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

We investigated amino acid metabolism in the Zucker diabetic fatty (ZDF Gmi fa/fa) rat during the prediabetic insulin-resistant stage and the frank type 2 diabetic stage. Amino acids were measured in plasma, liver, and skeletal muscle, and the ratios of plasma/liver and plasma/skeletal muscle were calculated. At the insulin-resistant stage, the plasma concentrations of the gluconeogenic amino acids aspartate, serine, glutamine, glycine, and histidine were decreased in the ZDF Gmi fa/fa rats, whereas taurine, alpha-aminoadipic acid, methionine, phenylalanine, tryptophan, and the 3 branched-chain amino acids were significantly increased. At the diabetic stage, a larger number of gluconeogenic amino acids had decreased plasma concentrations. The 3 branched-chain amino acids had elevated plasma concentrations. In the liver and the skeletal muscles, concentrations of many of the gluconeogenic amino acids were lower at both stages, whereas the levels of 1 or all of the branched-chain amino acids were elevated. These changes in amino acid concentrations are similar to changes seen in type 1 diabetes. It is evident that insulin resistance alone is capable of bringing about many of the changes in amino acid metabolism observed in type 2 diabetes.
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PMID:Amino acid metabolism in the Zucker diabetic fatty rat: effects of insulin resistance and of type 2 diabetes. 1538 98

Chryseobacterium indologenes is a non-fermentative Gram-negative bacillus that is a rare pathogen in humans. Its occurrence in diabetic children has not been previously reported. In this report, a case is described of C. indologenes bacteraemia possibly associated with the use of a peripheral venous catheter. A 2-year-old boy with type I diabetes mellitus was admitted due to a coma caused by cerebral oedema and was successfully treated for his neurological condition but presented on the tenth day after admission with fever of 40 degrees C, agitation, restlessness, lack of appetite, somnolence and fatigue. His pulse rate was 90 min(-1) and his respiratory rate was 20 min(-1). Laboratory studies revealed a white blood cell count of 4900 mm(-3) with 67% neutrophils and 27% lymphocytes. Two separate blood cultures yielded C. indologenes. Treatment with ceftriaxone was started before the culture results were obtained, and was continued after susceptibility test results were obtained. The patient became afebrile after 48 h, and his general condition improved within 36 h. The infection did not recur. This is believed to be the third case of bacteraemia outside of Asia due to C. indologenes and the first in a diabetic child not otherwise immunocompromised. This case indicates that C. indologenes infection can occur in diabetic children without ventilator or central venous catheter and might be treated with a single agent after in vitro susceptibility tests have been performed.
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PMID:Chryseobacterium indologenes bacteraemia in a diabetic child. 1594 33

Exenatide is an incretin mimetic indicated for the treatment of type 2 diabetes mellitus in combination with a sulfonylurea, a thiazolidinedione, metformin, or metformin plus a sulfonylurea or thiazolidinedione. Exenatide lowers postprandial blood glucose levels by stimulating glucose-dependent insulin secretion, inhibiting glucagon secretion, slowing gastric emptying, and increasing satiety. Therapy with exenatide often results in weight loss, which further assists in decreasing insulin resistance. This feature makes the drug an attractive therapeutic option for obese patients. We report the successful off-label use of exenatide in an obese, 40-year-old man with type 1 diabetes and human immunodeficiency virus (HIV) infection who had gastrointestinal intolerance to pramlintide. The patient had experienced a dramatic weight gain secondary to his antiretroviral drugs. This weight gain led to insulin resistance and the development of type 2 diabetes; thus he had characteristics of both types 1 and 2 diabetes, or double diabetes. Before the start of exenatide therapy, he weighed 123 kg, had a body mass index of 42.3 kg/m(2), and had a suboptimal hemoglobin A(1c) value of 8.7%. After 11 months of therapy, the patient lost 24 kg (19.5% of his body weight) and achieved a hemoglobin A(1c) value of 7.3%. His basal insulin requirement was reduced by 25%, and his use of short-acting insulin before breakfast and before dinner was discontinued. In addition, the patient's quality of life substantially improved, as he was able to return to work and exercise after being nearly incapacitated by his weight. To our knowledge, this is the first published case report of the use of exenatide in a patient with type 1 diabetes mellitus or human immunodeficiency virus infection. Given this experience, exenatide may prove to be a useful alternative in selected patients with type 1 diabetes.
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PMID:Off-label use of exenatide for the management of insulin-resistant type 1 diabetes mellitus in an obese patient with human immunodeficiency virus infection. 1789

