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)

Nineteen patients affected by non-insulin dependent diabetes mellitus (NIDDM), in good glycemic control (fasting plasma glucose 7.2 +/- 0.3 mmol/L, glycosylated hemoglobin 6.3 +/- 0.2%), underwent three isocaloric dietary phases. In phases 1 and 3 the diet was rich in complex carbohydrates (Carbo) whereas in phase 2 it was rich in monounsaturated fatty acids (Mono). Plasma glucose concentrations were 7.1 +/- 0.3 and 7.2 +/- 0.3 mmol/L for the two Carbo phases and 7.5 +/- 0.4 mmol/L for the Mono phase (NS). Plasma total cholesterol values for the Carbo phases were 6.2 +/- 0.2 and 6.4 +/- 0.2 mmol/L, respectively, and 6.5 +/- 0.2 mmol/L on the Mono phase (NS). Similarly, no significant changes were noticed for plasma triglycerides and high-density-lipoprotein (HDL) cholesterol. Thus, both diets were well-tolerated and did not alter glucose homeostasis or worsen plasma lipid concentrations. Consequently, these results suggest that a wider dietary choice can be made available to NIDDM patients without producing unwanted side effects.
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PMID:Carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus: effects of a low-fat, high-carbohydrate diet vs a diet high in monounsaturated fatty acids. 187 14

Geographic/population variation in the prevalence of diabetic nephropathy is well recognised. In a study of 'native' Indians, we screened 102 non-proteinuric diabetes mellitus patients (64 NIDDM, 38 IDDM; mean age and diabetic duration 48.7 and 6.5 years, 21.6 and 6.2 years, respectively) with blood pressure less than or equal to 170/105 and without congestive heart failure, ketonuria or urinary tract infection, for the presence of microalbuminuria (albumin excretion rate greater than 20 micrograms/min). Fifty-six patients (34 NIDDM, 22 IDDM) also underwent detailed fundus examination. Seventeen NIDDM (26.6%) and 3 IDDM (7.9%) patients had microalbuminuria. Glycated hemoglobin was significantly higher in microalbuminurics in the NIDDM group (P less than 0.05). Diabetic retinopathy tended to occur more frequently in microalbuminurics (NIDDM and IDDM).
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PMID:The prevalence of microalbuminuria in diabetes: a study from north India. 187 3

Albumin excretion rate measured by new immunoassays and semiquantitative tests is advocated as a means for early detection of diabetic nephropathy. We determined albumin excretion rate in 276 patients. Albumin excretion rate was normal in 66%, within the microalbuminuric range in 27%, and within the macroproteinuric range in 7%. Significant predictors of albumin excretion rate included presence of hypertension and glycosylated hemoglobin level in type I diabetes mellitus, and years since diagnosis in type II diabetes mellitus. A semiquantitative test was deemed to be of limited diagnostic value. We conclude that testing for early diabetic nephropathy in routine clinical practice gives valuable information and that determination by a quantitative immunoassay based on a single 24-hour urine sample is preferable. The optimal frequency of screening and the levels that determine progressive renal disease have yet to be established.
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PMID:Microalbuminuria in clinical practice. 188 40

Many investigators suggest that insulin resistance of the peripheral tissues is the primary defect that results in non-insulin dependent diabetes mellitus (NIDDM). It is also generally accepted that multifactorial controls, playing in concert for gene expression trigger this disease. Previous research reports indicated that uric acid metabolism plays a role in the pathogenesis of NIDDM. To investigate this hypothesis, we studied 53 NIDDM patients by using a double blind cross over control study, of allopurinol and placebo administration. We found a statistically significant elevation in the level of hemoglobin A1c (HbA1c) after the allopurinol intervention period of 12 weeks compared with the placebo period of the same duration (p less than 0.003). The elevation was also found in a subgroup with Body Mass Index (BMI) less than 25 kg/m2 (p less than 0.001) and BMI more than or equal to 25 kg/m2 (p less than 0.05). No statistically significant differences between fasting plasma glucose, glucose tolerance test, serum insulin, total cholesterol, triglycerides, high density lipoprotein cholesterol, creatinine, prior to and after use of allopurinol were noted except for serum uric acid (p less than 0.001). No relationship between changes in HbA1c and changes in uric acid, analysed by linear regression analysis and correlation was demonstrated (r = 0.15, p = 0.29). We conclude that the changing of hemoglobin A1c may be a direct effect of allopurinol or support the role of uric acid in the pathogenesis of NIDDM.
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PMID:The relationship between glucose and uric acid metabolism: influence of short term allopurinol on glucose metabolism. 205 62

Twenty seven subjects with Type II diabetes mellitus underwent analysis of the Self-Administered Alcoholism Screening Test (SAAST) and hemoglobin associated acetaldehyde levels (HbAA). The SAAST scores and HbAA levels correlated with one another (r = .48, p = 0.009). No correlation between glycated hemoglobin levels (GHb) and HbAA levels or SAAST was found. Glucose incubation of whole blood led to an increase in GHb but no change in HbAA. We conclude that HbAA and SAAST correlate with each other when measured in patients with diabetes. Therefore each test appears clinically useful in quantifying alcohol consumption in individuals with Type II diabetes mellitus.
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PMID:Hemoglobin associated acetaldehyde correlates with the Self-Administered Alcoholism Screening Test but not glycated hemoglobin in type II diabetes mellitus. 206 32

