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

Hyperglycaemia, a raised fibrinogen, an increased serum triglyceride and a reduced HDL-cholesterol are common metabolic features of non-insulin dependent diabetes mellitus (NIDDM). Hypertension is frequently associated with NIDDM, however the influence of antihypertensive therapy on these combined factors in the diabetic is at present unclear. In a double-blind placebo-controlled crossover study in 20 stable NIDDM subjects with hypertension, the metabolic effects of 6 weeks' treatment with the alpha-blocker, doxazosin, was compared with treatment with the beta-blocker, atenolol. Similar and significant reductions in BP were produced by both drugs. Significant increases in weight, HbA1, apoprotein B, serum triglyceride and cholesterol/HDL ratio were observed with atenolol therapy. Doxazosin therapy was associated with opposite patterns of changes in fasting glucose, lipids and lipoproteins but only for serum triglyceride was difference between treatments significant. Fibrinogen was not altered by either treatment. Conclusions from this study indicate; 1) adrenergic mechanisms may be an important influence on glucose homeostasis and lipid metabolism in NIDDM and 2) the beta-blocker, atenolol, has a small adverse effect on weight, glycaemic control and the atherogenic lipid profile, whereas the alpha-blocker, doxazosin, has no such effect and may, in part, correct the disturbances of lipoprotein metabolism characteristic of NIDDM.
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PMID:Alpha-blocker therapy; a possible advance in the treatment of diabetic hypertension--results of a cross-over study of doxazosin and atenolol monotherapy in hypertensive non-insulin dependent diabetic subjects. 198 Sep 30

Benfluorex has been reported to decrease blood glucose in different dismetabolic conditions, particularly in noninsulin-dependent diabetic (NIDD) patients, but the mechanism of this effect is poorly known. We evaluate fasting glucose production (3H-glucose infusion) and B-cell secretion (phi 1, phi 2 and glucose utilization SI) (minimal model technique) in 7 mild, diet treated, NIDDM patients after 6-week administration of benfluorex (450 mg/day) and placebo, in random sequence and double blind design. Body weight, HbA1c, plasma glucose profile, fasting plasma insulin, lactate, pyruvate, beta-OH-butyrate, total cholesterol, HDL-cholesterol and triglycerides were also measured at the end of each treatment. Mean values of body weight (71 +/- 4 vs 69 +/- 4 kg, p less than 0.01), HbA1c (8.3 +/- 0.2 vs 7.7 +/- 0.2%, p less than 0.01), fasting plasma glucose (137.0 +/- 6.5 vs 121.4 +/- 5.6 mg/dl, p less than 0.01), lactate (1.82 +/- 0.13 vs 1.22 +/- 0.11 mmol/l, p less than 0.0025) pyruvate (0.164 +/- 0.011 vs 0.095 +/- 0.010 mmol/l, p less than 0.0005), and beta-OH-butyrate (0.91 +/- 0.06 vs 0.66 +/- 0.04 mmol/l, p less than 0.005) were significantly lower after benfluorex than after placebo. phi 1, phi 2 and SI values were not significantly different in the two treatments. Fasting glucose production was significantly lower after benfluorex than after placebo: 2.46 +/- 1.57 vs 1.84 +/- 0.85 mg/kg.min, p less than 0.02. These results demonstrate that 6-week treatment with benfluorex produces a significant blood glucose lowering effect in mild NIDDM patients, mainly by decreasing glucose production.
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PMID:Benfluorex and blood glucose control in non insulin-dependent diabetic patients. 206 66

Currently our knowledge of the role of lipid abnormalities as risk factors for CHD in diabetes is insufficient. We need to define exact risk parameters to target correctly the therapy of lipid disorders and to outline optimum therapeutic strategies. Therefore it is necessary to identify quantitative and qualitative abnormalities of lipoproteins and apoproteins which signify the risk of CHD and to define their predictive power in prospective trials. Obviously we need to know more about the pathophysiology of lipid abnormalities and the action of insulin. Because diabetic patients carry a high inherent risk of CHD, target values recommended for non-diabetic populations may not be optimal for diabetic populations, but should be lower. To date no primary or secondary intervention trials in diabetic populations have been carried out to show that the lowering of lipid values (serum and LDL cholesterol) will reduce the risk of CHD morbidity or mortality or will prevent the progression of CHD in diabetes. Since hypertriglyceridaemia and low HDL levels are typical abnormalities in NIDDM it is a unique target group to test whether lowering of triglycerides and raising of HDL cholesterol levels will reduce the risk of CHD. Therefore there is a pressing need for clinical trials in both IDDM and NIDDM to provide adequate information on the benefits of lipid-lowering therapy and to confirm treatment strategies.
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PMID:Hyperlipidaemia in diabetes. 208 5

