UMLS:C0011860 - FACTA Search

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

Increased plasma concentrations of homocysteine have been found in patients with coronary artery disease (CAD) and essential hypertension (EH) and in patients with diabetic complications. The 677C/T methylenetetrahydrofolate reductase (MTHFR) gene polymorphism is related to the MTHFR enzyme activity and to the plasma homocysteine concentration. This study was designed to investigate an association of this polymorphism with CAD, EH, and type II diabetes mellitus in the Czech population. The MTHFR genotypes were assessed by the polymerase chain reaction-based methodology in a sample of 1199 unrelated Caucasian subjects with CAD, EH, type II diabetes, or a combination of these diseases, and in healthy subjects. Allele frequencies of the MTHFR polymorphism differed considerably between women with and without type II diabetes mellitus (P = 0.00069), with a higher frequency of the C allele in the diabetic women. In addition, the MTHFR T allele frequency was significantly higher in normotensive subjects with CAD compared with normotensive subjects without this disease (P = 0.020). Both associations were confirmed by multiple logistic regressions. In conclusion, while the C allele of the 677C/T MTHFR polymorphism is associated with type II diabetes mellitus in women, the T allele is associated with CAD only in normotensive subjects of Czech origin.
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PMID:Methylenetetrahydrofolate reductase polymorphism, type II diabetes mellitus, coronary artery disease, and essential hypertension in the Czech population. 1138 55

Prostaglandylinositol cyclic phosphate (cPIP), functionally a cAMP antagonist, is a novel, low-molecular weight mediator of insulin action. Both essential hypertension and type 2 diabetes may be associated with a reduction of cPIP synthesis. In intact cells and in plasma membranes, cPIP synthesis is stimulated by insulin, which activates cPIP synthase by tyrosine phosphorylation. We measured the activities of cPIP synthase in the homogenates of freeze-clamped and then lyophilized liver samples from five insulin-resistant, adult rhesus monkeys, obtained under basal fasting conditions and again under maximal insulin stimulation during a euglycemic hyperinsulinemic clamp. The mean cPIP synthase activity in basal samples (0.33 +/- 0.09 pmol/min/mg protein) was not significantly different at the end of the clamp (0.24 +/- 0.11 pmol/min/mg protein). Basal cPIP synthase activityVoL 12, No. 1, 2001 was directly related to both basal cAMP content and basal fractional activity of cAMP-dependent protein kinase (PKA): r=0.85, p<0.05 and r=0.86, p<0.05, respectively. In turn, insulin-stimulated cPIP synthase activity was inversely related to both the insulin-stimulated fractional activity of PKA (r=0.89, p<0.02) and the insulin-stimulated total PKA activity: r=0.94, p<0.005. The findings suggest that in the liver of insulin-resistant rhesus monkeys, cPIP synthase activity, which leads to the synthesis of the low-molecular weight mediator cPIP, may oppose cAMP synthesis and PKA activity.
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PMID:Prostaglandylinositol cyclic phosphate synthase activity in the liver of insulin-resistant rhesus monkeys before and after a euglycemic hyperinsulinemic clamp. 1141 4

