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

Both hyperinsulinemia and free oxygen radicals have been implicated in the pathogenesis of atherosclerosis, but the relationship between insulin levels or insulin action and the oxidant/antioxidant balance has not been explored. We measured the effect of physiologic hyperinsulinemia on plasma concentrations of vitamin E, a major free radical scavenger molecule. Isoglycemic clamps (at an insulin infusion rate of 6 pmol . min-1 . kg-1) were performed in four groups of subjects: (1) 12 non-insulin-dependent diabetic (NIDDM) patients, (2) eight patients with essential hypertension, (3) 11 nondiabetic obese individuals, and (4) 12 healthy subjects. In 10 healthy volunteers, a time-control experiment was performed by replacing the insulin infusion with normal saline. Vitamin E and plasma lipid levels were determined at baseline and after 2 hours of insulin/saline infusion. Insulin sensitivity was reduced in diabetic, obese, and hypertensive groups in comparison to healthy controls, but fasting plasma vitamin E concentrations were similar in all groups. A consistent decrement in plasma vitamin E concentrations (averaging 12% of baseline, P < .0001) was observed in all subjects receiving insulin regardless of the level of insulin sensitivity, whereas no significant changes in plasma vitamin E were seen in subjects receiving saline infusion (P < .001 v insulin infusion groups). The insulin-induced decrement persisted in all study groups when plasma vitamin E concentrations were corrected for total serum cholesterol levels (-8.9% +/- 1.2% v -0.4 +/- 2.3% of saline controls, P = .0004) or serum low-density lipoprotein (LDL(-10.0% +/- 1.2% v -0.4% +/- 2.2%, P = .0002). We conclude that insulin infusion acutely depletes vitamin E in circulating lipids regardless of insulin resistance. This effect may represent a physiologic means of transferring vitamin E into cell membranes; alternatively, it might reflect a pro-oxidant action of insulin in vivo.
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PMID:Insulin decreases circulating vitamin E levels in humans. 876 59

Increased erythrocyte (RBC) sodium-lithium (Na-Li) counter transport (CT) has been reported to be a genetic marker for essential hypertension (EHT). In addition, increased RBC Na-Li CT has been demonstrated in insulin-dependent diabetic (IDDM) patients with nephropathy, indicating that a predisposition to hypertension may cause renal damage and impaired renal function. Therefore, the present study was designed to determine RBC Na-Li CT in subjects with essential hypertension (EHT) and non-insulin-dependent diabetics (NIDDM) with or without hypertension (NIDDMHT or NIDDMNT), using the method of Canessa et al. with a slight modification by flame photometry and expressed as nmol Li/5 x 10(6) RBC/h. Na-Li CT in patients with EHT (0.159 +/- 0.051 (S.D.), n = 26) or NIDDMHT (0.168 +/0 0.083, n = 42) was higher than that in NIDDMNT patients (0.127 +/- 0.059, n = 27, P < 0.05). Among the NIDDMHT patients, those with clinical nephropathy had the same levels of Na-Li CT as those without nephropathy. When the NIDDM patients were divided into two groups with or without insulin treatment, the Na-Li CT in hypertensives was higher than that in normotensives, irrespective of whether or not they were on insulin therapy. Addition of insulin to RBCs in vitro did not augment the Na-Li CT activity. These results suggest that an increase of Na-Li CT may not be due to the stimulatory effect of endogenous or exogenous insulin, and reflect a genetic predisposition for hypertension, and hence diabetic nephropathy, not only in IDDM but also NIDDM patients.
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PMID:Elevated erythrocyte sodium-lithium counter-transport in hypertensive patients with non-insulin-dependent diabetes mellitus. 879

One hundred newly diagnosed IGT and type 2 diabetic subjects both normotensive and hypertensive and of age between 40-55 years were studied by oral glucose stimulation. Serum insulin concentrations were measured in the fasting and at 30, 60 and 120 minutes after glucose administration. Postglucose serum insulin responses were found to be significantly higher in the hypertensive subjects with FPG < 7.8 mmol/l (p < 0.05 at 30, 60 and 120 minutes) as compared with the corresponding values of the normotensive subjects with comparable fasting hyperglycemia. No significant difference in insulin responses between hypertensive and normotensive subjects was found in those with FPG > 7.8 mmol/l. A positive correlation was observed between diastolic blood pressure and 2 hour postglucose serum insulin concentration in those with FPG < 7.8 mmol/l (P < .05). The results suggested that hyperinsulinemia is a feature of hypertensive subjects with mild glucose intolerance and not of those with severe glucose intolerance. The absence of elevated insulin response in hypertensive subjects with advanced type 2 diabetes might be due to severe B cell decompensation. It appears that insulin resistance is somehow associated with essential hypertension and hyperinsulinemia is not necessary for the maintenance of raised blood pressure.
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PMID:The relationship between blood pressure and serum insulin response in glucose intolerant subjects. 881 63