Diabetes mellitus is frequently associated with lipid metabolism abnormalities. In the present study the lipid and apolipoprotein profiles have been compared in type II diabetic subjects with (n = 30) and without (n = 30) coronary heart disease (CHD). All subjects were studied after good metabolic control had been achieved. Significant differences in plasma lipids and apolipoproteins were seen in diabetic patients with CHD in comparison with diabetics without CHD. Patients with CHD presented higher total cholesterol, triglyceride, LDL-cholesterol, apo B, apo CII and apo CIII levels and total cholesterol/HDL-cholesterol and LDL-cholesterol HDL-cholesterol ratios and lower HDL-cholesterol values and apo A1/apo B ratio than the patients without CHD. The same findings were found in females; while male subjects with CHD had significantly increased total cholesterol, LDL-cholesterol and apo B levels and total cholesterol/HDL-cholesterol and LDL-cholesterol/HDL-cholesterol ratios and significantly decreased apo A1/apo B ratio compared with males without CHD. These findings support the concept that the apolipoprotein profile plays a remarkable role as risk factor for CHD in type II diabetes mellitus.
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PMID:Apolipoprotein profile in type II diabetic patients with and without coronary heart disease. 208 39

The borderline between diabetes and intolerance to carbohydrates has been drawn on the basis of prospective studies which determined a glycaemic threshold marking the risk for microangiopathy. On the other hand, the borderline between intolerance to carbohydrates and normal glucose tolerance remains arbitrary: 25% for subjects who are intolerant to carbohydrates return to normal glucose tolerance within 10 years. This is due to the fact that intolerance to carbohydrates is a heterogeneous entity which should be dismembered according to the severity of insulin deficiency and to the degree of insulin resistance. Alteration of insulin secretion is perhaps the most specific marker of susceptibility to non insulin dependent diabetes, but insulin resistance is certainly the principal factor exhausting insulin secretion and leading to non insulin dependent diabetes. Insulin resistance and the hyperinsulinism it creates seem to facilitate atherogenesis, even when glucose tolerance is still normal, so that the oral glucose tolerance test is not only poorly reproducible but loses a great deal of its value in the early detection of vascular risk. Measurements of fasting and post-prandial glucose levels and of A1C haemoglobin, cholesterol, triglyceride, and HDL cholesterol levels usually make it possible to classify subjects into one of the three following categories: (1) no risk of macro- or microangiopathy; (2) diabetes with a risk of macro- or microangiopathy; (3) intolerance to glucose with risk of atherogenesis but no risk of microangiopathy. The oral glucose tolerance test probably remains useful within a small set of values that are either very slightly above normal or dissociated. Measuring blood insulin levels might be a better way of assessing the risk of atherogenesis, but the clinical use of this test requires evaluation.
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PMID:[Intolerance to carbohydrates: the seven questions]. 209 35

Nine patients with non-insulin-dependent diabetes (NIDDM) treated with glibenclamide (3.5 mg b.i.d.) participated in this randomized double-blind placebo controlled crossover study to evaluate the effects of granulated guar gum (5 g t.i.d. with meals) on the absorption of glibenclamide and metabolic control and serum lipids. Each treatment period lasted for 4 weeks, and there was a wash-out period of one week between the treatments. The fasting blood glucose (10.5 +/- 3.4 mmol/l on guar gum vs 11.3 +/- 3.7 mmol/l on placebo, p less than 0.05) and serum total cholesterol (5.9 +/- 1.4 mmol/l on guar gum vs 6.6 +/- 1.6 mmol/l on placebo; p less than 0.05) levels were lower after the treatment with guar gum than placebo. No significant differences were observed in serum triglycerides or HDL cholesterol between guar gum and placebo treatments. The administration of guar gum together with glibenclamide did not change significantly the maximum concentration (223 +/- 196 ng/ml on guar gum vs 184 +/- 138 ng/ml on placebo; n = 7, NS) or area under the curve (AUC0-6) [729 +/- 813 (ng/ml) X h on guar gum vs 560 +/- 513 (ng/ml) X h on placebo; NS] of glibenclamide. The fasting serum glibenclamide concentrations were similar at the end of the 4-week treatment period with guar gum and placebo. In conclusion, guar gum improved the metabolic control and decreased serum lipids of patients with NIDDM. In addition, guar gum ingested with glibenclamide did not interfere with the absorption of glibenclamide.
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PMID:Effects of a gel forming dietary fiber, guar gum, on the absorption of glibenclamide and metabolic control and serum lipids in patients with non-insulin-dependent (type 2) diabetes. 211 Sep 37