Microalbuminuria (MA) is defined as persistent elevation of albumin in the urine, of 30-300 mg/day (20-200 microg/min). These values are less than the values detected by routine urine dipstick testing, which does not become positive until protein excretion exceeds 300-500 mg/day. Use of the albumin-to-creatinine ratio is recommended as the preferred screening strategy for all diabetic patients. MA is measured in spot morning urine obtained from the patient in the office and sent for measurement of both albumin and creatinine. A value above 0.03 mg/mg suggests that albumin excretion is above 30 mg/day and therefore MA is present. MA should be checked annually in everyone, and every 6 months within the first year of treatment to assess the impact in patients started on antihypertensive therapy. MA is an established risk factor for renal disease progression in type 1 diabetes and its presence is the earliest clinical sign of diabetic nephropathy. In addition, a number of studies suggest that MA is an important risk factor for cardiovascular disease and defines a group at high risk for early cardiovascular mortality in both type 2 diabetes and essential hypertension. MA also signifies abnormal vascular permeability and the presence of atherosclerosis. Among nondiabetic patients with essential hypertension, MA is associated with higher blood pressures, increased serum total cholesterol, and reduced serum high-density lipoprotein cholesterol. Thus, taken together these data support the concept that the presence of MA is the kidney's notice to the physician/patient that there is a problem with the vasculature. MA can be reduced, and progression to overt proteinuria prevented, by aggressive blood pressure reduction. The National Kidney Foundation recommends that blood pressure levels be maintained at or below 130/80 mm Hg in anyone with diabetes or renal disease. This should be accomplished with antihypertensive agents that prevent the rise in MA and hence prevent development of proteinuria. Such agents are angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and, to a lesser extent, Beta blockers, non-dihydropyridine calcium antagonists, and diuretics. In summary, the presence of MA is a marker of endothelial dysfunction and a harbinger of markedly enhanced cardiovascular risk. All patients with diabetes and/or hypertension should be screened for the presence of microalbuminuria with use of spot morning urine. To maximize prevention of MA development, the following goals should be instituted: 1) blood pressure should be maintained at less than 130/80 mm Hg and a low-salt, moderate-potassium diet instituted; 2) in diabetics, HbA1c should be kept at less than 7%; 3) in obese patients, a weight loss program should be implemented, with a goal BMI of less than 30; and 4) the physician and patient, working together, should maintain low-density lipoprotein cholesterol at less than 120 mg/dL, and less than 100 mg/dL if diabetes is present. (c)2001 by Le Jacq Communications, Inc.
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PMID:Microalbuminuria: what is it? Why is it important? What should be done about it? 1141 91

Valsartan is an orally active, selective antagonist of the angiotensin II-1 (AT1) receptor developed for the treatment of hypertension. The Valsartan Antihypertensive Long-term Use Evaluation (VALUE) Trial of Cardiovascular Events in Hypertension is a double-blind, randomized prospective, parallel group study designed to compare the effects of valsartan with those of the calcium-antagonist amlodipine on the reduction of cardiac morbidity and mortality. Patients with essential hypertension, aged 50 years and older, and at particularly high risk of coronary events were enrolled. 18,119 patients were screened and 15,314 patients in 31 countries were randomized mainly between January 1998 and December 1999. These hypertensives had a mean blood pressure of 154.7/87.5 mmHg at the time of their randomization to blinded medication. The population comprises both genders (men 57.6%), Caucasians (89.1%), mean age 67.2 years, mean body mass index 28.6 kg/m2, coronary heart disease (45.8%), high cholesterol (33.0%), type 2 diabetes mellitus (31.7%) and smokers (24.0%). More than 92% of the randomized participants had been treated for high blood pressure for at least 6 months when screened for the study. The randomized population is now being treated (goal blood pressure < 140/90 mmHg) in adherence with the protocol until at least 1450 patients experience primary cardiac endpoint defined as clinically evident or aborted myocardial infarction, hospitalization for heart failure or death caused by coronary heart disease.
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PMID:Characteristics of 15,314 hypertensive patients at high coronary risk. The VALUE trial. The Valsartan Antihypertensive Long-term Use Evaluation. 1146 64

To investigate the role of intracellular potassium (K(i))and other ions in hypertension and diabetes, we utilized (39)K-, (23)Na-, (31)P-, and (19)F-nuclear magnetic resonance (NMR) spectroscopy to measure K(i), intracellular sodium (Na(i)), intracellular free magnesium (Mg(i)), and cytosolic free calcium (Ca(i)), respectively, in red blood cells of fasting normotensive nondiabetic control subjects (n=10), untreated (n=13) and treated (n=14) essential hypertensive subjects, and diabetic subjects (n=5). In 12 subjects (6 hypertensive and 6 normotensive controls), ions were also measured before and after the acute infusion of 1 L of normal saline. Compared with those in controls (K(i)=148+/-2.0 mmol/L), K(i) levels were significantly lower in hypertensive (132.2+/-2.9 mmol/L, sig=0.05) and in type 2 diabetic subjects (121.2+/-6.8 mmol/L, sig=0.05). K(i) was higher in treated hypertensives than in untreated hypertensives (139+/-3.1 mmol/L, sig=0.05) but was still lower than in normals. Although no significant relation was observed between basal K(i) and Na(i) values, saline infusion elevated Na(i) (P<0.01) and reciprocally suppressed K(i) levels (142+/-2.4 to 131+/-2.2 mmol/L, P<0.01). K(i) was strongly and inversely related to Ca(i) (r=-0.846, P<0.001), and was directly related to Mg(i) (r=0.664, P<0.001). We conclude that (1) K(i) depletion is a common feature of essential hypertension and type 2 diabetes, (2) treatment of hypertension at least partially restores K(i) levels toward normal, and (3) fasting steady-state K(i) levels are closely linked to Ca(i) and Mg(i) homeostasis. Altogether, these results emphasize the similar and coordinate nature of ionic defects in diabetes and hypertension and suggest that their interpretation requires an understanding of their interaction.
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PMID:Relation of cellular potassium to other mineral ions in hypertension and diabetes. 1156 62

