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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inability to secrete the water-soluble glycoprotein form of the ABO blood group antigens is a genetic characteristic associated with susceptibility to superficial fungal infections and also insulin-dependent diabetes mellitus (IDDM). As oral carriage of Candida albicans in healthy adults is associated with non-secretion, we examined oral carriage of yeasts among 275 patients attending diabetic outpatient clinics, 137 with IDDM and 138 with non-insulin dependent diabetes mellitus (NIDDM) with reference to ABO blood group, secretor status and yeast species. Of the 166 yeast isolates, 109 (66.7%) were C. albicans, a lower proportion compared with 94% reported for healthy individuals. There was no association between ABO blood group and carriage. There was no increase in the proportion of non-secretor carriers of C. albicans among patients with IDDM; but among those with NIDDM, 44% of non-secretors were carriers compared with 21% who were non-carriers (p less than 0.01). The results are discussed in the context of host-parasite interactions influencing colonization.
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PMID:Blood group, secretor status and oral carriage of yeasts among patients with diabetes mellitus. 269 83

The use of dietary fiber (DF) in the diet of diabetics, although recommended, is often prevented by a limited tolerance and/or by the high cost and unpalatability of fiber supplements. Knowing that only or mainly the water soluble fraction of DF is effective in modulating postprandial hyperglycemia, the DF content (soluble, insoluble, and total) of a variety of common foodstuffs was determined. Such data were then utilized in the formulation of two complete meals, isocaloric and isoglucidic, characterized by a high-soluble, low-soluble, and total fiber content. The meals were administered to 13 NIDDM patients in good metabolic control. The data confirmed a significant reduction (p less than 0.001) of postprandial hyperglycemia and a moderate less significant reduction of insulinemia after the high fiber meal.
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PMID:Food fiber choices for diabetic diets. 282 13

Two sources of dietary fibre were discussed in this presentation: soybean and fenugreek. Soybean dietary fibre (SDF) was found to be effective in reducing plasma glucose levels in diabetic and fa/fa rats, ob/ob mice and in non-insulin dependent diabetes mellitus (NIDDM) subjects. Supplementation of SDF in bread was more effective in glucose reduction than powder. SDF was also found to be more effective in subjects with fasting blood glucose levels above 7.2 mmol/l. SDF had no effect on insulin levels in rats or NIDDM subjects although the insulin levels in ob/ob mice were lower after 180 d feeding. SDF had no effect on body weight or lipid levels in rats and human subjects. However, in diabetic rats with high levels of blood cholesterol, SDF feeding decreased the cholesterol levels after 45 d SDF administration. Addition of powdered fenugreek to an oral glucose tolerance test significantly reduced the subsequent postprandial blood glucose level in diabetic rats. Inclusion of fenugreek to the meal tolerance test given to NIDDM also decreased the postprandial blood glucose levels. Fenugreek was found to reduce the rate of gastric emptying and to inhibit glucose transport, indicating the blood modulating effect of fenugreek to be due mainly to delayed gastric emptying with direct interference with intestinal glucose absorption. Soybean and fenugreek dietary fibres reveal a potential benefit for the control of glucose metabolism in diabetes with additional advantages resulting from their ease in usage either in a mixture of water or milk products or in cooking.
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PMID:New sources of dietary fibre. 303 26

Erythrocyte sodium, potassium and water contents and sodium fluxes were measured in both normotensive and hypertensive patients with either insulin dependent or non-insulin dependent diabetes mellitus. Hypertensive patients were studied again after two months' treatment with captopril. There were no differences in erythrocyte ion contents or concentrations but sodium fluxes may have been lower in insulin dependent patients and in hypertensive patients. The most marked erythrocyte defects associated with hypertension were low erythrocyte water content and increased potassium concentration in non-insulin dependent diabetic patients. Treatment with captopril caused an increase in erythrocyte water and a decrease in ion content and concentration. In non-insulin dependent diabetic patients, who had the greatest increases in erythrocyte water and falls in potassium concentration, frusemide-sensitive sodium-potassium co-transport activity was reduced. The reduction in blood pressure with captopril treatment was related to the initial erythrocyte sodium content.
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PMID:Hypertension and diabetes mellitus: erythrocyte electrolytes and the effect of captopril treatment. 307 39

