Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ceruloplasmin (Cp) is an acute-phase-responsive oxidase enzyme. Prior reports suggest that Cp is increased in diabetes mellitus, perhaps reflecting greater oxidant stress. However, the situation in insulin-dependent diabetes mellitus (IDDM) per se remains unclear. Furthermore, vitamin C can interfere with one indirect assay for Cp, and vitamin C metabolism is altered in IDDM. We measured Cp levels by both a direct radial immunodiffusion (RID) assay and an indirect oxidase assay in 10 subjects with IDDM and 10 nondiabetics, both at baseline and after 30 days of vitamin C supplementation (100 or 600 mg daily, five subjects per group). Plasma copper level was measured independently also. Our data show that circulating levels of Cp are significantly increased in IDDM subjects as a group, and specifically that Cp is abnormally high in a subset of IDDM individuals. Vitamin C supplementation at either dose interfered with the oxidase assay for Cp in both groups, but vitamin C did not alter the RID assay. The observed increase in plasma copper suggests that circulating holo-Cp is increased. The finding of increased Cp in some individuals with IDDM supports the hypothesis of increased oxidant stress as a variable factor in the spectrum of chronic complications in diabetes. Measurements of Cp level by the oxidase assay must be considered unreliable for subjects taking vitamin C supplements of > or = 100 mg/d.
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PMID:Elevated plasma ceruloplasmin in insulin-dependent diabetes mellitus: evidence for increased oxidative stress as a variable complication. 763 57

The susceptibility of LDL to copper-catalyzed oxidation was evaluated in 24 patients with insulin-dependent and 16 patients with non-insulin-dependent diabetes mellitus, 14 abdominal and 14 gluteal-femoral obese women, 22 familial hypertriglyceridemic and 28 control subjects. Differences in the LDL susceptibilities were studied by measuring the changes of fluorescence intensity and expressed as lag-phase. The lag-phase was significantly shorter in patients with insulin-dependent, non-insulin-dependent diabetes mellitus, abdominal obesity and familial hypertriglyceridemic patients than in gluteal-femoral obese subjects and controls (p < 0.01). The shortest lag-phase was found in familial hypertriglyceridemic patients while intermediate values were found in insulin-dependent, non-insulin-dependent and abdominal obese patients who had only a slight increase in triglyceride values. Similarly the lowest value of the LDL cholesterol to protein ratio, as expression of LDL particle size, was found in familial hypertriglyceridemic patients (p < 0.01), while the patients with insulin-dependent, non-insulin-dependent diabetes mellitus and abdominal obesity had intermediate values. The ratio was found to be directly correlated with the length of the lag-phase (r = 0.87, p < 0.001). In spite of similar triglyceride and cholesterol to protein ratio values, however, the length of the lag-phase was significantly shorter in patients with insulin-dependent diabetes mellitus than in those with abdominal obesity. So it is concluded that the different susceptibility to oxidation found in the different groups of patients is only partially explained by plasma triglyceride values.
Diabetes Res 1994
PMID:Increased susceptibility of LDL to in vitro oxidation in patients with insulin-dependent and non-insulin-dependent diabetes mellitus. 764 91

The mechanisms underlying the teratogenicity of maternal copper deficiency, zinc deficiency, and diabetes are largely unknown. Here we investigated whether these insults are associated with altered patterns of cell death in gestation day (GD) 11.0 rat embryos. Four weeks prior to mating, rats in the copper-deficient group (CuD) were fed a copper-deficient diet supplemented with the chelator, triethylenetetramine, to facilitate the depletion of tissue copper stores. Rats in this group were switched to a triethylenetetramine-free copper-deficient diet 1 week prior to mating. Dams in the diabetic and control groups were fed a control (8 micrograms copper, 25 micrograms zinc/g) diet throughout the study. On GD 3.0, one subset of the control dams was assigned to the zinc-deficient group (ZnD) and fed a zinc-deficient diet. A second subset of control dams was assigned to a restricted fed group and fed the control diet in quantities consumed by the zinc-deficient dams. Litters were taken by cesarean section on GD 11.0. Embryos were examined for gross morphology and assessed for patterns of cell death using Nile blue sulfate. Embryos from the CuD dams were characterized by edematous hindbrain. Embryos from the diabetic group were characterized by delayed development. Altered patterns of cell death were only detected in embryos from the ZnD dams. Within the ZnD group, embryos were either characterized by small size, edematous head region, and control patterns of cell death, or normal size, normal morphology, and increased cell death. These different patterns of morphology and cell death in the embryos of ZnD dams were associated with different patterns of maternal food intake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Maternal zinc deficiency, but not copper deficiency or diabetes, results in increased embryonic cell death in the rat: implications for mechanisms underlying abnormal development. 766 Mar 26

