Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight insulin-dependent adolescents (4 boys, 4 girls) participated in an 8-wk program of supervised exercise, and 8 matched controls were encouraged to exercise on their own without supervision. All 16 subjects were asked to follow a standard ADA diet plan, kept a self-reported log of caloric intake, and met with a dietitian weekly to review their diets. Exercise for the supervised subjects was scheduled between the routine afternoon snack and the evening meal, and subjects were asked not to consume additional food on exercise days. After the 8-wk program, glycemic control, as measured by glycosylated serum albumin and blood glucose values (but not by glycosylated hemoglobin), improved in the supervised-exercise group despite reduced daily insulin dosage. Cardiorespiratory fitness, as measured by voluntary maximum treadmill time (Bruce protocol) and submaximal exercise heart rates, also improved. No changes were observed in the unsupervised control group.
Diabetes Care
PMID:Improved glycemic control after supervised 8-wk exercise program in insulin-dependent diabetic adolescents. 331 15

Of 22 immunomodulatory substances screened 12 were effective in modulating the course of hyperglycemia following low dose streptozotocin treatment. In this animal model diabetes is induced by administration of low doses of streptozotocin (30-40 mg/kg) body weight to male C57BL/6J/Bom, C57BL/KsJ and C3H/He/Bom mice on 5 consecutive days. Conventional immunosuppressants (azathioprine, cyclophosphamide) largely protected from diabetes development. Partial suppression of hyperglycemia was also seen after administration of B. pertussis, fetal tissue extracts, FTS, inosine pranobex, metronidazole and ADA 202-718. The majority of these substances, when applied with another regimen, and TP5 caused enhancement of diabetes. In conclusion, several substances with a therapeutic potential in experimental diabetes have been identified. Those with little risk of side-effects may deserve further analysis.
Diabetes Res 1987 Sep
PMID:Analysis of 22 immunomodulatory substances for efficacy in low-dose streptozotocin-induced diabetes. 331 52

Acetonemia is generally associated with the ketogenic states of fasting and diabetes. Disulfiram (DS), an inhibitor of aldehyde dehydrogenase (AlDH) that is used as an alcohol deterrent drug, is also known to elevate blood acetone in humans, but in the absence of a commensurate increase in its metabolic precursor, acetoacetate. We reexamined the effects of DS and other AlDH inhibitors on circulating ketone body levels in male rats of Sprague-Dawley descent and again demonstrated a 6- and 16-fold increase in blood acetone along with normal levels of acetoacetate at 6 and 24 hr after DS. Pargyline, another inhibitor of AlDH, maintained normal blood acetone levels in the presence of reduced acetoacetate levels. A third inhibitor of AlDH, cyanamide, administered to fasted and nonfasted rats, elevated blood acetone levels 10-fold over controls, with, however, a commensurate 5- and 7-fold increase in blood acetoacetate levels. The threshold values for the cyanamide-induced elevation of blood acetone and acetoacetate were equivalent, i.e. approximately 0.25 mmol/kg body weight (i.p.). The elevation of acetoacetate and the inhibition of hepatic catalase activity by cyanamide are not mechanistically linked, since 3-amino-1,2,4-triazole, another inhibitor of catalase, elevated blood acetone but not acetoacetate levels. These findings suggest that DS-induced acetonemia is due to inhibition of acetone metabolism, whereas enhanced acetone formation through acetoacetate contributes significantly to cyanamide-induced acetonemia.
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PMID:Acute effects of the aldehyde dehydrogenase inhibitors, disulfiram, pargyline and cyanamide, on circulating ketone body levels in the rat. 334 79

We have recently reported that type II diabetic subjects with macroangiopathy have a higher activity of aldehyde dehydrogenase (ALDH) in blood than those without clinical vascular disease. ALDH activity was measured as the elimination of acetaldehyde added to a blood homogenate in vitro. We have re-examined our clinical material with another assay of ALDH which uses indole-3-acetaldehyde as substrate and measures the formation of indole-3-acetic acid. A negative correlation between the half-life of acetaldehyde and the formation of indole-3-acetic acid was found in the group of subjects free from vascular disease (r = -0.55, p less than 0.01). Thus, a rapid elimination of acetaldehyde corresponded to a rapid formation of indole-3-acetic acid. No such correlation was found in subjects with macroangiopathy. These results suggest that the 2 groups, with and without clinical vascular disease, have differences in isoenzyme composition, in the kinetic properties of the enzyme, or in the non-enzymatic binding of acetaldehyde.
Diabetes Res 1987 Oct
PMID:Aldehyde dehydrogenase activity and vascular disease in type II diabetes--a comparison between 2 different assays for activity. 342 70

A survey was conducted to ascertain to what extent dietitians use techniques cited in the literature considered to affect adherence by patients with non-insulin dependent (Type II) diabetes. A survey instrument listing techniques related to changing behavior, the counseling process, and content of teaching was developed and mailed to 500 members of the ADA Diabetes Care and Education Practice Group. Responses were received from 39% of the sample. For a majority of techniques, data analysis showed statistical association between frequency of use, perceived importance, and adequacy of practitioner training. Dietitians regularly used only 40% of the cited techniques related to changing behavior and the counseling process, but they said most of the items were important. Only half of the items related to the content of teaching were rated as important, and dietitians felt prepared to use only 70% of them. Most dietitians did not teach concepts related to glucose utilization, energy metabolism, and the metabolic role of insulin in diabetes. Those findings suggest that dietitians do not regularly use many techniques considered effective in obtaining dietary adherence of patients with diabetes. Since other studies show compliance is directly influenced by skills of the provider, dietitians could improve cost-effective health care by developing further professional expertise in the area of counseling patients with diabetes.
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PMID:Motivational techniques of dietitians counseling individuals with type II diabetes. 379 31

