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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

Alterations in Relative Plasma Viscosity (RPV) and Plasma Fibrinogen Concentration (PFC) were compared in 24 insulin-dependent (IDDM) and 33 non-insulin-dependent (NIDDM) black Nigerian diabetics, during the course of treatment. Both PFC and RPV were significantly (p less than 0.001) increased in the diabetics, as a group, compared to a non-diabetic control group. PFC and RPV showed consistently marginal, though insignificant, increases in the IDDM vs NIDDM. Hypertensive diabetics, as a group, had significantly greater PFC (p less than 0.025), and RPV (p less than 0.025) than normotensive diabetics. Although PFC was significantly (p less than 0.05) raised in hypertensive IDDM, there was no marked change in RPV, compared to normotensive IDDM. Neither PFC nor RPV revealed a significant change between hypertensive and normotensive NIDDM. The implication of the present findings is that insulin-dependent diabetics may be more prone than non-insulin-dependent diabetics to develop haemorheological and hence circulatory disorders.
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PMID:Comparison of plasma viscosity and fibrinogen concentration in African insulin-dependent and non-insulin-dependent diabetics with and without hypertension. 226 27

Increased plasma plasminogen activator inhibitor type 1 (PAI-1), coagulation factor VII (FVII) and fibrinogen levels have been recognized as risk factors for cardiovascular disease. Because a substantially high incidence of cardiovascular disease has been reported in diabetic patients with nephropathy compared with those without nephropathy, we measured plasma levels of PAI-1, FVII activity and fibrinogen in non-insulin-dependent diabetic patients (NIDDM) with normoalbuminuria (without nephropathy), microalbuminuria (incipient nephropathy) and macroalbuminuria (overt nephropathy). PAI-1 and FVII levels were significantly increased in NIDDM with overt nephropathy compared with NIDDM without nephropathy. Fibrinogen levels were comparable between the patients with normo-, micro- and macro-albuminuria. Univariate regression analysis indicated that PAI-1 and FVII levels were significantly correlated with the albumin excretion rate (AER) in urine. PAI-1, FVII and fibrinogen levels were significantly correlated with the degree of insulin resistance estimated by the steady state plasma glucose concentration (SSPG) during the continuous infusion of glucose, insulin and octreotide. PAI-1 levels were correlated with plasma triglyceride (TG) levels. Multiple regression analysis revealed that AER was significantly associated with PAI-1 and FVII levels, whereas TG lost significant correlation with PAI-1 when AER, SSPG and plasma TG were entered as independent variables. SSPG retained an independent correlation with fibrinogen, PAI-1 and FVII levels. These results suggest that elevated plasma levels of PAI-1 and FVII in NIDDM patients with nephropathy are directly associated with renal damage, whereas insulin resistance widely regulates hemostatic components in NIDDM patients, irrespective of the presence of nephropathy.
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PMID:Albuminuria is directly associated with increased plasma PAI-1 and factor VII levels in NIDDM patients. 918 10

Fibrinogen is a strong cardiovascular risk factor in the general population, and increased fibrinogen plasma concentrations have been reported in type 2 diabetic patients. However, the mechanisms leading to hyperfibrinogenemia in type 2 diabetes are not known. It is also not known whether possible alterations of fibrinogen turnover may precede clinical diabetic micro- and macrovascular complications and therefore potentially contribute to their onset. To address these questions, fibrinogen production was determined in six male type 2 diabetic patients without detectable micro- and macrovascular complications (age, 45 +/- 4 yr; body mass index, 27 +/- 0.9 kg/m2) and in seven nondiabetic matched controls using leucine isotope precursor-product relationships. Plasma glucose (P < 0.001), insulin (P < 0.05), and glucagon concentrations (P < 0.01) were increased in the patients. Diabetic patients also had increased plasma fibrinogen concentration (+ approximately 50%; P < 0.01) and pool (+ approximately 40%; P < 0.01) as well as fractional (+ approximately 35%; P = 0.08) and absolute (+ approximately 100%; P < 0.01) synthetic rates. The plasma glucagon concentration was positively related (P < 0.005 or less) to the fibrinogen concentration as well as to fractional and absolute synthetic rates. Thus, fibrinogen production is markedly enhanced, and this alteration is likely to determine the observed hyperfibrinogenemia in type 2 diabetic patients. Hyperglucagonemia may contribute to the increased fibrinogen production. These findings in normoalbuminuric patients without clinical complications support the hypothesis that increased fibrinogen production and plasma concentrations may precede and possibly contribute to the onset of clinical cardiovascular complications in type 2 diabetes.
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PMID:Increased fibrinogen production in type 2 diabetic patients without detectable vascular complications: correlation with plasma glucagon concentrations. 1099 96