ATP-thymidine 5'-phosphotransferase (TK) is a cellular enzyme involved in DNA synthesis, activated during the G1/S phase of the cell cycle. Elevated TK serum levels can be found in cancer patients due to the active proliferation of tumor cells. TK serum activity was tested by a radioenzymatic technique (Prolifigen TK REA, Sangtec Medical, Sweden) based on the conversion of 125 I deoxyuridine to 125 I deoxyuridine monophosphate. A total of 181 patients were enrolled in this study: 133 lymphomas (Hodgkin, HL and Non-Hodgkin, NHL) 48 benign diseases including acute (n = 17) and chronic inflammatory diseases (n = 13), myocardial infarction (n = 11), liver cirrhosis (n = 2), renal failures (n = 2), and diabetes (n = 3). Lymphoma patients were classified according to the Ann Arbor staging system, and 103 NHL patients were classified according to the Working Formulation histologic grade (21 low, 72 intermediate, and 10 high grade lymphomas). The patients were treated with standard chemo-radiotherapeutic protocols according to the stage and the histologic grade; the evaluation of the response to the treatments and the follow-up were performed according to the serial examinations currently used in our Institute. Given a TK cut-off of 5 U/L, the diagnostic sensitivity of TK test at lymphoma presentation was 81.8% and 75.7% in HL and NHL patients, respectively. Values exceeding 50 U/L were found only in NHL patients. The overall sensitivity of TK resulted higher than that of LDH (16.7%), copper (42.6%), IgG (23.5%), IgM (26.8%) and IgA (9.8%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thymidine kinase (TK) activity as a prognostic parameter of survival in lymphoma patients. 766 Aug 54

In 20 patients with insulin-dependent diabetes mellitus the concentration of zinc in serum was 56.53 +/- 2.36 micrograms/dl (mean +/- SD). This was significantly lower (p < 0.01) than the levels measured in matched controls. In the same patients the concentrations of serum copper and magnesium were 123.46 +/- 6.59 micrograms/dl and 17.38 +/- 0.52 mg/l respectively. These copper values were higher and the magnesium levels were lower than in the control subjects (p < 0.01). These changes may be associated with the development of insulin resistance and it is proposed that patients will improve if trace elements are given as part of the therapy.
Diabetes Res 1994
PMID:Zinc, copper and magnesium status in insulin-dependent diabetes. 766 36

Male weanling rats were fed diets containing either adequate (6.2 mg/kg) or deficient (0.82 mg/kg) quantities of copper for 35 days. Six rats from each group (n = 12) were then injected with streptozotocin to induce diabetes. Rats were killed after a further 16 days and tissues removed for the analysis of the copper level and antioxidant enzyme activities. Diabetes resulted in increased cardiac catalase, glutathione S-transferase (GST), copper-zinc superoxide dismutase and manganese superoxide dismutase activities. Renal catalase levels were decreased in diabetes, while glucose-6-phosphate dehydrogenase activity (G6PDH) was increased. Diabetes significantly decreased the activities of hepatic GST and G6PDH. The combination of diabetes and copper deficiency resulted in increased levels of hepatic GST, glutathione peroxidase and glutathione reductase. Hepatic and renal tissue copper levels were also increased in diabetes, apparently improving copper status in the copper-deficient rats. Alterations of antioxidant enzyme activities in diabetes were suggestive of increased oxidant stress, especially in cardiac tissue.
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PMID:Effects of copper deficiency and experimental diabetes on tissue antioxidant enzyme levels in rats. 771 Feb 61

