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)

Recently, linkage between the ADA gene locus and MODY, a subtype of NIDDM, has been reported. The possibility that the region of chromosome 20q containing the ADA locus also may play a role in susceptibility to NIDDM needs to be investigated. Therefore, we examined the linkage between the ADA locus and NIDDM in affected siblings of 50 European white diabetic pedigrees--21 Italian and 29 British. Departure from independent segregation of the disease and an Alu VpA polymorphism within the 5' flanking region of the ADA locus was tested in the affected sib-pairs with the APM statistical method. After DNA amplification by the PCR and PAGE, five alleles were identified in the ALU VpA tract at the ADA locus in the two populations. Allele frequencies did not differ significantly between the two populations (chi 2 = 2.426, P > 0.05 [NS]). Analysis of the 50 diabetic sib sets, and independently of the Italian and British groups of affected sib pairs, revealed no segregation distortion between the marker locus and NIDDM. We conclude that mutations within or around the ADA locus are unlikely to play a major role in the etiology of NIDDM.
Diabetes 1992 Dec
PMID:Sib-pair analysis of adenosine deaminase locus in NIDDM. 144 5

Twenty-four hour urinary albumin concentrations were measured in 113 (mean age 51.1 years) non-insulin-dependent (NIDDM) Nigerian diabetics (50 males, 63 females). A high prevalence of microalbuminuria (> or = 30 mg/24 hour) was observed in male (54%) as well as female diabetics (59%). Microalbuminuria was also observed in a high proportion of diabetics (52%) with a short duration (< 5 years) of disease. Elevated blood pressure and retinopathy were present in 41% and 16% of patients respectively. Among the 49 patients with normoalbuminuria (< 30 mg/24 hour), six (12%) had retinopathy compared with 12 (18%) in the microalbuminuria group. Diastolic blood pressure levels were significantly higher (P < 0.01) in male diabetics with retinopathy but this was not associated with higher albuminuria. Urinary albumin concentrations were not influenced by elevated blood pressure. There were no significant differences in age, duration of diabetes, blood pressure or serum creatinine between diabetics with and without microalbuminuria. These results suggest that though there is a high prevalence of microalbuminuria amongst NIDDM Nigerian diabetics it may not predict retinopathy and occurs independently of either glycaemic control or elevated blood pressure levels.
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PMID:Microalbuminuria in non-insulin-dependent (type 2) Nigerian diabetics: relation to glycaemic control, blood pressure and retinopathy. 144 4

Glucokinase is thought to play a glucose-sensor role in the pancreas, and abnormalities in its structure, function, and regulation can induce diabetes. We isolated the human glucokinase gene, and determined its genomic structure including exon-intron boundaries. Structure of the glucokinase gene in human was very similar to that in rat. Then, by screening Japanese diabetic patients using polymerase chain reaction--single strand conformation polymorphism (PCR-SSCP) and direct-sequencing strategies, we identified a missense mutation substituting arginine (AGG) for glycine (GGG) at position 261 in exon 7 of the glucokinase gene in a patient with early-onset non-insulin-dependent diabetes (NIDDM).
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PMID:Structure of the human glucokinase gene and identification of a missense mutation in a Japanese patient with early-onset non-insulin-dependent diabetes mellitus. 146 39

The prevalence of nonadherence in IDDM and NIDDM populations and conceptual and methodological issues relevant to measuring diabetes regimen adherence are reviewed. The prevalence of nonadherence varies across the different components of the diabetes regimen, during the course of the disease, and across the patient's life span. Although prevalence rates might be expected to differ between IDDM and NIDDM populations, this rarely has been evaluated. Conceptual problems in defining and measuring adherence include: the absence of explicit adherence standards against which the patient's behavior can be compared; inadvertent noncompliance attributable to patient-provider miscommunication and patient knowledge/skill deficits; the behavioral complexity of the diabetes regimen; and the confounding of compliance with diabetes control. Methods for measuring adherence include: health status indicators, provider ratings, behavioral observations, permanent products, and patient self-reports, including behavior ratings, diaries, and 24-h recall interviews. A measurement method should be selected on the basis of reliability, validity, nonreactivity, sensitivity to the complexity of diabetes regimen behaviors, and measurement independence from the patient's health status. The timing of measurements should be based on the stability of adherence behaviors and temporal congruity with other measures of interest (e.g., indexes of metabolic control). Directions for future research and suggestions for clinical practice are provided.
Diabetes Care 1992 Nov
PMID:Methodological issues in diabetes research. Measuring adherence. 146 98

