Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus type 1 (DM-1) was modeled by a single intraperitoneal injection of streptozotocine (STZ) in a dose 65 mg/kg in two groups of Wistar rats: control (n=6) and test (n=14). Clinical and pathomorphological examinations of different organs were conducted for 4.5 months. It was found that the above model represents clinical picture and vascular diabetic complications (microangiopathy with parenchymal lesions) accompanied with destruction and depression of spleen activity. It is shown that rats, more resistant to the toxic action of STZ restore the ability for regeneration of the pancreatic islets and regress of glycemia and angiopathy, for positive changes in splenic structure and function.
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PMID:[Diabetic complications in rats in long-term modeling of type I diabetes mellitus]. 1815 83

In human diabetes, degenerative and functional disorders of the central nervous system, including depression, are common findings. Defective dentate gyrus (DG) neurogenesis is associated with affective-related disorders and depression. We previously demonstrated reduced DG neurogenesis in a pharmacological type 1 diabetes model, the streptozotocin (STZ)-treated mouse. Here, we explored DG neurogenesis in a spontaneous T1D model, the nonobese diabetic (NOD) mouse, at prediabetic and diabetic stages. Cell proliferation was assessed in the DG of 5, 8 and 12-week-old control C57BL/6 and BALB/c strains and NOD mice, killed 2 h after bromodeoxyuridine (BrdU) administration. Survival of the newly generated cells was studied in 15-week-old animals that were killed 21 days after BrdU injection. The number of proliferative BrdU-positive cells in the DG was, regardless of age, constantly and significantly lower in NOD than in control strains, showing the presence of hippocampal alterations far before clinical diabetes onset in NOD mice. Diabetes also strongly decreased cell survival in NOD DG. However, cell phenotype proportion, as assessed by co-localization with neuronal or glial markers and confocal microscopy, was not modified. Hippocampal neurogenesis is strongly diminished in the spontaneous NOD model, like in the STZ model. Notably, NOD hippocampal DG cell proliferation defect takes place during the prediabetic stage. Whether this early alteration might result, in this autoimmune strain, from hypothalamo-pituitary adrenal axis alterations and/or ongoing brain inflammatory process sharing many characteristics of aging is discussed and deserves further investigation.
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PMID:Prominently decreased hippocampal neurogenesis in a spontaneous model of type 1 diabetes, the nonobese diabetic mouse. 1819 Sep 10

True euglycemic diabetic ketoacidosis [blood glucose <200 mg/dl (11.1 mmol/l)] is relatively uncommon and in type 1 diabetes can be caused by starvation of any cause in conjunction with an intercurrent illness. We report a case of euglycemic diabetic ketoacidosis precipitated by starvation resulting from severe depression in a patient with type 1 diabetes. He was acidotic with ketonuria, but his blood glucose was only 105 mg/dl (5.8 mmol/l). He was rehydrated, the acidosis was corrected, and his depression was later treated. This case involves the complex interplay among type 1 diabetes, depression, ketoacidosis, and starvation physiology resulting in glucose concentrations in keeping with euglycemic diabetic ketoacidosis. The case also highlights that even in the absence of hyperglycemia, acid/base status should be assessed in an ill patient with diabetes, and in cases of euglycemic diabetic ketoacidosis, the diagnosis of depression should be considered as a cause for suppressed appetite and anorexia.
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PMID:Starvation-induced true diabetic euglycemic ketoacidosis in severe depression. 1897 36

Diabetic neuropathic cachexia is characterized by bilateral, painful neuropathy usually involving the anterior thighs, with dramatic weight loss. The cause is unknown. Most patients to date have been middle-aged type 2 diabetics on oral agents, and it has rarely been reported in patients with type 1 diabetes. Most patients recover spontaneously, although residual deficits may persist. No specific therapy has been found useful. Antidepressants aid in managing neuropathy and depression. Therapy of painful neuropathy is challenging. Tramadol, dextromethorphan, topical capsaicin, clonidine, tricyclic antidepressants, and gabapentin are often effective. Opioids are rarely beneficial and carry a high risk of addiction. Proper nutrition is essential to avoid further deterioration.
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PMID:Diabetic neuropathic cachexia: a rare manifestation of diabetic neuropathy. 1920 23

The hippocampus, a limbic structure linked to higher brain functions, appears vulnerable in diabetic subjects that have a higher risk of stroke, dementia, and cognitive decline. The dentate gyrus (DG) of the hippocampus is one of the limited neurogenic brain areas during adulthood; neurons born in the DG are involved in some types of learning and memory processes. We found a decrease in the ability for proliferation and neuronal differentiation of newborn cells, measured by bromodeoxyuridine incorporation in the DG, from streptozotocin-induced diabetic mice. The hilar region, formed by mature neurons presenting higher sensitivity to brain damage, showed a reduced neuronal density in diabetic mice with respect to vehicle-treated mice. Interestingly, in a spontaneous model of type 1 diabetes, we corroborated a decrease in the rate of neurogenesis in the nonobese diabetic mice compared to control strains, and this reduction was also found during the prediabetic stage. The antidepressant fluoxetine administered over a period of 10 days to diabetic mice was effective in preventing changes in proliferation and differentiation of new neurons. Confocal microscope studies, including using neuronal and glial markers, suggested that differentiation toward a neuronal phenotype was decreased in diabetic animals and was reversed by the antidepressant treatment. In addition, the loss of hilar neurons was avoided by fluoxetine treatment. Several reports have demonstrated that high susceptibility to stress and elevated corticosterone levels are detrimental to neurogenesis and contribute to neuronal loss. These features are common in some types of depression, diabetes, and aging processes, suggesting they participate in the reported hippocampal abnormalities present in these conditions.
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PMID:Neuronal plasticity and antidepressants in the diabetic brain. 1923 43