We report a case of latent autoimmune diabetes in adults (LADA), also known as slowly progressive type 1 diabetes (SPT1D), followed up for changes, including reactivity to the GAD65 antibody epitope for the 9-year period from impaired glucose tolerance (IGT) to the insulin-dependent stage (IDDM). This 69-year-old male was identified as having IGT by health checkup in 1998. As he was GAD65-positive (high titer), we initiated close clinical follow-up. In 2003, a 75-g oral glucose tolerance test showing a diabetic pattern confirmed that he had progressed to diabetes. During this period, fasting plasma glucose remained within normal range and insulin secretion was unchanged compared to that at the time of IGT diagnosis. His fasting plasma glucose and HbA1c levels began to increase in 2004 and serum C-peptide began to decrease in 2005. Insulin treatment was started in August 2006. GAD65 antibody titer was high (13900 U/ml) in 1998 and has remained high throughout follow-up. The patient's GAD65 antibodies were initially directed to the b96.11-defined epitope only, recognized as an indicator of T1D-like pathogenesis in our former study. During follow-up, he developed reactivity to more epitopes (MICA-3 and MICA-4, DPC, and DPA). The course of this case suggests that the b96.11-defined epitope is important for distinguishing LADA patients who progress to IDDM from those who do not and that epitope maturation is restricted to LADA patients who progress to IDDM, an observation similar to that in children at risk for developing typical IDDM.
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PMID:Latent autoimmune diabetes in an adult. 1912 Mar 10

Antibodies against glutamic acid decarboxylase (GAD) are involved in the pathophysiology of stiff-person syndrome (SPS) and type 1 diabetes. GAD catalyses the conversion of glutamate to gamma-aminobutyric acid (GABA). GABA acts as a neurotransmitter between neurones, while in pancreatic beta cells it plays an integral role in normal insulin secretion, hence the clinical presentation of muscular spasms in SPS and insulin deficiency in diabetes. Despite this apparent major overlap in pathophysiology, SPS only rarely occurs in individuals with type 1 diabetes. We report the case of a 41-year-old man presenting with a simultaneous diagnosis of both these conditions. His case is unusual in that it is the first reported case in the literature of these conditions occurring in someone with celiac disease (CD) and dermatitis herpetiformis. We discuss why SPS and type 1 diabetes co-exist in only a minority of cases and speculate on the underlying mechanism of the association with CD and dermatitis herpetiformis in our patient.
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PMID:A case of stiff-person syndrome, type 1 diabetes, celiac disease and dermatitis herpetiformis. 1947 52

A 14 year male adolescent born of 2nd degree consanguineous marriage presented with asymptomatic proteinuria and severe anemia. He had leucopenia, anisopoikilocytosis, megaloblastic erythropoiesis, megakaryocytes with low serum B12 level. His younger sibling was similarly affected. This combination suggested Imerslund-Grasbeck syndrome. The hemoglobin levels improved with injection of vitamin B12 but proteinuria persisted. During follow-up, he developed ketoacidosis due to insulin dependent diabetes mellitus. This rare combination has not been reported in the Indian literature.
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PMID:Imerslund-Grasbeck syndrome: association with diabetes mellitus. 1934 73

In this study, we reported a complete solitary living related orthotopic partial pancreatic transplantation (LROPPT) with duct to duct drainage of pancreatic juice. A 29-year old man, who has suffered from type I diabetes mellitus (DM) since age 2, underwent LROPPT on 2007 August 9th. He had hypoglycemia for several times per week. His preoperative hemoglobin A1c (HbA1c) was 8.4%. He has little diabetic complications of 2 degree of nephropathy with albuminuria and slight neuropathy. The donor was a 57-year old his father, whose preoperative 75gOGTT and ivGTT revealed normal pattern. Donor was performed hand-assisted distal pancreatectomy with spleen. Operative time was 5 hours and 18 min and intraoperative hemorrhage was 75 ml. Recipient was explored by upper abdominal L-shaped incision. Distal pancreatectomy with spleen with enough expose of both splenic vein and artery, and main pancreatic duct. Both the splenic vein and the arterial anastomosis was made, thereafter, pancreatic duct to duct anastomosis was made by 6-0 PDS with pancreatic duct stent. The pancreatic duct stent lead to extra abdomen through Papilla Vater and duodenum. Pancreatic tissue was anastomosis by 6-0 prolene using fibrin-glue. After that, absorbed thin mesh was rolled around the pancreatic anastomosis with fibrin-glue. The operative time was 10 hr 10 min and the blood loss was 435 ml. Patient was discharged without a pancreatic leakage and vessel thrombosis 16th days after transplantation. LROPPT is a complete physiologic procedure. In Japan, almost of donor is marginal donor aged above 50 years old. The portal drainage might be comfortable for the stress of the partial pancreatic graft.
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PMID:A complete physiological orthotopic living related partial pancreatic transplantation alone with pancreatic duct to duct anastomosis for type I diabetes mellitus. 1945 68