The aim of this study was to assess the chronic effects of a highly selective dihydropiridine calcium channel blocker, israpidine, in its sustained release form (I-SRO), on platelet functions and fibrinolytic parameters in subjects with essential hypertension (EH) combined or not with other well-known cardiovascular risk factors, such as cigarette smoking (EH+S) and type II diabetes mellitus (EH+DM). Thirty-six patients with essential hypertension with sitting diastolic blood pressures of 96-104 mmHg without (EH, n = 12) or with other risk factors (EH+S, n = 12, EH+DM, n = 12) were enrolled. After a 4-week, single-blind, placebo run-in period, the subjects received I-SRO 5 mg once daily for 18 weeks. After both placebo and 6 and 18 weeks of I-SRO treatment, the following parameters were measured: sitting blood pressure by mercury sphygmomanometer; platelet aggregation, plasma beta-thromboglobulin (BTG), platelet factor-4 (PF4), and plasminogen activator inhibitor 1 (PAI-1) by means of ELISA methods; and euglobulin lysis time before (ELT) and after standardized (10 min) venous occlusion (ELT-VO). In the group of patients as a whole compared with placebo, I-SRO significantly reduced SBP/DBP platelet aggregation, BTG, PF4, ELT, and ELT-VO. Significant reductions in these parameters were also observed in each group. In addition to the antihypertensive effect, I-SRO chronic treatment may favorably affect the platelet function and fibrinolytic system in essential hypertension with or without other cardiovascular risk factors.
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PMID:Effects of isradipine sustained release on platelet function and fibrinolysis in essential hypertensives with or without other risk factors. 884 3

Urapidil, a new alpha-blocker that peripherally antagonizes postsynaptic alpha 1 receptors and centrally causes a reduction in sympathetic tone as agonist of the serotoninergic receptors, was assessed for its antihypertensive effect and its role on glucose and lipid metabolism and insulin sensitivity in diabetic hypertensive patients. Thirty-three non-insulin dependent diabetes mellitus (NIDDM) patients with diastolic blood pressure (BP) of 95-115 mm Hg were treated with either 30 or 60 mg urapidil twice a day, with a gradual increment up to a maximum of 90 mg b.i.d., in order to reduce diastolic pressure to < 90 mm Hg or by at least 10% in the sitting position. A significant reduction in systolic and diastolic arterial pressure, not accompanied by an increased heart rate, was achieved after 12 weeks of treatment. Lipid and carbohydrate homeostasis and glycemic control, as assessed by HbA1C levels, were not affected. The fasting insulin concentration before the glucose load remained similar, but there was a trend toward reduction in peak insulin concentration, and the ratio of insulin change to glucose change between fasting levels and peak levels was significantly lowered by treatment, suggesting improved insulin sensitivity. In conclusion, urapidil is an effective antihypertensive agent in NIDDM patients with essential hypertension, with a neutral effect on lipids and carbohydrates and a possible beneficial effect on insulin resistance.
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PMID:Efficacy and tolerability of slow release urapidil (ebrantil) in hypertensive patients with non-insulin dependent diabetes mellitus (NIDDM). 886 67

The open trial was designed to evaluate the effects of long-term antihypertensive treatment with the calcium-channel blocker, manidipine and the angiotensin converting enzyme (ACE) inhibitor, delapril on insulin sensitivity in Japanese non-insulin dependent diabetes mellitus (NIDDM) patients with essential hypertension. We measured the insulin sensitivity index (SI) and the glucose-effectiveness (SG) by the use of Bergman's minimal model method in 18 hypertensive NIDDM patients before and after administration of manidipine (group A) or delapril (group B) for 3 months. Manidipine treatment for 3 months significantly improved SI in group A from 3.35 +/- 0.61 (x 10(-4) min-1 microU-1 ml-1) to 4.70 +/- 1.34 (P < 0.05). Delapril treatment for 3 months also significantly improved SI in group B from 3.56 +/- 1.04 to 5.00 +/- 0.87 (P < 0.05). Manidipine significantly improved SG in group A from 1.60 +/- 0.64 (x 10(-2) min) to 2.19 +/- 0.38 (P < 0.05). Delapril treatment also significantly improved SG in the group B from 1.41 +/- 0.56 to 1.91 +/- 0.35 (P < 0.05). Manidipine and delapril did not affect urinary C-peptide excretion for 24 h in the hypertensive NIDDM patients. Treatment with manidipine or delapril significantly reduced systolic and diastolic blood pressures in the hypertensive NIDDM patients. There were no differences between plasma glucose, serum total triglycerides, and cholesterol or lipoprotein cholesterol fractions, heart rate and body weight after 3 months on manidipine or delapril. This study confirmed the improving effects on SI and SG by long-term treatment with manidipine or delapril in the hypertensive NIDDM patients.
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PMID:Effect of manidipine and delapril on insulin sensitivity in type 2 diabetic patients with essential hypertension. 887 75