Diabetes has been associated with depression since Thomas Willis' work in 1684 (Rubin and Peyrot in Diabetes Metab Rev 18:173-175, 2002). The aim of this study is to identify social and clinical factors independently associated with depression in individuals with type 1 diabetes. We carried out a descriptive transversal study with 110 type 1 diabetes patients, administered a questionnaire and obtained demographical and diabetes-related data (number of years from diagnosis, initial admission at diagnosis, glycated hemoglobin, number of complications, insulin dose, number of insulin injections per day, admission for ketoacidosis or hypoglycemia at diagnosis, and specific diabetes complications such as nephropathy, retinopathy, peripheral neuropathy, coronariopathy, and amputation). Depressive symptoms were quantified using the Hamilton Score. We used T tests to investigate potential relations between the covariates and depression (Hamilton score). We concluded the following: as few as 10% of our patients had glycated hemoglobin under 7%; women had more symptoms of depression, and there are four independent factors associated with depression in individuals with type 1 diabetes mellitus: age, Graffar score, admission for ketoacidosis, and insulin dose.
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PMID:Independent factors associated with depression in type 1 diabetes mellitus. 1930 Aug 97

Previous studies in children with diabetes found that hyperglycemia induces memory dysfunction. In this study, we investigated memory and synaptic plasticity in streptozotocine (STZ)-induced diabetic rats during the juvenile period. We further investigated the effects of glucagon-like peptide-1 (GLP-1) on the diabetes-induced profiles. STZ (85 mg/kg, i.p.) was administered to 17-day-old Wistar rats to induce type-1 juvenile diabetes mellitus (JDM). In the Y-maze test, JDM rats showed significant impairment of learning and memory, which were improved by GLP-1 (7-36) amide (1 microg/5 microl/rat, i.c.v.). Extracellular recording at Schaffer collateral synapses in the CA1 region of hippocampal slices showed that long-term potentiation and paired-pulse facilitation in JDM rats were similar to age-matched control rats. However, the input-output relation was strengthened, and long-term depression (LTD) and responses of N-methyl d-aspartic acid through NR2B subunits were weakened in the JDM rats. GLP-1 (7-36) amide (100 nM) increased the magnitude of LTD and the responses through NR2B in the JDM rats. These results indicate that the lack of LTD and NR2B responses may contribute to impairment of memory associated with JDM, suggesting the potential usefulness of GLP-1 in the treatment of memory dysfunction in JDM.
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PMID:The influences of juvenile diabetes on memory and hippocampal plasticity in rats: improving effects of glucagon-like peptide-1. 1932 Nov 33

Girls and women with type 1 diabetes have increased rates of disturbed eating behaviors and clinically significant eating disorders than their nondiabetic peers. Type 1 diabetes is strongly associated with several empirically supported eating disorder risk factors (eg, higher body mass index, increased body weight and shape dissatisfaction, low self-esteem and depression, and dietary restraint). It may be that specific aspects of diabetes treatment increase the risk for developing disordered eating. Disturbed eating behaviors and clinical eating disorders predispose women with diabetes to many complex medical risks and increase risk of morbidity and mortality. For this reason, it is critical that diabetes clinicians understand more about eating disorders to improve the likelihood of early risk detection and access to appropriate treatment. This article presents a review of the current scientific literature on eating disturbances in type 1 diabetes and synthesizes the existent findings into recommendations for screening and treatment.
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PMID:Disturbed eating behaviors and eating disorders in type 1 diabetes: clinical significance and treatment recommendations. 1932 58

This study examined symptoms of anxiety and depression in mothers of young children with type 1 diabetes (T1D) in relation to mothers' fears of hypoglycemia, perceptions of coping, and children's metabolic control. Sixty-seven mothers of children less than 8 years of age diagnosed with T1D completed self-report measures, and children's metabolic control was measured with glycosolated hemoglobin (HbA1c). Twenty-one percent of mothers reported clinically significant levels of symptoms of anxiety, and twenty-four percent reported clinically significant levels of depression. Lower income level and finding it more upsetting to cope with diabetes-related stress accounted for higher symptoms of anxiety and depression in mothers. Mothers' symptoms were not related to children's metabolic control. Recommendations are made for screening mothers and providing supportive interventions to alleviate their distress.
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PMID:Coping and Psychosocial Adjustment in Mothers of Young Children with Type 1 Diabetes. 1941 55

259 adults with type 1 diabetes completed measure of anxiety, depression and diabetes specific distress, HbA1c from medical records. Anxiety not depression predicted HbA1c, this association was mediated by illness specific cognitions. Targeting illness specific cognitions may be more productive than treatment of general dysphoria in type 1 diabetes.
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PMID:The relationship between generic and diabetes specific psychological factors and glycaemic control in adults with type 1 diabetes. 1950 Aug 69


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