have suggested an increased incidence of eating disorders in young women with IDDM, whereas others have not detected such an increase. These differences may be attributable, at least in part, to methodological issues in study design, measurement tools, and relatively small sample sizes. Whether the prevalence of eating disorders in IDDM is increased will be resolved only by larger studies that use standardized diagnostic interviews. We suspect that certain aspects of IDDM and its management may trigger the expression of an eating disorder in susceptible individuals. Required dietary restraint and weight gain related to diabetes management are the factors most likely to be implicated. Eating disorders are relatively common in young women with IDDM and may contribute to impaired metabolic control with hypoglycemia and DKA, and to long-term microvascular complications of diabetes. Omission or reduction of required insulin, an extremely common means of weight control in these young women, is likely an important factor in this regard. Further research is required to determine more precisely the relationship between IDDM and eating disorders, and the effects of eating disorders on metabolic control and chronic complications of IDDM.
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PMID:Eating disorders and IDDM. A problematic association. 142 9

Diabetes may be associated with many genetic disorders. The scientific importance of these often rare disorders resides in the insight they may provide into the possible mechanisms of common diabetes. The type of diabetes varies in these syndromes. Non-insulin-dependent diabetes (NIDDM), clinically similar to common NIDDM, may be found in some syndromes (e.g. Werner's syndrome). In others there may be considerable insulin resistance, such as that present in ataxia telangiectasia. Extreme insulin resistance due to abnormal insulin receptor function is found in the Mendenhall syndrome. The mechanism of diabetes is more obscure in acute intermittent porphyria (AIP), although haem deficiency affecting the cytochrome chain raises interesting possibilities. In glycogen storage disease type I, the diabetes is associated with insulinopenia, following an earlier period in the disease when hypoglycaemia is the rule. IDDM, clinically similar to the common form, is present in the autoimmune polyglandular syndromes. Although a change in the lean:fat ratio is common in many neuromuscular disorders, mechanisms other than insulin resistance would seem to operate. The increased incidence of diabetes in heterozygotes for some of these genetic disorders raises the possibility that many common diabetics are, in fact, heterozygotes for some other disorder. The increased frequency of diabetes in Klinefelter's syndrome, Turner's syndrome and possibly Down's syndrome leads to the hypothesis that non-disjunction may, in some way be associated with the predisposition to diabetes. In several syndromes there is an increased incidence of diabetes in otherwise unaffected relatives of individuals with these syndromes. It is impossible to assess what proportion of common NIDDM or IDDM is made up of heterozygotes for these genetic syndromes.
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PMID:Diabetes secondary to genetic disorders. 144 74


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