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

Plasma lipid profiles--total cholesterol (TC), LDL-cholesterol, HDL-cholesterol, triglycerides and phospholipids--were studied in relation to two parameters of diabetic control (fasting blood sugar (FBS) for short-term control and glycosylated haemoglobin (HBA1C) for long-term control) in 46 diabetic patients (22 insulin-dependent (IDDM) and 24 non-insulin dependent (NIDDM] and 22 non-diabetic control subjects. We confirmed the positive correlation between FBS and HBA1C. All diabetic patients had significantly higher triglyceride levels (P less than 0.05) than controls, which were not influenced by degree of glycaemic control. NIDDM patients tended to have higher than normal TC levels (P less than 0.05). In IDDM, TC level was positively correlated with HBA1C (r = 0.37, P less than 0.05), and negative correlations were established between FBS and HDL-cholesterol (r = -0.46, P less than 0.02) and the HDL-cholesterol:TC ratio (r = -0.49, P less than 0.01), suggesting an increased atherogenic risk with poorer diabetic control. It is concluded that lipoprotein abnormalities exist in Nigerian diabetics, though not as consistently as in Caucasians. The differences may be due to, among other factors, differences in genetic make-up, diet (typical African diet being rich in plant fibre and poor in cholesterogenic nutrients) and aetiology of the diabetic state (tropical diabetes being highly heterogeneous and now thought to be linked to malnutrition).
Afr J Med Med Sci 1989 Sep
PMID:Plasma lipid profiles in relation to diabetic control in Nigerians. 255 Nov 65

The BB/Wor rat spontaneously develops autoimmune insulin dependent diabetes mellitus and lymphocytic thyroiditis (LT). Excess iodine ingestion enhances and low iodine diet decreases the incidence of LT in this rat model but does not affect the incidence of diabetes mellitus. The administration of a low dose of methimazole (MMI; 870 ng/gm bw ip daily) from 30-90 days of age had no significant effect on thyroid function or on the incidence of iodine induced LT and serum anti-thyroglobulin (Tg) antibodies measured by an ELISA assay. A large dose of MMI (0.05% in the drinking water) induced goiter and hypothyroidism. In addition, the incidence of LT was markedly attenuated (76% vs 6%, p less than 0.001) and reduced titers of serum anti-Tg antibodies (0.59 +/- 0.1 OD vs 0.08 +/- 0.01, p less than 0.001) were observed. This inhibitory effect of MMI on the occurrence of iodine induced LT in the BB/Wor rat may be due to the lower antigenicity of the poorly iodinated Tg secondary to MMI therapy and/or to an immunosuppressant effect of MMI itself.
J Endocrinol Invest 1989 Sep
PMID:The inhibitory effect of large doses of methimazole on iodine induced lymphocytic thyroiditis and serum anti-thyroglobulin antibody titers in BB/Wor rats. 259 41

The renal function in a group of diabetic children (n=29;age;4-17 yr; IDDM duration: 1,5-13 yr) was studied with a 3 year interval. At the first evaluation glomerular filtration rate (GFR) as assessed by inulin clearance was significantly increased compared to control values (167 +/- 32 vs. 124 +/- 18 ml/min/1.73 m2; pl less than 0.01). Eighteen out of 29 children exhibited a glomerular hyperfiltration (GFR greater than 160). Three years later mean GFR was identical (169 +/- 25 ml/min/1.73 m2) and 16 children were hyperfiltrating. Among them, 11 have had a persisting glomerular hyperfiltration over the 3-year period. Renal plasma flow (RPF) was positively correlated to GFR (r=0.7; p less than 0.01) and remained elevated at both evaluations (794 +/- 163 and 812 +/- 157 ml/min/1.73 m2, p greater than 0.01 vs, control values). When the children were separated into 3 groups according to IDDM duration no significant differences were observed in the results for GFR and RPF, Mean urinary albumin excretion was comparable at the 3-year interval, and not significantly different from the control values (5.2 +/- 3.7 and 8.2 +/- 6.6 respectively vs. 8.65 +/- 4 microgram/min). None of the children demonstrated a persistent microalbuminuria. This study reveals a high proportion of diabetic children with a persisting glomerular hyperfiltration, without any other symptom of incipiens nephropathy, If elevated GFR plays an important role in the development of diabetic nephropathy, this study emphasizes the value of regular evaluation of renal function in diabetic children.
Acta Paediatr Scand 1989 Sep
PMID:Persisting glomerular hyperfiltration in short-term diabetic children without microalbuminuria. 259 78