Progressive signs of ataxia in a eight years old girl prompted neurological investigation. The girl had unstable gait with incoordination of limb movements, impairment of position and vibratory senses, dysarthria, pes cavus, positive Babinski sign and scoliosis. At the age of fourteen the girl was referred in a comatose condition, in a severe diabetic ketoacidosis. Ataxia and hypoactive knee and ankle jerks prompted the analysis of the frataxin gene (FXN; 606829). The most common molecular abnormality: GAA trinucleotide repeat expansion in intron 1 was found with + 300 GAA repeats (1490bp) (normal individuals have 5 to 30 GAA repeat expansions, whereas affected individuals have from 70 to more than 1,000 GAA triplets). Electrocardiogram showed diffuse T wave inversion with sinus bradycardia, while ultrasound revealed concentric, symmetric hypertrophy of left ventricle leading to the diagnosis of hyperthrophic cardiomyopathy. At the age of 14 years, the patient was bound to the wheel-chair, unable to walk. Her brother started to show ataxia at the age of 8 years, and subsequent analysis showed hyperthrophic cardiomyopathy, too. His mutational analysis revealed the same frataxin abnormality, with + 300 GAA repeats. So far, no signs of diabetes occurred. The parents are heterozygous with FXN of 9 -10 GAA (490 bp). Both children received a beta blocker, while the girl's diabetes mellitus was treated by insulin preparations. This is a report of two siblings with Fridreich ataxia and hyperthrophic cardiomyopathy. In addition, the girl developed type 1 diabetes mellitus.
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PMID:Friedreich ataxia (FA) associated with diabetes mellitus type 1 and hyperthrophic cardiomyopathy. 1948 41

Progressive signs of ataxia in a eight year old girl with hypo-active knee and ankle jerks, prompted the analysis of the frataxin gene (FXN; 606829). The most common molecular abnormality--GAA trinucleotide repeat expansion in intron 1--was found with +300 GAA repeats (1490 bp) (normal individuals have 5 to 30 GAA repeats expansions, whereas affected individuals have from 70 to more than 1000 GAA triplets). Additionally she had unstable gait with incoordination of limb movements, impairment of position and vibratory senses, dysarthria, pes cavus, positive Babinski sign and scoliosis. At the age of fourteen the girl was referred in a comatose condition, in severe diabetic ketoacidosis. Insulin dependent diabetes mellitus was since treated with insulin preparations. Electrocardiogram showed diffuse T wave inversion with sinus bradycardia, while ultrasound revealed concentric, symmetric hypertrophy of the left ventricle leading to the diagnosis of hypertrophic cardiomyopathy. At the age of 14, she is bound to the wheelchair, unable to walk. Her brother started to show ataxia at the age of 8 years and subsequent analysis also showed hypertrophic cardiomyopathy. His mutational analysis revealed the same frataxin abnormality with +300 GAA repeats. So far, no signs of diabetes occurred. The parental DNA was not available for analysis.
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PMID:Friedreich's ataxia (FA) associated with diabetes mellitus type 1 and hypertrophic cardiomyopathy: analysis of a FA family. 1953 71

A 63-year-old male was admitted to our hospital with diabetic ketoacidosis. He had flu-like symptoms 10 days before admission and developed thirst, polyuria and anorexia with 9 kg of body weight loss in a week. Plasma glucose level on admission was 983 mg/dL and HbA1c was 7.5%. Despite high levels of serum pancreatic enzymes, lack of severe abdominal pain and no morphological change of pancreas in the abdominal CT scan eliminated the complication of classical acute pancreatitis. These findings suggested the diagnosis of fulminant type 1 diabetes. However, urinary and plasma C-peptide levels showed that insulin secretion was not completely depleted at onset. Furthermore, an examination of islet-related antibodies revealed the presence of high titer anti-GAD antibody. His HLA typing showed that DRB1*0901-DQB1*0303 and A24 were present. He has been doing well with continuation of insulin therapy. Over two years after onset, his plasma C-peptide level was gradually lowered, and anti-GAD antibody was still positive. Taken together, this is a rare case of abrupt onset autoimmune type 1 diabetes with transient but apparent exocrine pancreatic impairment at onset. Similar cases should be accumulated to clarify pathophysiological similarities and/or differences between fulminant type 1 diabetes and abrupt onset autoimmune type 1 diabetes.
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PMID:A case of abrupt onset autoimmune type 1 diabetes mimicking fulminant type 1 diabetes. 1968 7


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