The concentrations of Cu and Zn were determined in the plasma, granulocytes and mononuclear cells of 26 patients with diabetes mellitus and 26 age and sex-matched controls. In addition, Cu was measured in both washed and unwashed red blood cells, and Cu,Zn-superoxide dismutase (SOD) activity measured in washed red blood cells. Cu and Zn were determined by Zeeman-effect graphite furnace atomic absorption spectrometry following separation of plasma and red blood cells, and the white blood cell fractions (granulocytes and mononuclear cells) by density gradient centrifugation. There were no significant differences in any of the matching factors, or lipid profiles, between the groups. Plasma Zn was reduced by 17% in diabetics, compared with the controls (P = 0.0001). Neither the plasma nor the red blood cell Cu concentrations were significantly different. Of the white blood cell fractions, only mononuclear cell Cu was significantly different (30% lower in diabetics P = 0.0035, The red blood SOD activity was reduced in diabetics by over 12%, but this difference was non-significant (P = 0.0872). There was a significant negative correlation between washed red blood cell Cu and the duration of diabetes (r = -0.613, P = 0.0069). In conclusion, the copper and zinc status of these diabetic patients was reduced, providing further evidence of a role for these antioxidant trace elements in this disease.
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PMID:Plasma, granulocyte and mononuclear cell copper and zinc in patients with diabetes mellitus. 774 Dec 48

Endogen malondialdehyde (MDA), diene conjugate levels, the susceptibility to copper-induced lipid peroxidation and antioxidant activity of serum were determined in patients with atherosclerotic diseases such as diabetes mellitus and myocard infarction. Lipid peroxidation susceptibility and antioxidant activity did not change, however, an increase in endogen MDA and diene conjugate levels was observed in serum of these patients. These results indicate the presence of oxidative stress in diabetes mellitus and myocard infarction.
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PMID:Peroxidation potential and antioxidant activity of serum in patients with diabetes mellitus and myocard infarction. 775 Sep 4

We report two brothers with complete caeruloplasmin deficiency. The brothers presented with dementia and diabetes mellitus. Twelve relatives have partial caeruloplasmin deficiency. There is no copper overload. Transmission is autosomal recessive. DNA analysis showed genetic linkage between the deficiency and various polymorphic markers flanking the caeruloplasmin gene on chromosome 3q25. This is consistent with a mutation of the caeruloplasmin gene. Caeruloplasmin catalyses the oxidation of ferrous iron to ferric iron. Both brothers have low serum iron and increased liver iron. The index patient was given caeruloplasmin-containing, fresh-frozen plasma. A dose of 2.6 mg caeruloplasmin increased serum iron from 5 microM/l to 10 microM/l. A dose of approximately 72 mg increased serum iron from 5 microM/l to 19 microM/l. The abnormal serum and liver iron levels, and the caeruloplasmin-induced rise in serum iron, confirm a previous suggestion that caeruloplasmin maintains the normal rate of flow of iron from store to transferrin. Dementia and diabetes mellitus have been described in only one other homozygote. The absence of copper overload, and the linkage of the deficiency with chromosome 3q25, distinguish this condition from Wilson's disease.
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PMID:Hereditary caeruloplasmin deficiency, dementia and diabetes mellitus. 782 May 40

In diabetic plasma, glycated albumin and glycated LDL coexist with augmented levels of peroxides, conditions frequently associated with the development of accelerated atherosclerosis. The direct interaction between irreversibly glycated albumin, LDL and oxidation have not been explored yet. We tried to elucidate whether irreversibly glycated albumin (AGE-Alb) induces changes in the chemistry and morphology of LDL particle, and if AGE-Alb has the ability to scavenge free radicals, as reported for native albumin. LDL isolated from normal (nLDL) or diabetic human subjects (dLDL) was incubated in vitro with AGE-Alb in conditions of autoxidation (37 degrees C, 24-48 h in the absence of oxidation inhibitors) or of Cu2+ induced-oxidation. The results showed that, especially in the latter condition, AGE-Alb induced marked physico-chemical modifications of both nLDL and dLDL without significant changes in the level of peroxides. Incubation with AGE-Alb decreased the cholesteryl esters/unesterified cholesterol ratio of nLDL by 30% and of dLDL by approximately 50%. Concomitantly, in oxidative conditions a marked increase (approximately 3-fold) in the lysophosphatidylcholine/phosphatidylcholine ratio of dLDL was detected. Apolipoprotein B integrity as well as the morphology of the lipoprotein particles were drastically affected. To a lesser extent, these modifications occurred also in the presence of inhibitors of oxidation at 37 degrees C, but not at 4 degrees C. The above described effects were constantly more pronounced in the case of dLDL. These results indicated that in the absence of other plasma or vascular tissue components (e.g., endothelial cells, extracellular matrix) AGE-Alb by itself induces alterations in the chemistry and morphology of LDL, especially of glycated LDL, modifications that may account for the occurrence of accelerated atherogenesis in diabetes.
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PMID:Irreversibly glycated albumin alters the physico-chemical characteristics of low density lipoproteins of normal and diabetic subjects. 782 32


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