Studies on the role of parental history on the risk of developing metabolic syndrome (MS) show inconsistent data that may depend on misclassification of the parental history. Confirming carefully the parental phenotype (PF) of type 2 diabetes mellitus (DM) and essential hypertension (EH) of participants' parents, we determined the relationship between PF of either DM or EH and the risk of developing MS in Mexican individuals. A case-control study of 210 subjects randomly recruited from Durango, Mexico was carried out. Subjects with MS (cases) were compared with a control group of subjects without MS matched by age and gender. MS was defined by the presence of two or more of the following: fasting glucose > or =7.0 mmol/l; blood pressure > or =160/90 mmHg; fasting triglycerides > or =1.7 mmol/l and/or HDL-cholesterol <1.0 mmol/l; and obesity (body mass index > or =30 kg/m2 and/or waist-to-hip ratio > or =0.85). The PF of DM and EH was confirmed by direct clinical examination and/or review of certificates of death of each of the participants' parents. Incomplete or unclear data about PH were exclusion criteria. Multivariate analysis showed that PF of DM without EH (odds ratio (OR) 2.6; 95% CI, 1.3-7.8, p=0.044) and PF of both DM and EH (OR, 3.1; 95% CI, 1.5-9.1, p=0.0001), but not the PF of EH without DM are independent predictors for developing MS in Mexican individuals. In the offspring generation of Mexican subjects, the PF of DM seems to increase the risk of developing MS, whereas PF of EH does not.
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PMID:The parental phenotype of diabetes, but not of essential hypertension, is linked to the development of metabolic syndrome in Mexican individuals. 1175 7

Proteinuria is the hallmark of renal disease and proteinuria exceeding 1 gm a day in patients with renal disease augers a poorer prognosis. Proteinuria has been shown to be tubulotoxic and directly contributes to renal deterioration. Patients with non-selective proteinuria are more likely to have progressive renal disease. Diabetic patients with persistent microhaematuria have about 20 times the risk of developing diabetic nephropathy. In essential hypertension, the onset of de novo proteinuria after years of adequate BP control is a marker of subsequent decline in renal function. In glomerulonephritis, more severe proteinuria is associated with faster rate of progression. Even though the initial phase of proteinuria in patients with glomerulonephritis is usually of immunological origin, in the vast majority of patients with established disease, the latter progressive phase of proteinuric glomerulopathy is the result of glomerular hyperfiltration which shifts glomerular non-selective pores to larger dimensions resulting in excessive leakage of protein in the urine. Endothelial injury resulting from glomerular hyperfiltration causes increase in local generation of Angiotensin II in the kidney as part of the hemodynamic response. ACE inhibitors and angiotensin II receptor antagonists (ATRA) can improve glomerular pore-selectivity by remodelling the glomerular basement membrane. In addition, these agents also have beneficial effects by decreasing TGF-beta production therapy decreasing mesangial cell proliferation, hence ameliorating disease progression in patients with diabetic nephropathy and IgA nephropathy. A number of recent clinical trials have shown that ACEI and ATRA therapy can retard the progression of renal deterioration in patients with NIDDM and those with IgA nephropathy and even restore normal renal function in those with mild renal impairment. Treatment and control of proteinuria in patients with renal disease should be regarded as important as treatment of hypertension as it can prevent renal failure.
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PMID:Proteinuria: clinical signficance and basis for therapy. 1176 58