Factors to be checked concerning local and systemic condition were studied statistically in order to clarify the methodology for clinical management of diabetic retinopathy. NIDDM (n = 1517) and IDDM (n = 30) persons participating in baseline and follow-up examinations were included. The vitreous fluorophotometric values were selected for local check factors. Glycosylated hemoglobin was selected for systemic check factors. To determine the retinopathy status at both the baseline and follow-up examinations, all fundus photographs were graded in a masked fashion, using the author's classification scheme (1983) which specified six levels of retinopathy for each excepted from the interrupted proliferative retinopathy. Level 0: no retinopathy, Level 1: microaneurysms only (AI), Level 2: microaneurysms and retinal hemorrhages (AII), Level 3: preproliferative retinopathy (soft exudates, increased capillary occlusion and intraretinal microvascular abnormalities) (BI), Level 4: neovascularization elsewhere (BII), Level 5: neovascularization of the disc (BIII), Level 6: vitreous hemorrhages or proliferative tissue (BIV, V). A positive correlation between the progression of retinopathy and glycosylated hemoglobin or vitreous fluorophotometric values were observed. The coefficient of correlation was 0.67 between posterior vitreous fluorophotometric values and levels (scores) of retinopathy. The coefficient of correlation was 0.41 between glycosylated hemoglobin and levels of retinopathy. These data suggest that these two factors can predict the progression of diabetic retinopathy.
Nippon Ganka Gakkai Zasshi 1989 Sep
PMID:[Clinical management of diabetic retinopathy]. 261 Jan 68

The potential value of positron emission tomography (PET) in evaluating the myocardial energy metabolism was studied in two previously healthy mini-pigs before, during and after the induction of non-insulin dependent diabetes with alloxan. The distribution and kinetics of radioactivity derived from trace amounts of 11C-pyruvate and 1-11C-palmitate were followed in different sections of the myocardium. The early distribution of both tracers was similar even after the development of diabetes. The elimination of 11C-pyruvate derived radioactivity was slower in the diabetic heart. The rate of beta-oxidation was also decreased as suggested by the elimination curve of 11C-palmitate and the incorporation of 11C-palmitate into the triglyceride and phospholipid pool of the myocardium was increased in the diabetic animals. The results are consistent with previous observations using other techniques. Positron emission tomography offers the opportunity to characterize regional tissue metabolism quantitatively in vivo. This method may become a powerful tool in studying myocardial metabolism and the metabolic basis for the cardiac dysfunction in diabetes mellitus.
Diabetes Res 1989 Sep
PMID:The diabetic heart: a porcine model evaluated with positron emission tomography using 1-11C-palmitate and 3-11C-pyruvate. 263 Jan 51

The quantitative distribution of mutans streptococci and lactobacilli in saliva of insulin-dependent diabetic children was compared with a group of healthy children and related to the metabolic control of the disease. The study group, consisting of 94 boys and girls (age 4-19) with type 1 diabetes was matched by sex and age with a non-diabetic control group. Stimulated whole saliva was collected and flow rate, buffer capacity and the levels of mutans streptococci and lactobacilli were analysed in all children. In the diabetic group, total salivary proteins and glucose content of saliva were determined. Data on caries experience were recorded from the dental cards of all children. There were no difference in the distribution or number of mutans streptococci between the groups, but significantly (p less than 0.05) lower levels of lactobacilli were found among the diabetic children. The number of lactobacilli was positively correlated (p less than 0.05) to glucose concentration in saliva. There was no difference in the prevalence of caries between the groups. The present findings suggest that the dietary treatment of young insulin dependent diabetics gives rise to a reduced number of lactobacilli in saliva but does not affect the mutans streptococci.
Oral Microbiol Immunol 1989 Sep
PMID:Mutans streptococci and lactobacilli in saliva from children with insulin-dependent diabetes mellitus. 263 1

Antibodies in serums from newly diagnosed insulin-dependent (type I) diabetes mellitus (IDDM) patients and individuals experiencing early phases of beta-cell destruction specifically immunoprecipitate a minor pancreatic islet cell membrane protein of 64,000 Mr (64K). In this report, we demonstrate the use of two-dimensional (2-D) gel electrophoresis to unambiguously identify the 64K antigen. By nonequilibrium pH-gradient gel electrophoresis in the first dimension and sodium dodecyl sulphate-polyacrylamide gel electrophoresis in the second dimension, the 64K protein separates into two components, designated alpha and beta, that differ in size but display identical charge heterogeneity. The high resolution of the 2-D method efficiently separates the 64K components from background proteins in immunoprecipitates from crude detergent lysates of islets. The background proteins were identified as major cellular proteins carried nonspecifically through the immunoprecipitation procedure. The high affinity and specificity of the 64K autoantibodies were demonstrated by the exclusive and greater than 1000-fold purification of this minor protein by immunoprecipitation with IDDM serums. The 2-D analyses did not reveal additional proteins specifically immunoprecipitated by IDDM serums, suggesting that the 64K protein is the only protein antigen specifically and consistently recognized by IDDM autoantibodies in the relatively stringent conditions of immunoprecipitation. Moreover, the 2-D analyses demonstrate that purification of membrane protein fractions from both human and rat islets before the immunoprecipitation efficiently removes background proteins and substantially increases the specificity of 64K autoantibody measurements by traditional methods.
Diabetes 1989 Sep
PMID:Revelation of specificity of 64K autoantibodies in IDDM serums by high-resolution 2-D gel electrophoresis. Unambiguous identification of 64K target antigen. 267 Jun 43