Fasting total cholesterol (TC), triglycerides (TG), HDL cholesterol (HDL C), apolipoprotein A1 (apo A1) and apolipoprotein B (apo B) were measured in 35 non-insulin dependent diabetic patients treated by diet with or without sulphonylureas and 35 control subjects matched for age, sex, and body mass index. Ratios of apolipoprotein and lipid were calculated. The diabetics were well controlled with a mean (+/- SD) glycosylated haemoglobin (HbA1) of 8.5 +/- 1.3% (normal range less than 8%). Compared to non-diabetic control subjects apo A1: HDL C, apo B: TC, and apo B: calculated LDL C were significantly higher in the NIDDM patients, (112.9 +/- 26.3 vs 83.0 +/- 28.7, p less than 0.001, 15.89 +/- 1.68 vs 14.22 +/- 3.48, p less than 0.01, and 24.32 +/- 3.19 vs 22.33 +/- 5.49, p less than 0.05 respectively). These findings reflect differences in cholesterol content in the absence of differences in apolipoprotein concentrations between the NIDDM and control groups. The cardiovascular risk ratio HDL C: non HDL C was significantly lower in the NIDDM patients (0.25 +/- 0.09 vs 0.31 +/- 0.15, p less than 0.01), but there was no difference in apo A1:apo B (1.42 +/- 0.42 vs 1.43 +/- 0.52, NS). Although apo A1: apo B correlated well with HDL C:non HDL C in both NIDDM and controls (r = 0.88, 0.72, p less than 0.001 respectively) the slope of the relationships differed b = 4.01 NIDDM vs 2.50 controls (95% confidence intervals for difference is 0.22-2.78). Simple widely available methods can identify abnormalities of lipoprotein content in treated NIDDM patients. Both HDL and LDL contain less cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoprotein and lipid ratios in treated non-insulin dependent diabetics. 213 96

Prospective studies have shown that increased urinary albumin excretion is a risk factor for cardiovascular morbidity and mortality in patients with Type 2 diabetes mellitus, but the nature of the association remains unknown. Eighty-five patients aged less than 65 years and not treated with insulin were studied. The overnight albumin excretion rate (AER) was measured in each patient and analysed in relation to several putative risk factors for cardiovascular disease. AER was used both as a continuous variable and after dividing patients into high-risk (AER greater than or equal to 10 micrograms min-1) and low-risk (AER less than 10 micrograms min-1) groups. By both methods of analysis AER was significantly correlated with both seated and supine diastolic blood pressure levels and with resting heart rate. Body mass index and waist-hip ratio appeared higher and HDL-cholesterol lower in the at-risk group, but differences were not statistically significant. The level of Factor VII was not significantly lower in the at-risk group. Little of the cardiovascular risk associated with raised AER can be attributed to associations with conventional risk factors.
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PMID:Microalbuminuria and cardiovascular risk factors in type 2 diabetes mellitus. 213 50

To investigate whether persistent microalbuminuria is related to altered levels of both lipids and apolipoproteins in Type 2 diabetes mellitus serum total-cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, apolipoprotein A-I, and apolipoprotein B were measured by standard methods in a group of Type 2 diabetic patients affected by persistent microalbuminuria (albumin excretion rate (AER) 20-200 micrograms min-1) as compared with a group of sex- and age-matched non-microalbuminuric patients (AER less than 20 micrograms min-1). The groups were stratified according to a short (less than or equal to 5 years) or a longer (greater than 5 years) duration of diagnosed diabetes. Microalbuminuria was not associated with significant changes of serum total-cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, and apolipoproteins in the group of patients with a duration of disease greater than 5 years, while microalbuminuric patients less than or equal to 5 years from diagnosis (n = 11) had serum total-cholesterol, triglycerides, LDL-cholesterol, and apoprotein B higher than non-microalbuminuric control patients (n = 26) (cholesterol 6.2 +/- 0.9 vs 5.1 +/- 1.0 mmol l-1 (p = 0.003); triglycerides 2.1 +/- 0.7 vs 1.7 +/- 1.3 mmol l-1 (p = 0.03); LDL-cholesterol 4.1 +/- 0.8 vs 3.0 +/- 0.7 mmol l-1 (p less than 0.001); apo-B 1.3 +/- 0.3 vs 1.1 +/- 0.3 g l-1 (p = 0.02). In these patients with shorter duration of diabetes many of the serum lipid measures correlated positively with AER.
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PMID:Serum lipids and lipoproteins in type 2 diabetic patients with persistent microalbuminuria. 214 34

10 non-insulin-dependent (NIDDM) diabetic patients of the University Hospital Basle completed a placebo-controlled open crossover study of three 3-month periods in which the response to 30 g wheat bran and 15 g guar gum daily, respectively, was compared with placebo response. No significant difference occurred in blood glucose or HbA1c. Only postprandial plasma insulin levels were significantly lower in the afternoon at the end of both treatments (p less than 0.05). Serum total cholesterol levels decreased under guar gum by 10% (p less than 0.01), as did LDL cholesterol and the ratio of total to HDL cholesterol (p less than 0.05). Triglycerides were significantly lower (p less than 0.05) after 8 weeks. We conclude that neither guar gum nor wheat bran improves the metabolic control of NIDDM, but guar gum may be useful in patients with high serum total cholesterol levels.
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PMID:[Comparison of guar gum, wheat bran and placebo on carbohydrate and lipid metabolism in type II diabetics]. 215 79


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