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)

Recombinant DNA technology allows the production of insulin analogues with faster absorption rates from subcutaneous tissue as compared to soluble human insulin. The human insulin analogue B10Asp (mono/dimeric) is absorbed twice as fast as soluble human insulin (hexameric). A double blind, randomised crossover study with a 1-month run-in period and two 2-month treatment periods was performed in 21 male insulin-dependent diabetic (IDDM) patients aged 18-40 years in order to compare the metabolic control obtained with equimolar doses of the analogue B10Asp vs soluble human insulin (Actrapid) given as mealtime insulin and intermediate acting isophane insulin (Protaphane) at bedtime. At the end of each 2-month study period, the patients were admitted to the metabolic ward. We found significantly higher plasma insulin/analogue levels after breakfast, lunch and dinner with B10Asp as compared to Actrapid (p < 0.05). The plasma insulin/analogue levels were significantly lower before lunch and dinner with B10Asp as compared to Actrapid (p < 0.05). Also, the plasma insulin/analogue level tended to be lower at bedtime when comparing B10Asp to Actrapid. The 24-h blood glucose profiles showed identical fasting blood glucose, significantly lower blood glucose after breakfast with the analogue (p < 0.05), no differences in blood glucose after lunch and dinner but a significantly higher blood glucose at midnight using the analogue (p < 0.05). The overall 24-h mean blood glucose concentrations, the daily insulin dose, HbA1c, diet, home blood glucose monitoring and frequency of hypoglycaemia were almost identical in the two treatment periods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term comparison of human insulin analogue B10Asp and soluble human insulin in IDDM patients on a basal/bolus insulin regimen. 748 43

In a prospective study, neonatal morbidity of newborn children of diabetic mothers and its association with the maternal metabolism was determined. Particular attention was directed on the somatic outcome of the children and their frequent metabolic imbalances. In addition, we determined the influence of maternal biological and somatometrical variables on the somatic outcome of newborns. Dependent upon the mothers' and children' variables, risk groups of newborns (fetopathy groups) were defined to optimize clinical care and surveillance of newborns. A total of 810 children were included born to mothers with primary insulin dependent diabetes mellitus (IDDM), non insulin dependent diabetes (NIDDM), or gestational diabetes (GDM). Among the study population, 41.7% of children had macrosomia, 27.2% had a weight-length index > 1.2, 17.9% developed hypoglycemia and 19.5% hyperbilirubinemia within the initial 72 hours after birth. The somatic outcome of the children was significantly associated with pregnancy duration, maternal age, weight, height, and HbA1. Increasing maternal HbA1 prior to delivery (categorized in < 8.5%, 8.6-10%, > 10%) was associated with increased relative risk of incidence of neonatal morbidity. Finally, risk groups (fetopathy groups I-III) were defined according to maternal HbA1 value and somatic outcome of the newborns. The importance of these fetopathy groups for criteria of neonatal morbidity is demonstrated. Based upon categorization of newborn children into fetopathy groups, children should be allocated to specific concepts of appropriate surveillance and clinical care. The fetopathy classification may also serve as an independent tool for retrospective quality control of diabetic pregnancy.
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PMID:[Risk groups of newborn infants of diabetic mothers in relation to their somatic outcome and maternal diabetic metabolic status in pregnancy]. 749 17

Arginine vasopressin (AVP) hypersecretion in response to metoclopramide or to insulin-induced hypoglycaemia has been described in type I diabetes mellitus. In the present study, we examined whether residual endogenous insulin secretion may play a role in the control of this abnormal AVP secretory pattern. For this purpose, 21 insulin-dependent diabetic men and 10 age- and weight-matched normal men were tested with MCP (20 mg in an i.v. bolus). On a different occasion, subjects were tested with insulin (0.15 IU kg-1). The diabetic patients were subdivided into C-peptide negative patients (CpN, 11 patients without detectable endogenous pancreatic beta cell activity) (group I) and C-peptide positive patients (CpP, 10 patients with residual endogenous insulin secretion) (group II). Experiments started after optimization of the metabolic status of the diabetic men by 3 days of treatment with continuous subcutaneous insulin infusion. The basal concentrations of AVP were similar in all groups. The administration of MCP induced a striking elevation in plasma AVP levels in the normal controls and in the diabetic subjects of groups I and II. However, the AVP rise was significantly higher in group I and group II than in normal controls. Furthermore, group I diabetics showed higher AVP increments than group II. Insulin induced a similar hypoglycaemic nadir in all subjects at 30 min, even though the diabetic subjects of groups I and II had a delayed recovery in blood glucose levels. The hypoglycaemic pattern was similar in group I and II. Hypoglycaemia induced a striking AVP increase in the normal controls.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Influence of residual C-peptide secretion on the arginine vasopressin response to hypoglycaemia and metoclopramide in insulin-dependent diabetes. 758 12

