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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is found that antioxidative activity (AOA) and activity of glutathione-transferase in postmitochondrial placenta fraction of pregnant women with diabetes mellitus is lowered. Depression of AOA in placenta associated with a decrease of UDA and ceruloplasmin amount in blood of the newborns shows the exhaustion of the antioxidative protection system. A decrease of enzyme activity at the sorbitol way of glucose exchange (sorbitol-dehydrogenase and aldose reductase) in placenta reflects accumulation of sorbitol in tissue, which intensifies the damage of membrane structures in placenta.
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PMID:[Status of the antioxidant system and sorbitol pathway of glucose metabolism in diabetes mellitus]. 823 22

The effect of sodium metavanadate (NaVO3) consumption on trace element metabolism, components of the antioxidant defense system and lipid oxidative damage were studied in control (CON) and streptozotocin-induced diabetic (DIAB) rats. Ten days after injection, CON and DIAB rats received either 0 mM NaVO3/80 mM NaCl (0 group) or 1.2 mM NaVO3/80 mM NaCl (1.2V group) in their drinking water. DIAB groups had higher food and fluid intakes than the CON groups; vanadium (V) groups had lower food and fluid intakes than the saline groups. Vanadium therapy lowered plasma glucose concentrations of DIAB rats. The following parameters were similar among the groups: plasma Zn, Cu and Fe concentrations, plasma ceruloplasmin activity, liver Zn, Cu, Mn and Fe concentrations, kidney Mn and Fe concentrations, liver non-Se-dependent glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Red) and Mn-SOD activities, liver reduced glutathione (GSH) and oxidized glutathione (GSSG) concentrations and kidney non-Se-dependent GSH-Px activity. Kidney Zn and Cu concentrations were higher in DIAB rats than in CON rats. The CON-1.2V and DIAB-1.2V groups had V accumulation in the liver and kidney. Liver CuZn-SOD and Se-dependent GSH-Px and kidney CuZn-SOD and GSH-Red activities were lower in DIAB rats compared to CON rats; kidney Mn-SOD and kidney Se-dependent GSH-Px activities were higher in DIAB rats than CON rats. Vanadium treatment did not cause significant alterations in the antioxidant defense system; however, tissue vanadium concentrations were positively correlated to TBARS production. These results show that diabetes caused significant alterations in the antioxidant defense system and that V therapy was associated with a marked deterioration in health of both control and diabetic rats.
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PMID:Vanadium treatment of diabetic Sprague-Dawley rats results in tissue vanadium accumulation and pro-oxidant effects. 824 40

Increased free radical activity in diabetes mellitus may contribute to the higher prevalence and mortality from macrovascular disease in diabetic patients. To investigate this, levels of plasma antioxidants (superoxide dismutase, caeruloplasmin, plasma, and lysate thiol), diene conjugates, lipid peroxides, and chemiluminescence were measured in diabetic and non-diabetic patients with peripheral vascular disease compared with healthy control subjects. Caeruloplasmin, diene conjugate ratio, and lipid peroxides were significantly increased in patients with vascular disease but there was no difference between diabetic and non-diabetic patients. Conjugated diene ratio correlated with caeruloplasmin (r = 0.40, p < 0.02) and inversely with superoxide dismutase level (r = 0.36, p < 0.05) but there was no significant correlation between other antioxidants and diene conjugates, lipid peroxides or chemiluminescence. The relationship between different indirect measurements of free radical activity is variable but there appears to be no additive effect of diabetes on the increased free radical activity associated with vascular disease.
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PMID:A comparison of different methods of assessing free radical activity in type 2 diabetes and peripheral vascular disease. 850 15

A novel mutation of the ceruloplasmin (Cp) gene was found in a patient with hereditary ceruloplasmin deficiency (HCD) with diabetes mellitus (DM). The patient had been treated for DM for about 13 years, and then his illness was diagnosed as HCD. One year later, he was found dead in his home. A decrease in insulin-immunostained cells was observed in the islets of the patient's pancreas tissue, which accounted for his DM. The polymerase chain reaction (PCR)-direct sequencing analysis of the Cp gene of his daughter revealed a novel point mutation, G to A, at nucleotide 2630 in exon 15. This mutation changes the Trp858 codon (TGG) to a stop codon (TAG) (nonsense mutation). PCR-restriction analysis for the mutation revealed that the patient as well as his daughter was a heterozygote for the mutation, indicating that the patient was a compound heterozygote.
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PMID:A nonsense mutation of the ceruloplasmin gene in hereditary ceruloplasmin deficiency with diabetes mellitus. 852 44

Hereditary ceruloplasmin deficiency with hemosiderosis (aceruloplasminemia) is a new disease characterized by systemic hemosiderosis, diabetes mellitus, neurological abnormalities and pigment degeneration of the retina. Loss of the ferroxidase activity of ceruloplasmin results in systemic iron deposition and tissue damage. Neuroimaging studies reveal iron deposition in basal ganglia and in the red and dentate nuclei. Cerebellar ataxia, extrapyramidal signs and dementia develop after middle age. We report a patient with undetectable serum ceruloplasmin levels and the above clinical manifestations. Sequence analysis of the cDNA of ceruloplasmin from this patient revealed an insertion of adenine in exon 3; this produced a premature stop codon.
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PMID:Hereditary ceruloplasmin deficiency with hemosiderosis. 864 92

