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)

In Madras city (India) 10,513 school students between 3 and 20 yr of age were investigated for glycosuria and its causes. While no previously known cases of diabetes mellitus of any type were encountered, four students (0.038%) in the survey population were found to have glycosuria. One (0.009%) had renal glycosuria, two (0.019%) were possibly NIDDY (MODY) and one (0.009%) had transient glycosuria while receiving anti-tuberculous chemotherapy. It is therefore concluded that neither diabetes mellitus nor glycosuria of non-diabetic causes is a crucial health problem in Indian children and adolescents. While the reasons for this are not known, further research in this field could be of global interest.
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PMID:Glycosuria and diabetes mellitus in children and adolescents in south India. 177 10

There are two approaches to identify diabetes-susceptibility genes. One approach is to isolate and characterize genes expressed in the beta-cell and in insulin target tissues whose mutation or altered expression may contribute to the development of diabetes mellitus. Another approach is to clone a diabetes-susceptibility gene by a reverse genetic strategy. The first step for this strategy is to identify a DNA polymorphism that is linked to the disease locus. Using the strategy of the first approach, several candidate genes were examined. Among these genes, the mutation of insulin genes and insulin receptor genes was found in the patient with diabetes. By cDNA cloning or PCR-direct sequencing methods, we identified several mutations in the insulin receptor genes of four insulin-resistant diabetic patients. At least two mutants of insulin receptor genes were expressed in Chinese hamster ovary cells and these mutated receptors showed impaired ability to transduce insulin action in these cultured cells. The expression of these mutant genes in animals such as transgenic mice will be indispensable to establish the relationship between the gene mutation and the abnormality found in the patient. Using the strategy of the second approach, Bell et al. recently reported that the gene responsible for MODY (maturity-onset diabetes of the young) is tightly linked to the adenosine deaminase gene on chromosome 20q. However, this strategy will not be applicable for identification of diabetes-susceptibility genes of NIDDM, since this disorder is likely to be genetically heterogenous, with mutations in several different genes able to cause hyperglycemia, and this heterogeneity could confound the linkage analysis.
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PMID:[Diabetes mellitus and molecular biology]. 177 65

Authors analyzed the case history of 25 young diabetic patients, whose disease has been diagnosed before the age of thirty. The question that has been raised: is it allowed to treat young diabetics with oral drugs? By classifying the patients, they stated followings: In the 1. group they classified 16 verified MODY/NIDDY patients. In the second group they classified 3 young diabetics, whose disease had been evaluated as slowly progressing IDDM (autoimmune form). 3 patients belonged to the 3 group. They had been classified as MODY/NIDDY patients, however an extremely long lasting remission period--due to the short observation time--can not be excluded. The remaining 3 diabetic patients belonged to the IDDM group, with a long remission period. They were treated incorrectly with oral hypoglycemic drugs. Young diabetics can be treated with oral drugs only in case, when they are proven MODY/NIDDY patients. The precise differential diagnosis between this form and autoimmune IDDM, as well as long lasting remission periode, is extremely important.
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PMID:[Is it permissible to treat young diabetics with oral antidiabetics?]. 185 36

We studied the association of obesity with serum lipid and lipoprotein concentrations in 117 patients (62 males and 55 females) with NIDDY and in 40 nondiabetic control subjects (21 males and 19 females). Obesity at a young age was related to increased lipid and lipoprotein levels both in the patients with NIDDM and the control group. Moreover, low HDL-c levels were aggravated by diabetic status only in males. The BMI and fasting insulin level had a statistically significant correlation with the TG and HDL-c level and various atherogenic factors. Therefore, it is suggested that the lipid abnormalities seen in obesity may be associated with hyperinsulinemia. We conclude that obesity in adolescence leads to aberrations of the serum lipid and lipoprotein levels, particularly in obese males with NIDDY.
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PMID:Adverse effects of obesity on lipid and lipoprotein levels in the patients with non-insulin dependent diabetes in the young. 228 36

The authors deal with the clinical picture of total remission in diabetes, among young patients (below 30 years). In their interpretation "complete remission" means total withdrawal of insulin treatment for at least 2 months. Out of 14 patients with complete remission, the classified 7 patients--by clinical and immunogenetical parameters--as noninsulin-dependent diabetes in the young (MODY-NIDDY). 1 diabetic patient belongs to the autoimmune-subgroup of IDDM. The remaining 6 patients could be classified as IDDM-s. However their clinical and immunogenetical parameters were rather atypical. In conclusion they raised the possibility that this subgroup is heterogenous with in IDDM.
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PMID:[Long-term remission in diabetes mellitus diagnosed at an early age]. 240 24

