Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied environmental risk factors which might contribute to the development of beta-cell autoantibodies in healthy children. Here, we investigated 6000 randomly selected children from the large All Babies in Southeast Sweden (ABIS) cohort, including 17 055 newborns recruited between 1997 and 1999. Questionnaires at birth and at 1 yr of age and the levels of autoantibodies to glutamic acid decarboxylase (GADA) and autoantibodies to tyrosine phosphatase (IA-2A) at 1 yr of age were analyzed. The 99th percentile cutoff for autoantibodies was proposed to identify children at risk of type 1 diabetes (T1D) and the 90th percentile cutoff to identify children in whom beta-cell autoimmunity has been induced. Using the 90th percentile cutoff level, 1156 children had either IA-2A (n = 574) or GADA (n = 582), while 126 children had both GADA and IA-2A. When the 99th percentile cutoff level was used, 114 children had either IA-2A (n = 57) or GADA (n = 57), and six children had both GADA and IA-2A. In logistic regression analysis, celiac disease in grandparents [odds ratio (OR) 2.2] and maternal gastrointestinal infection (OR 1.1) represented a risk for simultaneous occurrence of both IA-2A and GADA above the 90th percentile. Birth in spring (March to May) (OR 1.5) and male gender (OR 1.3) were risk factors for induction of IA-2A. Mother's low education represented a risk for induction of IA-2A (OR 1.5) and GADA (OR 1.4). T1D in first-degree relatives increased the risk for beta-cell autoimmunity above the 99th percentile (OR 2.6), whereas type 2 diabetes in grandparents was associated with GADA (OR 2.1). Exposure to cow's milk formulas <2 months of age implied an OR of 2.9 for IA-2A above the 99th percentile.
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PMID:Environmental factors related to the induction of beta-cell autoantibodies in 1-yr-old healthy children. 1639 Mar 88

The aim of the study was to describe serum adiponectin levels in a population-based sample of women with different degrees of glucose tolerance and to examine if the variability in serum adiponectin was explained by family history of diabetes, obesity, insulin resistance, glycemia, and inflammation. Repeated oral glucose tolerance tests were used in a screening procedure of a cohort of 64-year-old women to identify those with diabetes mellitus n = 210) and impaired glucose tolerance (n = 201). A random sample of women with normal glucose tolerance (NGT, n = 186) was also included. The examination included history of first-degree relatives with diabetes, anthropometry, measurement of circulating adiponectin, glutamic acid decarboxylase antibodies, blood glucose, HbA1c, insulin, proinsulin, C-peptide, high-sensitivity C-reactive protein, and homeostasis model assessment. Serum adiponectin concentration was lowest among diabetic women, highest in the random-sample NGT group, and intermediate in the impaired glucose tolerance group. This difference was partly explained by homeostasis model assessment, C-peptide, family history, and high-sensitivity C-reactive protein (R2 = 0.33, P < .001), but obesity and glycemia did not contribute to this variability in serum adiponectin. A family history of diabetes was associated with low serum adiponectin concentration independently of obesity, glycemia, or insulin sensitivity (P = .002). Glutamic acid decarboxylase-positive diabetic women (n = 17) had similar serum adiponectin as the NGT group in spite of hyperglycemia. In conclusion, serum adiponectin was lowered in women with type 2 diabetes mellitus, and this difference could only be partly explained by insulin resistance, insulin secretion, family history of diabetes, and inflammation. Family history of diabetes was independently associated with hypoadiponectinemia. Autoimmune diabetic women did not have low adiponectin levels.
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PMID:Serum adiponectin in a population sample of 64-year-old women in relation to glucose tolerance, family history of diabetes, autoimmunity, insulin sensitivity, C-peptide, and inflammation. 1642 25