The specific genes causing type 1 diabetes susceptibility in any species are unknown. Serological HLA studies have shown susceptibility to type 1 diabetes is linked to HLA DR3 and DR4 allels, whereas DR2 and DR5 alleles contain protective elements. DR4 chromosomes can be divided into diabetes prone or resistant by restriction fragment length polymorphism analyses with cDNA probes for DQ beta-gene. No type 1 diabetes-specific environmental factors have been revealed to be convincingly implicated in human type 1 diabetes. Congenital rubella, by its lasting influence on T cells creates susceptibility to many organ-specific autoimmune diseases. Certain dietary proteins shown in BB rats as well as hyperglycemia during the prenatal period increase the later incidence of type 1 diabetes. Human type 1 diabetes results from a progressive probably autoimmune loss of the pancreatic beta cells. The immunologic hallmarks of type 1 diabetes is the lymphocytic infiltration of pancreatic islets, the hyperexpression of class I MHC on all islet cells and the abarrent class II MHC expression on beta cells within inflamed islets, the increased frequency of activated T cells in islet and circulation. It is generally accepted that cellular immunity plays the major role in the pathogenesis of type 1 diabetes. The heightened autoimmune reactivity being detectable during the preclinical period, lasting months to years, has been proved by antibodies directed against cytoplasmic islet cell antigens (ICA), beta cell surface antigens (ICSA), insulin (IAA), and with a lower frequency against non-islet cell antigens. The presence of IgG insulin autoantibodies and complement fixing ICA confers increased risk for future type 1 diabetes development in genetically predisposed individuals than the presence of either marker alone. For ICSA a more specific and quantitative assay is needed. 90% of children developing type 1 diabetes were detected positive for ICA and/or IAA. By the time of clinical onset if type 1 diabetes some 90% of the insulin secretory beta cell mass has already been destroyed. For this reason, new approaches are needed to address the causes of diabetes and not just the consequences. The development of insulin-dependent diabetes may be reversible, or even preventable by early detection coupled with the judicious use of immunotherapy.
Exp Clin Endocrinol 1989 Sep
PMID:Immunological disorders of type 1 diabetes mellitus. 268 94

Glucocorticoid receptor binding characteristics were investigated in 8 males with poorly controlled Type 1 diabetes mellitus and 14 healthy males. The cell type studied was monocytes, and a method for correction for heterogeneity in glucocorticoid binding in a mononuclear leucocyte population was introduced. The number of receptors and the dissociation constant KD were, respectively, 13,699 and 2.93 X 10(-8) mol/l for the control group and 15,788 and 2.75 X 10(-8) mol/l for diabetics (p greater than 0.05). In diabetics, KD correlated negatively with blood glucose (r = 0.762, p less than 0.05) indicating an increased sensitivity to cortisol at high blood glucose levels. In 6 of the diabetics and 7 of the control group, a simultaneous insulin receptor study was carried out. However, glucocorticoid receptor binding characteristics did not correlate with insulin receptor binding characteristics or with HbA1c. In conclusion, no major abnormalities in glucocorticoid receptor binding characteristics could be demonstrated in Type 1 diabetes mellitus.
Clin Chim Acta 1989 Sep 29
PMID:Glucocorticoid receptors in monocytes in type 1 diabetes mellitus. 269 Nov 20

Insulin dependent diabetes is an organ specific immunologic disease caused by pancreatic B cell destruction, mediated by T lymphocytes Present knowledge about insulin dependent diabetes immunogenetics and their relationship with the HLA system is reviewed, highlighting the polymorphism of the D area of that system and its connectors with diabetes. Possible therapeutic interventions in the autoimmune destructive process are discussed.
Acta Med Port 1989 Sep
PMID:Diabetes mellitus type I. The present and the future. 269 81


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