In this study, 52 nonproteinuric Japanese patients with non-insulin-dependent diabetes (NIDDM) were followed from 1985 to 1990 to investigate the rate of development and progression of microalbuminuria and the factors which influence it. In 1985, 34 patients were normoalbuminuric, and 18 patients were microalbuminuric. Five years later, 11 of 34 initially normoalbuminuric patients (32.4%) developed microalbuminuria, and 6 of 18 initially microalbuminuric patients (33.3%) developed overt proteinuria. At the beginning of the study, hypertension existed more frequently in the patients who later developed microalbuminuria (8 of 11, 72.7%) than in the patients who stayed normoalbuminuric (4 of 23, 17.4%). Age-adjusted values of mean blood pressure (+/- SEM) at the beginning of the study in the patients who developed microalbuminuria (98.2 +/- 3.4 mm Hg, n = 11) were significantly higher than those in the patients who stayed normoalbuminuric (87.3 +/- 2.4 mm Hg, n = 23). In six patients who developed overt proteinuria, initial urinary albumin excretion rates (AER) were higher than those in the patients who stayed microalbuminuric, and four patients who presented with initial AER greater than 100 micrograms/min all developed overt proteinuria. These results indicate that, in Japanese patients with NIDDM, the rate of development of microalbuminuria is faster than that reported in Caucasian IDDM, and preexisting hypertension with relatively poor control of blood pressure may be a risk factor for the development of microalbuminuria.
J Diabetes Complications
PMID:High blood pressure is a risk factor for the development of microalbuminuria in Japanese subjects with non-insulin-dependent diabetes mellitus. 147 44

Prevalence of non-insulin-dependent diabetes (NIDDM) in India was reported to be 2.3% in the urban and 1.5% in the rural areas in the early 1970s by the Indian Council of Medical Research (ICMR). Recent studies both in the migrant Indians and in the native Indians have shown the prevalence to be much higher than the above values. Similar prevalence of NIDDM in the migrant and native Indians in affluent areas suggests that Indians as an ethnic group have a high genetic risk for diabetes. Our recent study in South India showed a high prevalence of diabetes in the urban area (8.2%) versus a low prevalence of 2.4% in the rural area. Age, urban-rural factor, body mass index (BMI) and the waist:hip ratio (WHR) were positively associated with diabetes. Interestingly, the prevalence of impaired glucose tolerance (IGT) was similar in urban and rural areas (8.7% and 7.8%, respectively) despite a four-fold lower prevalence of diabetes in the latter. The ratio of new to known diabetes was 1:2 in the urban and 3:1 in the rural areas. There was a male preponderance among Indian diabetic patients. Migration from rural to urban environment with changes in dietary habits and physical inactivity may have contributed to the increased prevalence of diabetes. A high rate of familial aggregation is noted in NIDDM in India and the genetic risk of NIDDM increases with increasing family history of diabetes. In the adult offspring of diabetic parents, hyperinsulinaemia and decreased insulin sensitivity are observed before the development of glucose intolerance.
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PMID:Genetic epidemiology of NIDDM among Asian Indians. 148 45

To investigate the frequency and etiology of diabetic osteopenia, we measured spinal bone mineral density (SBMD), total body bone mineral density (TBBMD), total body fat and lean body mass in 69 female diabetic patients (14 IDDMs and 55 NIDDMs). SBMD decreased with age in both IDDM and NIDDM, but when expressed as a percentage of age-matched normal Japanese females, some had lower SEMD, but others had normal or increased SBMD. Postmenopausal IDDM patients had lower SBMD than postmenopausal NIDDM patients. Thirteen out of 69 (18.8%) had an SBMD lower than 90% of age-matched controls. SBMD correlated positively with TBBMD. Those with lower SBMD had poor glycemic control, but there was no relation between SBMD and either duration of diabetes or presence of retinopathy and/or nephropathy. IDDM patients had lower 1.25 (OH)2D, osteocalcin than NIDDMs. SBMD correlated negatively with urinary pyridinoline and deoxypyridinoline excretion. SBMD correlated positively with body weight, and those with lower SBMD had significantly lower body mass index, body weight, fat weight and lean body mass than those with normal or increased SBMD. These results suggest that IDDM patients may be at higher risk of losing bone postmenopausally, and diabetic patients with lower SBMD have characteristics of poor diabetic control, lean habitus, low serum 1.25 (OH)2D.
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PMID:[Spinal bone mineral density in the female diabetic patients]. 149 83