Fibrinogen is an acute-phase reactant and an independent cardiovascular risk factor. Insulin without amino acid replacement acutely suppressed fibrinogen production in nondiabetic and type 1 diabetic individuals. Fibrinogen production and plasma concentration increase in insulin-resistant type 2 diabetes. It is not known whether altered response to insulin contributes to hyperfibrinogenemia in type 2 diabetes. Fibrinogen fractional (FSR) and absolute (ASR) synthesis rates were measured using a leucine isotopic model in type 2 diabetic men (n = 7; age = 51 +/- 3 years; BMI = 26.7 +/- 1 kg/m(2)) compared with matched nondiabetic subjects under basal conditions and following a 4-h euglycemic-, euaminoacidemic-hyperinsulinemic clamp. Basal fibrinogen concentration (+35%, P < 0.05) and ASR (+35%, P < 0.05) were greater in the diabetic subjects. Following clamp, fibrinogen FSR and ASR were unchanged in the control subjects. In contrast, fibrinogen FSR and ASR increased by 41 and 43%, respectively (P < 0.05), in the diabetic subjects. Thus, fibrinogen production is acutely increased by insulin when euglycemia and euaminoacidemia are maintained in type 2 diabetic individuals but not in nondiabetic individuals. Enhanced fibrinogen production by insulin is likely to be a key alteration contributing to hyperfibrinogenemia and therefore cardiovascular risk in type 2 diabetes. Unchanged fibrinogen production in nondiabetic individuals suggests a role of plasma amino acids in regulating fibrinogen production in humans.
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PMID:Insulin acutely increases fibrinogen production in individuals with type 2 diabetes but not in individuals without diabetes. 1282 56

Plasma fibrinogen level represents a strong cardiovascular risk factor and is regulated by an interplay of genetic and environmental factors. Hyperfibrinogenemia frequently occurs in cluster with dyslipidemia within the frame of insulin resistance syndrome (IRS) and type 2 diabetes mellitus. Genetic variants with a pleiotropic effect have been proposed to cause IRS features including hyperfibrinogenemia. We studied the influence of polymorphisms in lipoprotein lipase (LPL) gene, beta-fibrinogen gene (FIBB) and environmental factors on plasma fibrinogen levels in type 2 diabetes patients. 131 type 2 diabetes patients (mean age 62+/-10 years, 33% male) were genotyped for polymorphisms in LPL gene (intron 6 PvuII, intron 8 HindIII) and FIBB gene (-148C/T, -455G/A) by PCR-RFLP method. Fibrinogen was measured by thrombin coagulation method, albuminuria by immunoturbidimetric assay. Polymorphism LPL PvuII showed a gene-dose effect on fibrinogen levels, with the highest fibrinogen in P-P- homozygotes (p = 0.05, analysis of variance). P-carriers (P-P- and P+P- combined) had significantly higher fibrinogen levels compared with P+P+ homozygotes (3.74+/-1.40 g/l vs 3.06+/-1.20 g/l, p=0.03). Other studied polymorphisms were not significantly related to fibrinogen levels. Age- and sex-adjusted fibrinogenemia correlated significantly with albuminuria (r = 0.48, p=0.001), serum uric acid (r = 0.42, p=0.006) and serum creatinine (r = 0.32, p=0.04). Multiple stepwise linear regression identified interaction term of LPL PvuII and albuminuria as an independent predictor of fibrinogen level, explaining 18% of fibrinogen variance. Albuminuria thus appears to be the best predictor of fibrinogen plasma levels in type 2 diabetic patients. Relationship between albuminuria and fibrinogenemia may be modified by the genotype LPL PvuII, which also shows a weak association with plasma fibrinogen level in type 2 diabetes patients.
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PMID:Relationship among urinary albumin excretion rate, lipoprotein lipase PvuII polymorphism and plasma fibrinogen in type 2 diabetic patients. 1585 59

Inflammation is associated with insulin resistance, atherosclerosis and type 2 diabetes but whether it causes insulin resistance and accelerated atherosclerosis or an epiphenomena of insulin resistance is not clear. Thirty-eight young normoglycemic, non-obese, first degree relatives of type 2 diabetic subjects (FH(+)) and 38 control subjects without family history of diabetes (FH(-)) (age and sex matched), were studied to determine difference in inflammatory markers, insulin resistance and carotid intima-media thickness (IMT). Plasma glucose, insulin (fasting and 2h after 75gm oral glucose) lipids and serum levels of C-reactive protein (CRP), tumour necrosis factor (TNF)-alpha and fibrinogen were measured after an overnight fast of 10-12h. First degree relative group (FH(+)) have higher BMI (p<0.05), composite IMT (p<0.05) and CRP level (p<0.05), however, after adjustment for BMI, the two groups did not significantly differ. Fibrinogen was not significantly correlated with composite IMT in FH(+) group after controlling with BMI. In FH(+) group composite IMT was significantly correlated with systolic blood pressure (p<0.05), LDL-cholesterol (p<0.05), postprandial insulin level (p<0.05) and HOMA-IR (p<0.05) after adjustment of BMI. Thus insulin resistance is a major determinant of atherosclerosis in subjects with high risk of type 2 diabetes showing the strong relationship between inflammation, obesity and insulin resistance.
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PMID:Inflammation, insulin resistance and carotid IMT in first degree relatives of north Indian type 2 diabetic subjects. 1653 Feb 89