We report on a patient whose type 2 diabetes mellitus resolved during IFN-alpha therapy for hepatitis C virus (HCV). A 40-year-old man was diagnosed with type II diabetes in year 2000. His body mass index (BMI) was 30.8 kg/m and glycosylated haemoglobin (HbA1c) was 10.7%. He was treated with metformin. Later, his glycaemic control deteriorated despite additional dietary and lifestyle advice and the addition of glibenclamide. He was started on subcutaneous insulin in 2002 with the continuation of metformin. In 2003 he was diagnosed with chronic hepatitis caused by HCV. In September 2003 he was started on IFN-alpha and ribavirin. After 24 weeks of treatment his HCV polymerase chain reaction remained positive and treatment was stopped as per guidelines. At the commencement of antiviral therapy, HbA1c was 7.7%. In April 2004 his BMI of 29.38 kg/m had reduced and he then stopped insulin therapy because of repeated hypoglycaemia. After stopping insulin his HbA1c was 4.7%. Fasting plasma glucose of 6.2 mmol/l and anti-glutamic acid decarboxylase antibodies were negative. Urea and creatinine levels were normal. Most of the earlier literature describes diabetes developing in the course of IFN-alpha therapy for a variety of diseases. More recent research has described a relationship between hepatitis C infection and the development of diabetes and insulin resistance. Responders to IFN-alpha treatment manifest an improvement in insulin sensitivity compared with non-responders after the completion of IFN-alpha therapy. Our case shows the resolution of pre-existing diabetes in a patient with chronic HCV infection, which did not respond to IFN-alpha therapy. Whether this occurred as a direct result of IFN-alpha on insulin sensitivity or indirectly as a result of weight loss because the therapy for HCV precipitated additional lifestyle changes in the patient is as yet unclear.
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PMID:Resolution of diabetes in type 2 diabetic patient treated with IFN-alpha and ribavirin for hepatitis C. 1646 44

Type 1 diabetes results from a specific destruction of the insulin-producing beta-cells of the pancreas. The disease is characterized by the appearance of specific autoantibodies against islet cell antigens. Autoantibodies to insulin, glutamic acid decarboxylase, tyrosine phosphatase IA-2 and cytoplasmic islet cell antibodies are useful markers for the differential diagnosis of type 1 diabetes when clinical and metabolic criteria alone do not allow definite classification. Autoimmune diagnostics is of particular importance in adults to discriminate between type 1 and type 2 diabetes and to assess the diagnosis of latent autoimmune diabetes in adults.
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PMID:Autoimmune diagnostics in diabetes mellitus. 1647 96

We studied dietary risk factors by analysing a questionnaire administered at birth, 1 year and 2(1/2) years of age, as well as the level of glutamic acid decarboxylase autoantibodies (GADA) and tyrosine phosphatase autoantibodies (IA-2A), in 7208 2(1/2)-year-old children from the All Babies in Southeast Sweden cohort, using the 95th percentile cut-off for autoantibodies to identify children at risk of type 1 diabetes. A total of 657 children had either IA-2A (n 360) or GADA (n 335), and thirty-eight children had both GADA and IA-2A. In univariate analysis, male gender and maternal coeliac disease implied a risk of possessing IA-2A. Maternal type 2 diabetes, a high consumption of fresh cows milk at the age of 1 year and a late introduction of gluten were associated with a risk of GADA. Early cessation of breast-feeding (< 2 months of age) was associated with a risk of the simultaneous occurrence of both IA-2A and GADA. In logistic regression analysis, a high consumption of milk at the age of I year (odds ratio 2.6)represented a risk for GADA, and maternal coeliac disease (odds ratio 2.9) represented a risk for IA-2A. The combination of an early introduction of cows milk formula and a late introduction of gluten-containing food gave an odds ratio of 6.0 for positivity for at least one autoantibody at 1 and 21 years of age. The induction of autoantibodies by the age of 2(1/2) years has a male preponderance and is more common in children with maternal type 2 diabetes or maternal coeliac disease. Dietary risk factors for the induction of beta-cell autoantibodies in 21-year-old children are a short duration of breast-feeding, an early introduction of cows milk formula and a late introduction of gluten, as well as a high consumption of milk at the age of I year.
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PMID:Dietary risk factors for the emergence of type 1 diabetes-related autoantibodies in 21/2 year-old Swedish children. 1709 93