The acetylator phenotype was determined in 31 insulin-dependent (IDDM) and 110 noninsulin-dependent (NIDDM) Jordanian diabetics, and was compared to that of 160 healthy volunteers of the same ethnic group. Dapsone was used as the test drug. The rapid acetylator phenotype was slightly less frequent in IDDM and slightly more frequent in NIDDM. Neither of the differences was significant. When acetylator status in the two types of diabetes mellitus was compared, there was a significant difference among the two groups. Patients with IDDM had a higher percentage of the slow acetylator phenotype when compared to NIDDM patients. The association between acetylator status and IDDM in Jordanians, which agrees with that reported for the Saudi Arabian population, is the reverse of what is found in European populations. The results demonstrate ethnic differences in acetylator status among IDDM patients.
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PMID:Acetylator phenotypes of Jordanian diabetics. 149 43

In one third of patients who suffered an infarction NIDDM and arterial hypertension are present. In the absolute majority of patients with IHD, as apparent from the IRI and C-peptide response after a glucose load, hyperinsulinism is present. The blood sugar response can have the character of diabetes or of impaired glucose tolerance, the curve may be very flat or normal while the IRI and C-peptide response are excessive. Hyperinsulinism has a hypersecretory origin as suggested by the concurrently elevated C-peptide level but also reduced insulin utilization in the liver and peripheral target organs. Hyperinsulinism is thus a regular associated phenomenon of IHD and is a special risk factor independent on hyperglycaemia and associates with the other main risk factors of IHD such as arterial hypertension, HPLP (android obesity), hyperglycaemia (NIDDM) and hirsutism as a manifestation of a hyperandrogenic state in the female organism with the syndrome of polycystic ovaries. Hyperinsulinism plays an indirect role in the pathogenesis of coronary syndrome via the main risk factors (5H syndrome--hyperinsulinism, hypertension, HPLP, hyperglycaemia, hirsutism) and also directly by its action on endothelial paracrine mechanism of the coronary circulation where in the early stage vasoconstrictor factors predominate (endothelin-1, PGF2-alpha) over physiological vasodilatating factors (EDRF-NO, PGE2, PGI2) and this leads then to functional spasms. It seems that also the coronary X syndrome develops very frequently on the background of the hormonal metabolic X syndrome or the 5H syndrome.
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PMID:[Hyperinsulinism and the coronary syndrome]. 149 68

The prevalence and incidence of CHD, defined by ECG abnormalities according to the Tecumseh criteria for Minnesota Codes, were determined in Pima Indians greater than or equal to 25 yr of age. In a cross-sectional analysis, the age-sex-adjusted prevalence (+/- SE) of ECG abnormalities was higher in 1454 NIDDM patients (6.86 +/- 0.65%) than in 1696 nondiabetic subjects (3.23 +/- 0.63%; prevalence rate ratio = 2.12; 95% CI 1.39-3.25). In a prospective analysis, the age-sex-adjusted incidence (+/- SE) of ECG abnormalities was higher in 824 NIDDM patients (12.77 +/- 1.67) than in 935 nondiabetic subjects (5.93 +/- 1.43 cases/1000 person-yr; incidence rate ratio = 2.15; 95% CI 1.26-3.69). The prevalence of ECG abnormalities in insulin-treated NIDDM patients was significantly higher than in NIDDM patients not treated with insulin (age-sex-adjusted OR = 2.83; 95% CI 1.84-4.33); and this association persisted when adjusted for other factors such as sBP, BMI, duration of diabetes, serum cholesterol concentration, and oral hypoglycemic agents (OR = 2.12; 95% CI 1.34-3.37). In the prospective analysis, the incidence of ECG abnormalities in NIDDM patients treated with insulin was higher than in those NIDDM patients not treated with insulin, but, when controlled for age, sex, duration of diabetes, and oral hypoglycemic agents in a proportional-hazards model, the relationship with insulin treatment was not statistically significant (incidence rate ratio = 1.36; 95% CI 0.80-2.31). This suggests that insulin treatment may be a marker of more severe diabetes, and that factors associated with clinical indications for insulin treatment, rather than insulin treatment per se, are related causally to CHD. On the other hand, endogenous fasting and 2-h postload serum insulin concentrations were not associated with ECG abnormalities among 761 NIDDM patients not treated with insulin nor among 1226 nondiabetic subjects. Furthermore, in the prospective study, neither endogenous fasting nor 2-h postload serum insulin was associated with the subsequent development of ECG abnormalities in NIDDM patients or nondiabetic subjects.
Diabetes 1992 Sep
PMID:Insulin treatment, endogenous insulin concentration, and ECG abnormalities in diabetic Pima Indians. Cross-sectional and prospective analyses. 149 65


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