The relationship between type 2 diabetes, antioxidant-enzyme serum ceruloplasmin, pro-inflammatory blood fibrinogen and antioxidant activity (AOA) was investigated in 40 diabetics and 47 non-diabetics hailing from South India as a preliminary study aspiring to be a crucial stepping stone for a large study. Serum AOA was lower (p<0.01) in diabetics (0.68+/-0.03 mmol/L) than controls (0.92+/-0.07 mmol/L) and ceruloplasmin more (p<0.001) in diabetics (983.20+/-52.18 mg/L) than controls (470.79+/-39.20 mg/L). Plasma fibrinogen was higher (p<0.001) in diabetics (480.23+/-19.52 mg/dl) than controls (313.94+/-13.42 mg/dl). Males had more AOA. Fibrinogen increased with age. These significant findings point strongly to augmented oxidative stress and inflammatory states in South Indian diabetics.
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PMID:Increased ceruloplasmin and fibrinogen in type 2 diabetes corresponds to decreased anti-oxidant activity in a preliminary tertiary South Indian hospital study. 1983 73

Inflammation may play a role in the pathogenesis of cardiovascular disease and type 2 diabetes, and it has been suggested that the protective effects of whole-grain consumption could be mediated by an effect on inflammation, although few studies have examined the relationships between grain intakes and inflammatory protein concentrations. Our objectives in this study were to examine the associations of whole grain and refined grain intake with plasminogen activator inhibitor type 1 (PAI-1), C-reactive protein (CRP), and fibrinogen plasma concentrations. Cross-sectional data from the Insulin Resistance Atherosclerosis Study were used to perform multiple regression analyses using dietary information on whole and refined grain intakes from a FFQ and clinical measures of plasma inflammatory protein concentrations in participants free of type 2 diabetes. After adjustment for demographic, lifestyle, and dietary variables, whole-grain intake was inversely related to log PAI-1 (beta = -0.102; SEM = 0.038; P = 0.0077) and log CRP (beta = -0.102; SEM = 0.048; P = 0.0340). Adding insulin sensitivity, waist circumference, and 2-h postload glucose to the model attenuated both associations to nonsignificance. Refined grain was positively related to log PAI-1 in the multivariate model (beta = 0.076; SEM = 0.034; P = 0.0251) and the relationship remained unchanged by additional adjustment for metabolic variables. Fibrinogen concentrations were not related to whole or refined grain intake. In summary, whole grain intake was inversely related to PAI-1 and CRP plasma concentrations, but these relationships were attenuated by the addition of metabolic variables to the model. Refined grain intake was positively independently related to plasma PAI-1 concentrations.
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PMID:Whole and refined grain intakes are related to inflammatory protein concentrations in human plasma. 2008 89

Individuals with hypertension, dyslipidemia or diabetes are at a higher risk to suffer cardiovascular disease than other people; while impaired fibrin structure/function may contribute to further raise the cardiovascular risk in the former. The purpose of this work was to study the fibrin network and fibrin degradation properties in hypertensive (HT) patients, pharmacologically treated, 124 +/- 11 mmHg, systolic blood pressure, and 70 +/- 10 mmHg, diastolic blood pressure, n = 12; metabolic dyslipidemic patients (DL), cholesterol: 5.7 +/- 1.5 mmol/L, n = 10; patients with type 2 diabetes mellitus (T2D), fasting plasma glucose: 8.8 +/- 2.2 mmol/L, n = 10; and a control group of healthy individuals, n = 9. The fibrinogen concentration was determined by the gravimetric method. Fibrin network formation and porosity were assessed by turbidity and permeation techniques, respectively; fibrin elastic properties were evaluated by compaction and fibrin lysis, by turbidity after addition of external tPA prior to plasma clotting. Fibrinogen concentration was significantly higher only in T2D patients (p = 0.004), compared to the control group. The fibrin polymerization and lysis processes were similar for all patient and control groups. Permeation was significantly slower in DL and T2D patients, p = 0.022 and 0.0002, respectively, whereas the compaction coefficient was significantly smaller in T2D patients, p = 0.0015. Our results suggest that the fibrin structure was altered in DL and T2D patients, probably due to the increased cholesterol and glycation, respectively.
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PMID:Preliminary study of the fibrin structure in hypertensive, dyslipidemic and type 2 diabetic patients. 2130 90


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