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

Microalbuminura (MA) was determined in 127 children and adolescents (age 3-21 years) with type 1 (insulin-dependent) diabetes mellitus. Patients with clinical evidence of long-term complications or macroproteinuria were excluded. Urinary albumin excretion was measured in a nocturnal 12-h collection and correlated with the albumin/creatinine ratio of a urine sample freshly voided on the morning immediately following the collection. The patients were divided into group A (n = 83, age less than 16 years, duration of diabetes 1-13 years, mean 4.4) and group B (n = 44, age greater than 16 years, duration of diabetes 1-19 years, mean 8.7) and compared with appropriate controls. MA above 15 micrograms/min was present in 11 of 83 (13.3%) patients in group A and in 7 of 44 (15.9%) in group B. In a repeat urine collection at least 3 months later elevated MA persisted in 1 of 11 (group A) and in 4 of 7 (group B) patients. There was no correlation between increased MA in a 12-h urine collection and the albumin/creatinine ratio in a subsequently voided urine sample. MA was not strictly dependent on age, sex, duration of diabetes, haemoglobin A1, mean arterial blood pressure, plasma creatinine, creatinine clearance or serum beta-2-microglobulin. Further systematic studies and careful follow up are necessary to appraise whether intermittent MA is indeed an early manifestation of incipient kidney disease in children with type 1 diabetes.
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PMID:Intermittent microalbuminuria in children with type 1 diabetes mellitus without clinical evidence of nephropathy. 274 46

This paper reports our experience with the successful simultaneous transplantation of kidney and fetal pancreatic islets in 46-year-old diabetic man. No detectable C-peptide level was noted and the end-stage nephropathy required hemodialysis. The cadaver kidney and two masses of 8-week-cultured fetal islets were grafted simultaneously. After revascularization of the kidney, the islet masses were placed under the kidney capsule. Following transplantation, islet function was demonstrated by a higher C-peptide level, which subsequently persisted. Twenty-four months after grafting, islet function was provoked by glucagon and glucose, which led to elevations in the C-peptide and insulin levels. The insulin requirement fell from 58 to 24 U/day during the post-transplant period of 24 months. The mean value of HbA1C (5.6% +/- 0.3%) indicated a constantly normal carbohydrate metabolism. Improvements in retinopathy were also noted. Three periods of kidney rejection were diagnosed, but these proved reversible with high-dose steroid treatment. The serum and urine beta-2-microglobulin levels correlated well with rejection and recovery. More than 2 years after grafting, kidney functions is in the normal range. On sonography, the transplanted islet masses were repeatedly clearly visible, and 24 months following transplantation the volume was twice the original one. The results indicate that simultaneous kidney and fetal pancreatic islet grafting is advantageous in end-stage nephropathy secondary to type I diabetes mellitus.
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PMID:Successful simultaneous transplantation of kidney and fetal pancreatic islet masses. 762 85

Whole pancreas or beta-cell transplantation has opened the way for the treatment of advanced stage of diabetes mellitus. However, it is always limited by the scarcity of transplantation materials. The amniotic membrane is part of the fetal membrane and is composed of amniotic epithelium (HAE) and mesenchymal (HAM) cells that are derived from the inner cell mass in the blastocyst. Thus, HAE and HAM cells may have the potential to differentiate into various organs. The aim of our study was to assess the possibility of HAE cells differentiating into insulin-producing cells. In vitro, HAE cells stimulated with nicotinamide induced insulin mRNA in the culture cells. In vivo, HAE cells were capable of normalizing the blood glucose level of diabetic mice after several weeks of implantation into streptozotocin-induced diabetic mice. The distribution of human cells and human insulin secretion in mouse tissue studied by immunohistochemistry for anti-human-specific beta-2-microglobulin and anti-human-specific insulin shows the same location in mouse tissue. These studies suggest that HAE cells have the potential to differentiate into beta-cells in vivo, and hence that HAE cells have therapeutic potential for the treatment of type I diabetes mellitus.
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PMID:Human amnion-isolated cells normalize blood glucose in streptozotocin-induced diabetic mice. 1295 29

Genetic linkage analyses, genome-wide association studies of single nucleotide polymorphisms, copy number variation surveys, and mutation screenings found the human chromosomal 12q24 locus, with the genes SH2B3 and ATXN2 in its core, to be associated with an exceptionally wide spectrum of disease susceptibilities. Hematopoietic traits of red and white blood cells (like erythrocytosis and myeloproliferative disease), autoimmune disorders (like type 1 diabetes, coeliac disease, juvenile idiopathic arthritis, rheumatoid arthritis, thrombotic antiphospholipid syndrome, lupus erythematosus, multiple sclerosis, hypothyroidism and vitiligo), also vascular pathology (like kidney glomerular filtration rate deficits, serum urate levels, plasma beta-2-microglobulin levels, retinal microcirculation problems, diastolic and systolic blood pressure and hypertension, cardiovascular infarction), furthermore obesity, neurodegenerative conditions (like the polyglutamine-expansion disorder spinocerebellar ataxia type 2, Parkinson's disease, the motor-neuron disease amyotrophic lateral sclerosis, and progressive supranuclear palsy), and finally longevity were reported. Now it is important to clarify, in which ways the loss or gain of function of the locally encoded proteins SH2B3/LNK and ataxin-2, respectively, contribute to these polygenic health problems. SH2B3/LNK is known to repress the JAK2/ABL1 dependent proliferation of white blood cells. Its null mutations in human and mouse are triggers of autoimmune traits and leukemia (acute lymphoblastic leukemia or chronic myeloid leukemia-like), while missense mutations were found in erythrocytosis-1 patients. Ataxin-2 is known to act on RNA-processing and trophic receptor internalization. While its polyglutamine-expansion mediated gain-of-function causes neuronal atrophy in human and mouse, its deletion leads to obesity and insulin resistance in mice. Thus, it is conceivable that the polygenic pathogenesis of type 1 diabetes is enhanced by an SH2B3-dysregulation-mediated predisposition to autoimmune diseases that conspires with an ATXN2-deficiency-mediated predisposition to lipid and glucose metabolism pathology.
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PMID:12q24 locus association with type 1 diabetes: SH2B3 or ATXN2? 2493 53