Sixty-four insulin-dependent (Type 1) diabetic patients (IDDM) in Soweto, South Africa were followed over a 10-year period. Patients were assessed in 1982 and again in 1992. There were 10 deaths (16%), half of which were due to renal failure. Ketoacidosis, hypoglycaemia, and sepsis accounted for the rest. At the 10-year follow-up mean age (+/- SD) was 32.4 +/- 5.0 years and diabetes duration 13.6 +/- 2.6 years. Retinopathy affected 52%, peripheral neuropathy 42%, and nephropathy 28% (all significantly increased from the 1982 assessment). Microalbuminuria and autonomic neuropathy were also common. Serum cholesterol was over 6.5 mmol l-1 in 19%, hypertension affected 22%, and 28% were cigarette smokers; though no patient had evidence of macroangiopathy. We conclude that IDDM in South Africa is associated with excess mortality, a significant proportion of which is related to nephropathy. Diabetes of long duration is now not uncommon in South Africa, and although diabetic complications frequently occur, most patients have good life quality and freedom from large vessel disease.
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PMID:Mortality and outcome of insulin-dependent diabetes in Soweto, South Africa. 764 31

The islets of Langerhans provide energy storage and disposal, and protection from plasma glucose excursions, especially hypoglycemia. Insulin-dependent diabetes mellitus (IDDM) results from autoimmune beta-cell damage. Prevention of IDDM has already been achieved in animal investigation and some centers are now screening and treating individuals at high risk for developing IDDM. Immunosuppressive drugs can induce transient remission of recent-onset IDDM. Intensive insulin treatment of IDDM delays the onset and slows the progression of long-term complications. Non-insulin dependent diabetes mellitus (NIDDM) is the result of beta-cell malfunction and is strongly associated with X syndrome. Diet and exercise are of undoubted importance in NIDDM prevention and treatment. Functional endocrine tumors of the pancreas (FET) are rare hormone and peptide-secreting neoplasms. These peptides may or may not occur naturally in the islets. FETs often occur with multiple endocrine neoplasia 1 (MEN 1) so that MEN-1 screening should always be performed, and extended to family members whenever diagnosed. Drugs--alcohol, insulin and sulfonilureas--are the main cause of hypoglycemia. Insulinoma is the main cause of post-absorptive organic hypoglycemia. Non islet-cell tumors seldom cause hypoglycemia. Insulinoma often is a solitary tumor, but it may be multicentric and may coexist with cell hyperplasia and nesidioblastosis. Symptoms of neuroglycopenia may be mistaken for neuropsychiatric disease. The diagnosis is based on confirmation of post absorptive hypoglycemia and hyperinsulinism. Gastrinoma causes Zollinger-Ellison syndrome (ZES) which is characterized by fulminating peptic ulcer disease. The tumor is often malignant, and it may be multicentric and may occur with cell hyperplasia and nesidioblastosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The endocrine pancreas]. 765 6

Disturbed hemodynamic reactions to insulin-induced hypoglycemia have been documented in diabetic patients and considered related to hyperinsulinemia and impairment of autonomic nervous functions. In the present study we investigated the effect on skin microcirculation of insulin-induced hypoglycemia obtained during moderate hyperinsulinemia, in 7 men with type 1 diabetes and in 8 healthy age- and sex-matched controls. The patients had all normal cardiovascular reflexes as assessed by respiratory sinus arrhythmia and Valsalva ratio. The skin microcirculation of the left fourth finger nailfold was investigated by laser Doppler fluxmetry, and the skin temperature within the same area was measured by a thermistor. Hypoglycemia was induced by a constant insulin infusion of Actrapid Human, 0.034 U kg-1 h-1 during 120 min. Plasma adrenaline, noradrenaline and pancreatic polypeptide increased significantly in both groups during hypoglycemia and the insulin levels never exceeded 50 mUl-1. A close to identical arterial hypoglycemia was obtained in the two groups 60 min after onset of insulin infusion. During hypoglycemia the control subjects revealed a significant decrease in laser Doppler flux (p < 0.025), while it was unchanged in the diabetic patients. Simultaneously, the skin temperature decreased (p < 0.05) in the controls, but was unchanged in the diabetic patients. The present study indicates that type 1 diabetic patients with normal cardiovascular reflexes have an abolished vasoconstrictor response in skin microcirculation of fingers during insulin-induced hypoglycemia, despite the fact that neurogenic and neuroglucopenic symptoms developed in these patients during hypoglycemia.
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PMID:Patients with type 1 diabetes lack vasoconstrictor response in skin microcirculation during insulin-induced hypoglycemia. 770 86