The effect of fenugreek on postprandial glucose and insulin levels following the meal tolerance test (MTT) was studied in non-insulin dependent diabetics (NIDDM). The addition of powdered fenugreek seed (15 g) soaked in water significantly reduced the subsequent postprandial glucose levels. The plasma insulin also tended to be lower in NIDDM given fenugreek but without a statistical difference. Fenugreek had no effect on lipid levels 3 h following the MTT. Fenugreek may have a potential benefit in the treatment of NIDDM.
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PMID:Glucose-lowering effect of fenugreek in non-insulin dependent diabetics. 328 42

To determine the effects of very-low-calorie diets on the metabolic abnormalities of diabetes and obesity, we have studied 10 obese, non-insulin-dependent diabetic (NIDDM) and 5 obese, nondiabetic subjects for 36 days on a metabolic ward during consumption of a liquid diet of 300 kcal/day with 30 g of protein. Rapid improvement occurred in the glycemic indices of the diabetic subjects, with mean (+/- SEM) fasting plasma glucose falling from 291 +/- 21 to 95 +/- 6 mg/dl (P less than 0.001) and total glycosylated hemoglobin from 13.1 +/- 0.7% to 8.8 +/- 0.3% (P less than 0.001) (normal reference range 5.5-8.5%). Lipid elevations were normalized with plasma triglycerides reduced to less than 100 mg/dl and total plasma cholesterol to less than 150 mg/dl in both groups. Hormonal and substrate responses were also comparable between groups with reductions in insulin and triiodothyronine and moderate elevations in blood and urinary ketoacid levels without a corresponding rise in free fatty acids. Electrolyte balance for sodium, potassium, calcium, and phosphorus was initially negative but approached equilibrium by completion of the study. Magnesium, in contrast, remained in positive balance in both groups throughout. Total nitrogen loss varied widely among all subjects, ranging from 70 to 367 g, and showed a strong positive correlation with initial lean body mass (N = 0.83, P less than 0.001) and total weight loss (N = 0.87, P less than 0.001). The nondiabetic group, which had a significantly greater initial body weight and lean body mass than the diabetic group, also had a significantly greater weight loss of 450 +/- 31 g/day compared with 308 +/- 19 g/day (P less than 0.01) in the diabetic subjects. The composition of the weight lost at completion was similar in both groups and ranged from 21.6% to 31.3% water, 3.9% to 7.8% protein, and 60.9% to 74.5% fat. The contribution of both water and protein progressively decreased and fat increased, resulting in unchanged caloric requirements during the diet. This study demonstrates that short-term treatment with a very-low-calorie diet in both obese diabetic and nondiabetic subjects results in: safe and effective weight loss associated with the normalization of elevated glucose and lipid levels, a large individual variability in total nitrogen loss determined principally by the initial lean body mass, and progressive increments in the contribution of fat to weight loss with stable caloric requirements and no evidence of a hypometabolic response.
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PMID:Metabolic consequences of very-low-calorie diet therapy in obese non-insulin-dependent diabetic and nondiabetic subjects. 351 Sep 22

We have previously demonstrated that oral glipizide suppresses the absorption of xylose in diabetics treated with diet alone. We suggested that glipizide might influence postprandial glucose levels by interfering with absorptive mechanisms. In the present study we have extended our observations to insulin-dependent diabetics (IDDM). Nine non-obese diabetics without residual beta-cell function and with normal respiratory sinus arrhythmia and Valsalva ratio were studied on two occasions. Their ordinary insulin treatment was discontinued 24 hours before the study and glucose control was maintained by i.v. insulin infusion. The experiments began at 8 a.m. after an overnight fast. Insulin was given as a continuous i.v. infusion of 0.01 U/kg/h at 8-11 a.m. and 0.005 U/kg/h at 11 a.m. -2 p.m. At 8 a.m. the patients ingested 25 g of xylose and 15 g of glucose in 300 ml of water. Glipizide (5 mg) or placebo were given 30 min prior to the glucose-xylose load in random order, each patient serving as his own control. Blood samples were taken every 60 min for analysis of glucose, xylose, C-peptide and glipizide. The rise in blood glucose in the control experiment was similar to that previously seen in non-insulin-dependent diabetics (NIDDM) given the same xylose-glucose load. Glipizide did not exert any effects on either blood C-peptide, glucose or xylose levels. We conclude that oral glipizide administered in a therapeutic dose does not reduce xylose absorption in IDDM, in contrast to its previously demonstrated effect in NIDDM.
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PMID:Glipizide does not affect absorption of glucose and xylose in diabetics without residual beta-cell function. 351 65