We evaluated the prevalence of glutamic acid decarboxylase autoantibody (GADA) in nonobese patients with type 2 diabetes mellitus in Korea and investigated the characteristics of GADA-positive and GADA-negative patients. Two years later, we assessed the progression of beta-cell function in these patients. Of the 647 nonobese patients with type 2 diabetes mellitus enrolled in the study, 10.1% was positive for GADA. Glutamic acid decarboxylase antibody-positive patients had lower fasting and stimulated C-peptide levels compared with GADA-negative patients (1.70 +/- 0.72 vs 1.24 +/- 0.59 microg/L, P < .001; 2.59 +/- 1.51 vs 1.99 +/- 0.82 microg/L, P < .001). Patients treated with insulin had lower fasting and stimulated C-peptide levels than those not treated (1.13 +/- 0.52 vs 1.66 +/- 0.73 microg/L, P = .002; 1.85 +/- 0.69 vs 2.49 +/- 0.91 microg/L, P = .004) and had higher titers of GADA (30.5 +/- 7.3 vs 6.0 +/- 4.8 U/mL, P < .001). In terms of progression of beta-cell function, fasting and stimulated C-peptide levels were significantly lower in GADA-positive patients after 2 years (from 1.24 +/- 0.59 to 0.95 +/- 0.54 microg/L, P = .004; from 1.99 +/- 0.82 to 1.61 +/- 0.77 microg/L, P = .007), whereas no such difference was observed in the GADA-negative patients. We demonstrate that a significant proportion of Korean patients may be positive for GADA; this is consistent with studies of white subjects, although disagrees with previous reports on Korean subjects. By assessing the presence of GADA in Korean type 2 diabetic patients, we are able to predict their course of beta-cell function and identify in advance those who are likely to require insulin treatment.
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PMID:Clinical and biochemical characteristics of nonobese type 2 diabetic patients with glutamic acid decarboxylase antibody in Korea. 1683 48

The Japanese Brazilian population has one of the highest prevalences of diabetes worldwide. Despite being non-obese according to standard definitions, their body fat distribution is typically central. We investigated whether a subset of these subjects had autoantibodies that would suggest a slowly progressive form of type 1 diabetes. A total of 721 Japanese Brazilians (386 men) in the 30- to 60-year age group underwent clinical examination and laboratory procedures, including a 75-g oral glucose tolerance test and determinations of serum autoantibodies. Antibodies to glutamic acid decarboxylase (GADab) were determined by radioimmunoassay and to thyroglobulin (TGab) and thyroperoxidase (TPOab) by flow-cytometry assays. Mean body mass index was 25.2 +/- 3.8 kg/m2, but waist circumference was elevated according to the Asian standards. Diabetes, impaired glucose tolerance, and impaired fasting glycemia were found in 31%, 22%, and 22%, respectively, and 53% of the subjects had metabolic syndrome. Glutamic acid decarboxylase (GADab) was positive in 4.72%, TGab in 9.6%, and TPOab in 10% of the whole sample. When participants were stratified according to the presence of thyroid antibodies, similar frequencies of GADab were found in positive and negative groups. The prevalence rates of glucose metabolism disturbances did not differ between GADab positive and negative groups. Our data did not support the view that autoimmune injury could contribute to the high prevalence of diabetes seen in Japanese Brazilians, and the presence of co-morbidities included in the spectrum of metabolic syndrome favors the classification as type 2 diabetes.
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PMID:Autoimmunity does not contribute to the highly prevalent glucose metabolism disturbances in a Japanese Brazilian population. 1727 84