The aim of our study was to compare the effect of captopril--the angiotensin-converting enzyme inhibitor, nifedipine--the calcium antagonist, and prazosin--the alpha blocker, on the secretory function of pancreatic beta-cells in hypertensive patients with NIDDM and with normal glucose tolerance. The effect of a 2-week treatment with nifedipine, captopril and prazosin upon glycaemia, serum insulin (IRI) and C-peptide (CP) following oral and intravenous glucose load were investigated in three groups, each including 10 non-diabetic patients with essential hypertension (h) and 10 hypertensive type 2 (non-insulin-dependent) diabetics (h + d), aged 32-63 years. Nifedipine produced increase in glycaemia in the oral test in both groups. In the (h) group, but not in the (h + d) group, the drug caused reduction of the glucose-dependent increases in serum IRI and CP, more marked with respect to CP, as expressed by the decrease in the molar serum CP/IRI ratio. These results indicate that in non-diabetic patients, nifedipine reduces the early response of beta-cells to glucose, but this effect is partly compensated by a decreased insulin uptake by the liver. In patients with type 2 diabetes, this phenomenon does not become manifest because of absence or reduction in the early glucose-dependent insulin release. After captopril, lower values of glycaemia and serum IRI and CP were observed in both groups suggesting an improvement of insulin sensitivity. In conclusion, nifedipine has a small influence, and captopril and prazosin are devoided of any influence on the secretory function of pancreatic beta-cells. These drugs may be recommended for the treatment of hypertension in patients with type 2 (non-insulin-dependent) diabetes.
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PMID:Effect of nifedipine, captopril and prazosin on secretory function of pancreatic beta-cells in hypertensive patients with type-2 (non-insulin-dependent) diabetes and in hypertensive non-diabetics. 887 77

Incidence of essential hypertension has been reported to be significantly higher in the population afflicted with non-insulin dependent diabetes mellitus (NIDDM). The present studies were under taken in the insulin resistant, Zucker obese rats to evaluate various factors that could lead to the development of high blood pressure. Direct blood pressure measurements in the conscious obese rats indicated that they were not consistently hypertensive although the blood pressures of the obese rats tended to be higher than that of the control lean rats. However, after Inactin anesthesia blood pressures of the obese rats were significantly elevated which can be related to an increase in sympathetic tone since autonomic ganglionic blockade eliminated the differences between the pressures of the two groups. Under anesthesia, cardiac output per 100 gm body weight was significantly lower indicating inadequate tissue perfusion in the obese rats. In a separate series of studies carried out in conscious rats, reflexly mediated alterations in the heart rate to intravenous phenylephrine and sodium nitroprusside were significantly blunted in the obese rats. These observations which include enhanced central sympathetic discharge, inadequate systemic hemodynamics and attenuation of baroreceptor compensation collectively suggest that the insulin resistant obese rats are in a pre-hypertensive state and could develop sustained hypertension if they are exposed to other risk factors.
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PMID:Evaluation of hemodynamics, vascular reactivity and baroreceptor compensation in the insulin resistant Zucker obese rats. 892 47

There are striking similarities between Cushing's syndrome and the 'metabolic syndrome X' since both are characterised by hypertension, insulin resistance, glucose intolerance, hyperlipidaemia, and central obesity. The possibility that cortisol contributes to the associations between multiple risk factors for cardiovascular disease was rejected when it was demonstrated that there was no elevation in cortisol secretion or circulating concentration in patients with essential hypertension or type 2 diabetes mellitus. However, in recent years the enormous variability in tissue sensitivity to cortisol has become apparent. We have measured tissue sensitivity to glucocorticoids using an assay of skin vasoconstriction and have demonstrated its relationship with high blood pressure, insulin resistance, glucose intolerance, and hypertriglyceridaemia. Our data suggest that the increase in dermal glucocorticoid sensitivity is not a secondary phenomenon and may be explained by increased glucocorticoid receptor affinity together with impaired inactivation of cortisol by 11 beta-hydroxysteroid dehydrogenase. Importantly, we have not found that enhanced peripheral glucocorticoid sensitivity is associated with compensatory suppression of cortisol secretion, so that the maintenance of normal circulating cortisol concentrations in patients with cardiovascular risk factors may be paradoxical and inappropriate.
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PMID:Abnormal glucocorticoid activity in subjects with risk factors for cardiovascular disease. 896 30

Hypercholesterolaemia is a strong risk factor of coronary artery disease (CAD). The importance of high triglyceride and low HDL cholesterol in predicting risk of CAD is less well-established. This review presents data showing that high triglyceride and low HDL cholesterol are important risk factors of CAD and suggests that combined lipid profiles of triglyceride, HDL cholesterol, and total cholesterol provide more information about risk of CAD than total cholesterol alone. High triglyceride and low HDL cholesterol is the characteristic dyslipidaemia seen in subjects with insulin resistance, a basic abnormality in glucose- and insulin metabolism. Since insulin resistance and raised triglyceride and decreased HDL cholesterol can be identified in children of patients with NIDDM, essential hypertension, and CAD, we suggest that efforts to prevent CAD should include interventions against all these associated abnormalities in glucose-, insulin-, and lipid metabolism and not only high cholesterol.
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PMID:[High triglyceride, low HDL-cholesterol and risk of coronary heart disease]. 898 51


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