Both high morbidity and potentiation of systemic complications emphasise significance of diabetes mellitus and hypertension co-incidence. The aim of the study was to analyse the influence of hypertension accompanied with type 2 diabetes mellitus on calcium phosphorus and magnesium metabolism. The study was performed in standard low-calcium diet conditions on the group of 49 patients with type 2 diabetes mellitus (among them 27 had hypertension), 14 patients with essential hypertension and 20 healthy persons. Both serum and urine concentration of creatinine, calcium, phosphorus, hydroxyproline, hydroxylysine and uric acid were analysed. Oral calcium load test was done. Serum alkaline phosphatase activity and oxalic acid urine excretion were also estimated. There were no significant differences between diabetic patients with and without hypertension as far as calcium, phosphorus or magnesium metabolism were concerned.
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PMID:[Bone complications in diabetic subjects with good metabolic control and without any long-term complications--certain problems. Part III: The influence of hypertension and type 2 diabetes mellitus co-incidence of calcium, phosphorus and magnesium metabolism]. 1176 86

We have documented, contrary to expectation, that the renin-angiotensin-aldosterone system (RAAS) is stimulated normally by restriction of sodium intake inpatients with Type 2 diabetes mellitus (DM) and hypertension. Conversely, plasma renin activity (PRA)is suppressed less than in normal subjects by a high-salt diet in these patients. Increasing plasma angiotensin II (Ang II) concentration through intravenous Ang II infusion also suppresses renin release, via the short feedback loop. In this study, we sought to ascertain whether the limited renin suppression in Type 2 diabetes mellitus via high-salt intake is a unique defect or part of a more generalised abnormality of PRA suppression. We studied 38 patients with Type 2 DM and hypertension, 158 hypertensive control patients, and 61 normotensive controls. All patients were studied while in metabolic balance on a 10 mEq sodium (Na) diet. The response to the Ang II infusion at 3 ng/kg/min for 45 minutes was measured. We found that PRA fell significantly in normal subjects, from 4.0 +/- 0.33 to 2.5 +/- 0.23 ngAngI/ml/hr (p=0.0056). In patients with essential hypertension, the Ang II infusion also led to a fall in PRA from 3.51 +/- 0.23 to 2.76 +/- 0.17 ng Angl/ml/hr(p=0.014). In patients with DM, despite a similar basal PRA (3.7 +/- 0.40 ng AngI/ml/hr), the infusion of Ang II did nor influence PRA significantly (3.43 +/- 0.42ng AngI/ml/hr; p > 0.77), though these patients had the most robust mean arterial pressure response. Our data are in complete accord with the concept of high intrarenal Ang II in DM and suggest lower systemic Ang II despite comparable PRA.
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PMID:Blunted suppression of plasma renin activity in diabetes. 1188 Oct 33

Arterial wall stiffness is an important independent risk factor for cardiovascular disease in hypertensive patients, which is further exacerbated by co-existent diabetes mellitus. Increased arterial stiffness is directly associated with an increase in pulse wave velocity (PWV) and indirectly with increased central and peripheral blood pressure. Following a two-week placebo run-in period, 27 patients with mild to moderate essential hypertension and Type 2 diabetes mellitus, were randomised to once daily treatment with either telmisartan 40 mg or placebo for three weeks, and after a two-week washout period, crossed-over to the alternative treatment for a further three weeks. Carotid/femoral and carotid/radial PWV were measured non-invasively using the automatic Complior device, and central parameters (central blood pressure, pulse contour analysis, and augmentation index) were measured using the SphygmoCor system, at the start and end of each treatment period. Compared with placebo, treatment with telmisartan significantly reduced carotid/femoral PWV (mean adjusted treatment difference -0.95 m/s, 95% confidence intervals: -1.67, -0.23 m/s, p=0.013), as well as peripheral and central diastolic, systolic and pulse pressure. In conclusion, the results of the this study show that telmisartan is effective in reducing arterial stiffness in hypertensive patients with Type 2 diabetes mellitus, and may potentially have beneficial effects on cardiovascular outcomes, beyond blood-pressure lowering effects in the patient group.
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PMID:Effect of telmisartan on arterial distensibility and central blood pressure in patients with mild to moderate hypertension and Type 2 diabetes mellitus. 1188 Nov 2

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