We report here on the characterization of a mutation in the ceruloplasmin gene in a 45 year old woman with insulin-dependent diabetes mellitus who presented with the recent onset of gait disturbance and dysarthria. Physical examination revealed an ataxic gait, scanning speech and retinal degeneration. Magnetic resonance imaging of the brain was consistent with increased basal ganglia iron content and laboratory studies revealed a low serum iron concentration and no detectable serum ceruloplasmin. Nucleotide sequence analysis of the ceruloplasmin gene from this patient revealed a G to A substitution in exon 15 resulting in a nonsense mutation at amino acid 858 (Trp858ter). The patient's younger, neurologically asymptomatic brother was also found to be homozygous for this mutation. Taken together the clinical and genetic data support the concept of an essential and unique role for ceruloplasmin in human iron metabolism. Identification of this kindred extends the spectrum of ceruloplasmin gene mutations resulting in this autosomal recessive, late-onset neurodegenerative disease and highlights the importance of recognizing aceruloplasminemia as a genetic cause of diabetes and neurologic disease.
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PMID:Characterization of a nonsense mutation in the ceruloplasmin gene resulting in diabetes and neurodegenerative disease. 878 43

Aceruloplasminemia is a systemic degenerative disorder characterized by mutations in the ceruloplasmin gene, the absence of serum ceruloplasmin, and iron accumulation in the brain, liver, and other tissues. Iron is an important catalyst of oxyradical-mediated cellular and tissue injury, and beta-cells in the pancreatic islets are susceptible to the cytotoxic effects of oxidative stress. We report three patients with aceruloplasminemia who have late-onset diabetes mellitus (DM) and impaired glucose tolerance (IGT) as well as neurologic symptoms. Their basal lipid peroxide levels, measured as thiobarbituric acid-reactive products, in plasma samples were three times the values for the controls. This increased susceptibility to lipid peroxidation in patients with aceruloplasminemia suggests that free-radical-mediated tissue injury plays a role in the occurrence of DM and IGT.
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PMID:Late onset diabetes mellitus in patients with hereditary aceruloplasminemia. 889 30

A 58 year old patient with dementia, oral dyskinesia, and diabetes mellitus is described. He had an undetectable concentration of serum caeruloplasmin, as an autosomal recessive trait. Brain MRI disclosed a pronounced hypointensity in the bilateral putamina, caudate, and dentate nuclei on both T1 and T2 weighted images. Pathological findings were mainly in those regions of the brain and consisted of neuronal cell loss with gliosis, heavy iron deposition, and spheroids. Visceral organs also had iron deposition, especially severe in the liver and pancreas. The present patient and other recorded cases constitute a clinicopathological entity of hereditary caeruloplasmin deficiency, different from Wilson's disease.
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PMID:Hereditary caeruloplasmin deficiency: clinicopathological study of a patient. 893 46

Primary hemochromatosis is characterized by a specific pattern of clinical manifestations. It includes liver disease with hepatomegaly, glucose intolerance, e.g. diabetes, hyperpigmentation oft the skin, impotence/ amenorrhea, arthropathy, cardiomyopathy and fatigue. Laboratory investigation reveals significantly elevated serum ferritin and transferrin saturation with iron. The diagnosis is confirmed by liver biopsy and quantitative determination of elevated liver iron content. Wilson's disease represents a copper storage disease. Prominent clinical features are hepatomegaly and splenomegaly. Neurological alterations and detection of Kayser-Fleischer corneal rings are typical. In the acute initial phase the often young patients present with Coombs-negative hemolysis. Psychiatric alterations, cardiomyopathy, arthropathy, nephropathy, as well as thrombocytopenia and leucopenia are other clinical features. Laboratory parameters of Wilson's disease include low serum ceruloplasmin and serum copper. There is an elevated urinary copper excretion and elevated serum free copper concentration. The diagnosis is confirmed by liver biopsy with quantitative determination of an elevated liver copper content.
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PMID:[Current diagnosis: hereditary metabolic diseases of the liver (primary hemochromatosis, Wilson disease)]. 898 78

Diabetes mellitus (DM) is the important initial symptom of hereditary ceruloplasmin deficiency (HCD). We examined the pancreas of an autopsy case of HCD and revealed a marked reduction in insulin-containing cells in the islets despite no massive iron deposition, degeneration, nor necrosis. Non-insulin-containing cells in the islets had glucagon or somatostatin. This study indicates that DM in HCD results from depletion of insulin cells and this depletion does not seem to be caused by the direct effect of iron deposition. The present observation suggests that the defect of the ceruloplasmin gene may influence the population of islet cells.
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PMID:Islet changes in hereditary ceruloplasmin deficiency. 910 52


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