This investigation was performed in two groups of adult patients, 10 with type I and 10 with type II diabetes mellitus, all with arterial hypertension (160 to 200 mm Hg systolic and 95 to 120 mm Hg diastolic). Captopril, 50 mg twice a day, was administered for 12 weeks and was effective as monotherapy in 16 patients. Mean arterial pressure (+/- s.d.) in type I patients changed from 121.4 +/- 9.6 to 100.2 +/- 10.1 after 4 weeks and to 102.0 +/- 3.8 mm Hg after 12 weeks; in type II patients it changed from 132.8 +/- 5.7 to 123.9 +/- 13.5 after 4 weeks and to 109.1 +/- 11.1 mm Hg after 12 weeks. The differences were statistically significant. In only 4 patients was it necessary to add a thiazide after the first month of therapy. No significant change was induced by captopril in urine output, osmolar clearance, free water clearance inulin, and PAH clearances. No significant change was observed in serum and urine Na+, Cl-, Ca++ and Mg++, whereas a statistically significant reduction was found in the renal clearances of K+ and PO4-. No important change in serum aldosterone was found, while plasma renin activity was increased, as expected. No alterations in urine protein, glucosaminoglycans, gamma GT, and N-acetyl-beta-glucosaminidase were observed during follow-up. All patients maintained good metabolic control of their disease. No neutropenia and orthostatic hypotension were seen. Captopril appears to be an effective and safe drug for lowering blood pressure in diabetic patients, without affecting renal function, electrolyte balance and the metabolic control of diabetes.
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PMID:Captopril in the treatment of hypertension in type I and type II diabetic patients. 353 66

An epidemic of renal disease is occurring among the Zuni Indians in western New Mexico. In 1985, 1.6% of Zunis had clinically recognized renal disease and 1% had renal insufficiency. The incidence of end-stage renal disease (ESRD) in 1984 and 1985 was 14 times the rate for US whites, and three times the rates of other Indians in ESRD network 6. One third of the cases of renal disease and ESRD is due to type 2 diabetes, but the etiology of disease in most of the remainder is unknown. Affected subjects range from early childhood to old age. Early signs are hematuria, mild to moderate proteinuria, normal BP, and low total hemolytic complement, normal or low C3 and C4 levels, in about 40% of the cases. The clinical course varies from benign to rapidly progressive renal failure. Biopsies usually reflect an immune-complex mediated mesangiopathic glomerulonephritis, with IgA, IgG, IgM, and C3 variably present in the mesangium. In some cases, there is a very strong familial pattern suggesting autosomal dominant inheritance or a marked communal exposure effect. This may be a genetic disease educed by the consanguinity in the ethnically homogeneous Zuni population. Mesangiopathic renal disease is common in some Oriental populations, and this phenomenon may reflect the American Indians' Oriental ancestry. This disease may also be due to toxic exposures related to jewelry-making, potting, Zuni water, Zuni salt, or herbal or other products used for medicinal or religious purposes. This epidemic is much morbidity and generating huge costs for ESRD treatment. Further study is needed to better understand its etiology.
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PMID:Epidemic renal disease of unknown etiology in the Zuni Indians. 359 94

A general "glucoreceptor" defect, demonstrable in pancreatic islet and taste cells, may contribute to the metabolic and taste abnormalities of adult onset diabetes and possibly, if present at the level of the hypothalamus, could produce hyperphagia and the obesity seen in diabetics. To determine if a glucoreceptor defect generally accompanies obesity and glucose intolerance, behavioral responsiveness to glucose was examined in nine obese and nine lean female Zucker rats. Daily food and fluid intake were measured during three two-bottle preference tests, in which rats chose between water and one of several glucose solutions (1%, 3%, and 12%). Taste responsiveness to glucose of obese rats appeared normal; however, increased satiating effects of glucose were found in obese rats, possibly due to an enhanced delivery of glucose to neurons that inhibit feeding, caused by glucose intolerance. Also, obese rats had (a) increased brain weights, and (b) increased volumes of ventromedial and paraventricular hypothalamic nuclei. These findings, perhaps explainable by an increased delivery of nutrients to the developing brain, indicate that the hyperphagia of Zucker rats is due neither to an overt hypothalamic lesion nor to insensitivity to glucose.
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PMID:Sensitivity to satiating and taste qualities of glucose in obese Zucker rats. 401 22


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