Glucose intolerance often occurs in liver cirrhosis; therefore a long-term control of plasma glucose levels appears to be important. For this purpose glycated hemoglobin A (HbA1c) determination is proposed as a suitable method, while no data are available on fructosamine test. In 98 cirrhotic patients serum fructosamine and HbA1c levels were compared with those of normal controls and among cirrhotic patients grouped in non glucose-intolerant and with non insulin-dependent (NIDDM) or insulin-dependent diabetes mellitus (IDDM). The mean HbA1c values of cirrhotic patients with normal glycemic control were significantly lower than normal, and only a few IDDM and NIDDM cirrhotic patients showed high values of HbA1c, indicating that HbA1c is often underestimated in these patients. On the contrary, serum fructosamine levels were on the average higher than normal in nondiabetic patients, but they were significantly higher in IDDM and NIDDM patients than in nondiabetics, and the 72% of NIDDM and 85% of IDDM patients had fructosamine levels higher than the upper normal value. In conclusion, in diabetic patients with liver cirrhosis fructosamine seems to be a more suitable test than HbA1c for monitoring blood glucose levels.
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PMID:Fructosamine and glycated hemoglobin as indices of glycemic control in patients with liver cirrhosis. 207 78

We randomly administered thyrotropin-releasing hormone (200 micrograms, as an i.v. bolus) or control saline (in isovolumic amount) to 30 male diabetic subjects (23 IDDM, 7 NIDDM) in fair metabolic control (HbA1 9.7 +/- 0.3%, means +/- SEM) and to 12 healthy male controls on two different mornings. While GH in the basal state was similar in IDDM, NIDDM and normal subjects, TRH administration evoked a significant GH release only in a single IDDM individual. The only GH-responder to TRH was a newly-diagnosed (two weeks) IDDM patient, still with a high glycated hemoglobin level (HbA1 11.1%), despite normal plasma glucose levels. Saline infusion did not affect GH concentrations either in normals or in diabetics. Exaggerated GH responses to TRH are uncommon in diabetic patients in good metabolic conditions.
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PMID:Inappropriate growth-hormone (GH) response to thyrotropin-releasing hormone (TRH) occurs infrequently in well-regulated diabetes mellitus. 211 57

Debrisoquine hydroxylation was assessed in 54 type I and in 42 type II diabetic patients. The distribution of metabolic ratio debrisoquine/4-hydroxydebrisoquine (MR) in urine of the patients was compared with a MR-distribution of 176 healthy subjects, and the correlation of glucose balance parameters with the MR was investigated. One poor metabolizer of debrisoquine was found among type I diabetics but no poor metabolizers were found among type II diabetics. Despite the low frequency of the poor metabolizers, the prevalences of debrisoquine hydroxylation phenotypes did not differ from that in healthy volunteers in either diabetic group. No correlation was found between MR and fasting blood glucose or blood glycosylated hemoglobin A1c, whereas a negative correlation was evident between age and the excretion of 4-hydroxydebrisoquine in urine. In summary, debrisoquine hydroxylation is essentially unaltered in type I and type II diabetes mellitus, and no relationship exists between debrisoquine hydroxylation and glucose balance.
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PMID:Debrisoquine hydroxylation polymorphism in diabetic patients. 213 5

Staub Effect or improved glucose disposal after repetitive glucose loads does not occur in untreated diabetes. In non-insulin dependent diabetes (NIDDM) there is impaired insulin response to intravenous (i.v.) glucose injection, especially in early insulin release (EIR) and the lesser known post EIR suppression of insulin levels below basal, or acute insulin decrement (AID). To test the ability of a second generation sulfonylurea, glyburide, to affect glucose primed glucose disposal and insulin secretory patterns, sixteen NIDDM male subjects received three hourly intravenous glucose loads while untreated and again after six months of glyburide therapy. After treatment there was a fall of fasting glycemia from 204 +/- 11 to 147 +/- 8 mg/dl (p less than 0.001), of all glucose levels during the i.v. glucose tolerance tests (p less than 0.025) and glycosylated hemoglobin from 8 +/- 0.3% to 7.6 +/- 0.3% (p less than 0.005). Before treatment i.v. glucose disposal (K value) changed very little after successive glucose challenges, but after glyburide all mean K values were higher, and glucose primed glucose disposals were faster after the second (K2) and third (K3) glucose injection than after the first (K1) (p less than 0.025 and p less than 0.01 respectively). In the untreated state, there was higher and significant EIR by the third glucose load, (p less than 0.025) while AID was clearly more pronounced after the second load (p less than 0.001). After glyburide treatment EIR was significantly higher than before in all loads, and mean AID was no longer demonstrable. Insulin summation (S) after successive i.v. loads maintained a stepwise increase both before and after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recovery of Staub Effect and amelioration of insulin secretion defects after glyburide treatment in non-insulin-dependent diabetes. 213 1

Increased levels of lipid peroxides have been implicated in the pathogenesis of diabetic complications. A convenient and sensitive method for estimation of lipid peroxide concentration is the quantitative estimation of their metabolic end-product malonyldialdehyde (MDA) expressed in mumol/L using the thiobarbituric acid test. The mean fasting MDA value in the plasma of 26 Arab subjects with NIDDM was significantly higher than in healthy controls (14.3 +/- 8.3 vs 2.3 +/- 3.4, p less than 0.001). Within a group of nine diabetic patients with markedly elevated MDA values (greater than 20 mumol/L), eight subjects had retinal changes, four had evidence of coronary artery disease and three had manifest cerebrovascular disease. Macroproteinuria was documented in only three patients in this same group. The mean body mass index was 28.7 +/- 5.4 and the glycaemic control was unsatisfactory with a mean glycosylated hemoglobin of 10.1 +/- 1.5%. The MDA results in an Arabic population were similar to reports in Japanese and British patients and should prove useful as a laboratory test in assessing the severity of the diabetic state, as well as a complementary test in diagnosis and management.
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PMID:Thiobarbituric acid test as a measure of lipid peroxidation in Arab patients with NIDDM. 213 5


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