This study was designed as a quantitative study. Subjects ranging from the fourth grade of primary school to the third year of senior high school were drawn from the survey project of Taipei IDDM Registry and from the Kang-Tai IDDM Association. The mothers of these diabetic children were asked to complete questionnaires. The purpose of this paper was to explore the influences of maternal stress, management difficulties and family function on self-management of diabetes and HbA1c. Results indicated that family function was positively and significantly related with self-management. There was a significant correlation between the difficulty of diet control and self-management. The total self-management, blood glucose monitoring and preventive measures for hypoglycemia were negatively correlated with HbA1c. Forty-six point six percent of the variance of self-management could be explained by the family role function, paternal education, patient's school grade, religion and difficulty of diet control. Forty-two point six percent of the variance of HbA1c could be accounted for by total self-management, payment method, difficulty of blood glucose monitoring and frequency of hospitalization due to hypoglycemia.
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PMID:[The effects of management difficulty and family functions on metabolic control of insulin-dependent diabetes mellitus]. 770 65

Type 1 diabetes mellitus is caused by severe insulin deficiency secondary to the autoimmune destruction of pancreatic beta cells. Patients need to be controlled by periodic insulin injections to prevent the development of ketoacidosis, which can be fatal. Sustained, low-level expression of the rat insulin 1 gene from the liver of severely diabetic rats was achieved by in vivo administration of a recombinant retroviral vector. Ketoacidosis was prevented and the treated animals exhibited normoglycemia during a 24-hr fast, with no evidence of hypoglycemia. Histopathological examination of the liver in the treated animals showed no apparent abnormalities. Thus, the liver is an excellent target organ for ectopic expression of the insulin gene as a potential treatment modality for type 1 diabetes mellitus by gene therapy.
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PMID:Gene therapy for diabetes mellitus in rats by hepatic expression of insulin. 772 55

Brainstem auditory evoked potentials (BAEP) were studied in 10 type 1 diabetic children during normoglycaemia (5.5 +/- 0.4 mmol/l), hypoglycaemia and in the post-hypoglycaemic state. In addition, BAEP during normoglycaemia in diabetic children were compared with those of an age-, weight- and sex-matched group of healthy control children. No significant differences were observed between all latencies of the diabetic children compared with those of the healthy children during normoglycaemia. During induction of hypoglycaemia a minor (p < 0.05) prolongation of the inter-peak latency I-V at a blood glucose concentration of 4.1 +/- 0.5 mmol/l was observed. This prolongation was not aggravated at glucose nadir (1.7 +/- 0.3 mmol/l). In conclusion, and in contrast with previous findings in non-diabetic children and in adults with type 1 diabetes, no changes in BAEP were demonstrated during short-term severe hypoglycaemia in diabetic children and only minor transient changes were seen during the initial phase of a standardized induction of hypoglycaemia.
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PMID:Brainstem auditory evoked potentials during hypoglycaemia in insulin-dependent diabetic children. 773 73

The effect of insulin-induced hypoglycaemia on plasma coagulant activity was studied in 11 subjects with well-controlled, uncomplicated type 1 diabetes. Thrombin generation was determined in plasma by a computer ex-vivo assisted chromogenic method and by the activated partial thromboplastin time (APTT). In addition, factor VIII:C, thrombin-antithrombin III (TAT) complex and fibrinopeptide A (FPA) levels were measured. Hypoglycaemia induced a rise in mean (SD) factor VIII:C concentrations from a baseline level of 1.13 (0.32) IU/ml to a peak 15 min after onset of symptoms and they remained increased at 90 min [1.54 (0.57) and 1.5 (0.54) IU/ml, p < 0.001 respectively]. A corresponding reduction in time to generate 50% maximal thrombin activity occurred from a pre-insulin value of 56 (6) s to a minimum reading of 46 (7) s at 15 min (p < 0.001) and remained low at 90 min [48 (6) s, p < 0.001]. APTT shortened from 43.3 (4.8) s to 40.1 (4.6) s at 30 min (p < 0.001) but did not fall below the normal range (37.6-42.7 s) and no significant changes in TAT or FPA levels were noted. Factor VIII:C correlated inversely with time to generate 50% maximal thrombin activity and APTT (r = -0.580, p < 0.001; r = -0.673, p < 0.001, n = 66, respectively). The results show that the rise in plasma factor VIII:C levels induced by hypoglycaemia is accompanied by accelerated rates of generation of thrombin in contact-activated plasma, though concentrations of FPA and TAT remain unchanged, although TAT complexes are not a sensitive marker of in vivo thrombin generation.
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PMID:The effect of insulin-induced hypoglycaemia on factor VIII:C concentrations and thrombin activity in subjects with type 1 (insulin-dependent) diabetes. 779 37


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