We report the clinical records of 45 children with abnormalities regarding glycemic regulation characterized by a non-insulin deficient hyperglycemia (NIDH), known under the different names of chemical diabetes, sub-clinical diabetes and more recently MODY. These 45 children belong to 31 families with 532 relatives comprising 137 cases of NIDH which could have been studied. The symptoms of this biochemical abnormality, the pathophysiology of which is not yet clearly understood, are the following: lack of clinical manifestations, except for a variable and intermittent glycosuria; constant abnormal glucose tolerance tests, above 97 percentiles of the reference value with some variations over time; normal immunoreactive insulin levels; percentage of glycosylated hemoglobin at the upper range of normal; dominant autosomal genetic transmission and no association with HLA markers like in insulin-dependent diabetes; lack of degenerative complications of the micro-angiopathic type, at least on these cases even after more than 30 years of follow-up; finally, no tendency towards insulin-dependent diabetes. The NIDH should not be confused with the slow and progressive beginning of insulin-dependent diabetes for which prolonged delay is needed to affirm the diagnosis. The frequency of the biochemical phenomena is about 1.8% of the cases of authentic diabetes mellitus occurring before the age of 15.
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PMID:[Chronic non-insulin deficient hyperglycemia in children]. 265 58

In 12 members of a family with MODY, insulin and C-peptide release after intake of a test breakfast was measured as well as binding of insulin to its erythrocyte receptor. According to serum glucose concentrations, subjects were classified into: diabetic, carbohydrate intolerant, and normal subjects. The two diabetic patients had an insulin release pattern similar to that of non-insulin dependent diabetics. The two patients with carbohydrate intolerance presented hyperinsulinism either at base state and after stimulation. Of the eight normal subjects, three presented high concentrations of serum insulin either at base level and after stimulation; in the remaining five, base insulinemia was normal and the response after food intake was poor. Insulin binding to the receptor was decreased in diabetic patients and this anomaly was more evident in patients with carbohydrate intolerance. In the three patients with increased serum insulin concentration, no disturbances in insulin-receptor binding were detected; in the remaining five patients, insulin-receptor binding was significantly decreased. Our findings prove that these subjects present a disturbance of insulin release and an impairment of insulin-receptor binding with a predominance of one or the other alteration even before hyperglycemia is evident.
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PMID:[Insulin and peptide C secretion after food ingestion and the interaction of insulin with its erythrocyte receptor in a family with MODY type diabetes mellitus]. 269 74

Both early onset and late onset type II diabetes were present in one family of nine siblings. The three early onset type II diabetic siblings showed severe microvascular complications: proliferative retinopathy, diabetic nephropathy, and peripheral neuropathy. Early onset type II diabetes was not associated with any particular HLA haplotype. Early onset type II diabetes could be considered a clinical and genetic disease entity different from MODY type diabetes.
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PMID:Severe microvascular disease in type II diabetes of early onset. A family study. 275 Apr 46

Nineteen diabetics aged 9 to 18 years with the MODY type were investigated, incl. their families, by the oGTT. Diabetes in the parents was nine times and in siblings four times more frequent than in families of adolescents with IDDM. In parents the manifest form predominated, in siblings PGT. Vertical transmission of diabetes in three consecutive generations was found only in the MODY type (in 35%). Diabetes with the MODY type and their diabetic siblings did not differ significantly as to their mild glucose intolerance (blood sugar level up to 13 mmol/l), and their mild diabetic phenotypes did not differ either. Similarly diabetics with IDDM and their diabetic siblings did not differ substantially as to their severe glucose intolerance (blood sugar level up to 21 mmol/l), and their severe diabetic phenotypes did not differ either. IRI levels revealed five times a hyperinsulinaemic and three times a normal insulinaemic response. Obese diabetics were treated with a reducing diet and physical activity. To non-obese diabetics, if the above procedure was not sufficiently successful, sulphonylurea preparation were also administered. During check-up examinations fasting values and values three hours after a meal lower than 6.1 mmol/l were required. In the course of a four- to ten-year follow up it did not change. Existence of the MODY type already macroangiopathic complications developed; in one diabetic the glucose tolerance improved, in the remainder it did not change. Existence of the MODY type already in adolescents justifies early detection in families with a cumulated incidence of NIDDM and prophylactic procedures ensuring euglycaemia in confirmed diabetics.
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PMID:[MODY type diabetes mellitus in children and adolescents]. 275 88

Growth hormone (hGH) reserve following arginine administration and the paradoxical hGH response to thyrotropin-releasing hormone (TRH) were studied in 30 diabetics without evidence of vascular complications. The diabetics were divided into 4 groups according to the type of their disease and to the metabolic condition within the IDDM group (insulin-dependent: IDDM, in acceptable response and in poor metabolic control; non-insulin-dependent: NIDDM, and juvenile diabetics not requiring insulin at least for two years after diagnosing their disease: NIDDY). The results were compared with controls of identical age and normal weight. A paradoxical hGH response to TRH stimulation was found only in IDDM patients in poor metabolic control. In this group the hGH reserve revealed by arginine was significantly larger than in the others. It was shown that the induced hGH release was independent of the sex distribution of the groups and of the basal hGH values. Magnitude of the hGH reserve and appearance of the paradoxical hGH response were not necessarily correlated but the substantial reserve was frequently associated with a paradoxical response. It can be assumed that the unfavorable metabolic condition is of decisive importance in giving rise to these anomalies. Our observations seem to confirm the need for good metabolic control if the pathological hGH secretion in diabetics is to be prevented.
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PMID:Arginine induced growth hormone (hGH) response and paradoxical hGH secretion stimulated by TRH in diabetes mellitus. 311 18


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