Acquired generalized lipodystrophy (AGL) is a rare disorder of adipose tissue characterized by loss of fat from large regions of the body, occurring after birth. Its etiology remains unknown. Most AGL patients have had fasting and/or postprandial hyperinsulinemia, diabetes mellitus, hypertriglyceridemia, and fatty liver. We describe the case of a 30-year-old woman with a progressively unsteady gait and a generalized loss of body fat beginning at the age of 7. Cerebellar degeneration was revealed by imaging study, and the patient was eventually bedridden at the age of 15, due to progressive ataxia. She developed diabetes at the age of 25 without the presence of any evidence of ketoacidosis. The glutamic acid decarboxylase antibody was negative, C-peptide level 3.6 ng/ml, HbA1c 13%, triglyceride 412 mg/dl, total cholesterol 196 mg/dl, high-density lipoprotein-cholesterol 28 mg/dl, adiponectin 0.76 microg/ml, and resistin was 22.8 ng/ml at the initial state of diabetes. AGL accompanied by type 2 diabetes and cerebellar degeneration was diagnosed on the basis of the clinical features and metabolic derangements.
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PMID:A case of acquired generalized lipodystrophy with cerebellar degeneration and type 2 diabetes mellitus. 1749 4

In this paper, the islet autoimmunity status and relation to clinical characteristics, beta cell function and cardio-metabolic risk factors in young-onset Asian diabetic patients are evaluated at baseline. The study population consisted of 912 patients (from China, India, Malaysia and Singapore) with age 12-40 years and diabetes duration <12 months. Autoantibodies to glutamic acid decarboxylase (GADA) and tyrosine phosphatase (IA-2A), beta cell function and cardio-metabolic risk parameters were assessed. Among our young patient cohort, 105 (11.5%) patients were GADA and/or IA-2A positives (Ab +ve). Ab +ve patients were younger, leaner, had more severe hyperglycaemia and lower beta cell function. The frequency of metabolic syndrome was significantly lower in Ab +ve patients (27%) compared to Ab -ve patients (54%). However, a substantial proportion of patients in both groups of patients had atherogenic dyslipidaemia, hypertension and albuminuria (micro or macro). In our study cohort, only one in 10 Asian youth with new-onset diabetes had evidence of islet autoimmunity. At least 60% of Ab +ve and 50% of Ab -ve patients demonstrated classical features of type 1 and type 2 diabetes respectively. Regardless of autoimmunity status, the cardio-metabolic risk factors, in particular atherogenic dyslipidaemia, hypertension and albuminuria were common in our patients with young-onset diabetes.
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PMID:Islet autoimmunity status in Asians with young-onset diabetes (12-40 years): association with clinical characteristics, beta cell function and cardio-metabolic risk factors. 1820 2

We report an interesting and unique case of an overweight adolescent with a novel mutation of the maturity-onset diabetes of the young (MODY)3 gene [hepatocyte nuclear factor-1 alpha (HNF-1alpha)] and positive islet cell autoantibodies. The patient is a 17-yr-old Caucasian female, who was diagnosed with type 2 diabetes mellitus, treated with metformin and glipizide, with poor control for 18 months prior to being referred to the Endocrinology clinic. Family history was strongly positive for type 2 diabetes (father, paternal aunts, uncles, and grandmother). All were diagnosed at age 40-50 and treated with oral hypoglycemic agents. The patient's body mass index was 36.4 kg/m(2). She had no acanthosis nigricans. Initial hemoglobin A1c was 11.9%, with fasting glucose of 234 mg/dL and fasting insulin 10.7 microU/mL. She was started on insulin therapy (0.6 units/kg/d), resulting in good glycemic control. Oral hypoglycemic agents were discontinued. Immunologic studies showed positive islet cell (29 U/mL, normal <1.0) and glutamic acid decarboxylase-65 (0.9 U/mL, normal <0.5) antibodies. Sequencing for HNF-1alpha gene revealed a nucleotide A to G substitution (ACC to GCC), resulting in a missense mutation, T196A. To our knowledge, T196A has not been previously reported. The coexistence of type 1 diabetes autoimmunity and a mutation in the gene responsible for MODY3 in this overweight patient is intriguing and might explain the early onset of progressive insulinopenia compared with the later age of diabetes onset of the earlier generation in the family.
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PMID:Triple diabetes: coexistence of type 1 diabetes mellitus and a novel mutation in the gene responsible for MODY3 in an overweight adolescent. 1822 40


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