Type II diabetic subjects, 26 with symptoms and/or signs of large vessel disease (LVD group) and 26 free from clinical vascular disease (FVD group), matched for sex, age, body weight, and duration of diabetes after diagnosis, together with 28 healthy controls participated in a preliminary study on new potential risk factors of large vessel disease. The activity of erythrocyte aldehyde dehydrogenase (ALDH) was significantly higher (P less than 0.005) in the LVD than in the FVD group and in the controls, as indicated by a shorter half-life of acetaldehyde in homogenates of erythrocytes and plasma (100 +/- 11, 203 +/- 28, and 180 +/- 21 min, respectively). The results were unaffected by antidiabetes therapy, blood glucose control, alcohol consumption, or by recognized risk factors of angiopathy, such as blood pressure, hyperlipidemia, or smoking. Whether ALDH activity is a primary factor in large vessel disease or is merely a secondary phenomenon is unknown. However, ALDH activity is a critical factor determining chlorpropamide alcohol flush (CPAF), which has been suggested to be an inherited trait in some type II diabetic subjects. In conclusion, high ALDH activity was shown to be associated with an increased risk of large vessel disease in diabetes.
Diabetes 1986 Mar
PMID:Aldehyde dehydrogenase activity and large vessel disease in diabetes mellitus. A preliminary study. 394 78

The effect on plasma glucose concentration of four different, approximately isocaloric breakfasts designed using the American Diabetes Association food exchange lists was studied in eight type II diabetic patients. The meals were estimated to contain similar amounts of carbohydrate, protein, and fat and were given in random order. The plasma glucose responses to the different meals were similar except for one meal. This meal resulted in a greater glucose increase but the latter could be explained by the substitution of banana for orange juice in the meal. Banana contains starch as well as fructose and glucose, whereas orange juice contains glucose, fructose, and sucrose. In regard to the postmeal glucose response, these data indicate that the ADA food exchange list is useful in meal planning, at least for breakfast.
Diabetes Care
PMID:The glycemic effect of different meals approximately isocaloric and similar in protein, carbohydrate, and fat content as calculated using the ADA exchange lists. 640 Jul 1

Many diabetics who take chlorpropamide (a sulphonylurea compound) experience facial flushing after drinking even small amounts of alcohol. These flushers have a noticeably lower prevalence of late complications of diabetes (microangiopathy, macroangiopathy, and neuropathy) than non-flushers. This flush reaction is accompanied by increased blood acetaldehyde concentrations, suggesting an inhibition of aldehyde dehydrogenase activity. In the present study the activity of this enzyme in erythrocytes was assessed in the absence of chlorpropamide. Erythrocyte homogenates obtained from flushers and non-flushers were incubated with acetaldehyde and the rate of metabolism studies. Flushers eliminated acetaldehyde more slowly at a low range of concentrations (0--30 mumol/l), suggesting a difference in aldehyde dehydrogenase activity. Further studies are needed to clarify the role of this enzyme in the pathogenesis of diabetic complications.
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PMID:Chlorpropamide-alcohol flushing, aldehyde dehydrogenase activity, and diabetic complications. 681 Oct 34

There is an increasing interest on one of the smallest human chromosomes as it is shown by the First International Symposium on the Human Chromosome 20 and by the genetic map prepared by EUROGEN. The conserved part of the long arm of human chromosome 20 is synthenic with the distal part of the mouse chromosome 2 allowing for some analogies between them. Human chromosome 20 contains several important genes for the human pathology. Mutations of one of them, the vasopressin-neurophysin II gene, are responsible for hereditary neurohypophyseal diabetes insipidus. Severe combined immunodeficiency due to adenosin deaminase deficiency is the first human disorder successfully treated by somatic gene therapy. Spongiform encephalopathies are related to mutation and/or polymorphisms of the PRNP amyloid gene. One form of benign familiar neonatal convulsions is mapped to a specific locus on chromosome 20. In some families, maturity onset diabetes of the young (MODY) is caused by alterations of a hypothetical gene closely linked to the ADA locus. Allegile syndrome is often associated with deletions and microdeletions of the short arm of the chromosome. Finally, deletions of the long arm of the chromosome is a frequent finding in several hematologic malignities, specifically in myeloproliferative disorders and myelodysplastic syndromes.
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PMID:[The human genome--chromosome 20]. 748 83

Mutations of the glucokinase gene (chromosome 7p) have been shown to cause some cases of familial maturity onset diabetes of youth (MODY) but few, if any, cases of late onset familial Type 2 diabetes. A further single large pedigree with MODY has shown linkage to a marker for the adenosine deaminase gene (ADA, chromosome 20q), although the diabetes susceptibility gene at this locus has not been identified. We have studied members of 19 families with familial Type 2 diabetes (including 10 European families, 6 families from the Indian subcontinent, and 3 families of Afro-Caribbean origin), 2 of which were of MODY type (and both European), with a glucokinase marker and a marker linked to ADA, to examine whether glucokinase, or the unknown defect on chromosome 20, are implicated in diabetes in our pedigrees. Several models were constructed for standard two-point linkage analysis. Glucokinase is not the cause of diabetes in all of these families but was excluded in only one MODY family. It was possible to exclude both loci in the second MODY pedigree. No evidence was found of linkage to either marker in this multi-ethnic population under the models used. At least one further locus is involved in determining susceptibility to MODY.
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PMID:Genetic analysis of glucokinase and the chromosome 20 diabetes susceptibility locus in families with type 2 diabetes. 770 22


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