Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemin binds to isolated low-density lipoprotein (LDL) and thereby triggers LDL oxidation. In this study we investigated whether hemin can get together with LDL under physiological conditions. The relative affinity of three blood components to free hemin was as follows: RBCM < LDL < albumin. At physiological molar ratio of LDL/albumin all the hemin was bound to albumin. In molar excess of albumin over hemin, existing even under pathological conditions, albumin served as an efficient antioxidant for the plasma hemin-induced LDL oxidation. RBCM-embedded hemin, unlike plasma hemin, affected LDL: the mobile hemin was transferred from RBCM to LDL in the absence of albumin, whereas in the presence of albumin most of the mobile hemin finally reached the albumin but partially via LDL. Thus, a transient hemin is built up in LDL. This transient hemin triggered LDL oxidation which was not inhibited but rather promoted by albumin. The involvement of albumin in this oxidation was explained by its acting as a pump thereby increasing the transient hemin in LDL. It is suggested that increased membrane hemin level as in hemoglobinopathies and/or excess LDL in dyslipidemia provide conditions for hemin-induced LDL oxidation.
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PMID:The involvement of low-density lipoprotein in hemin transport potentiates peroxidative damage. 754 35

Changed endothelial function and dyslipidemia are features of insulin-dependent diabetes mellitus complicated with clinical nephropathy. The time relationship between the appearance of these abnormalities is however not well known. We have therefore studied the coincidence of microalbuminuria, endothelial dysfunction and dyslipidemia during a 10 year prospective study of 209 insulin-dependent diabetic patients with normal urinary albumin excretion. Twenty-three patients developed progressing microalbuminuria defined as a median urinary albumin excretion > 30 mg/24-h in two consecutive years and a progression rate in albuminuria higher than 5% per year. Thirty patients who remained normoalbuminuric throughout the observation period were randomly selected to obtain a control group with comparable degree of glycaemic control. The mean level of von Willebrand factor before onset of microalbuminuria tended to be higher in patients developing microalbuminuria than in the control group (NS), but there was no increase in von Willebrand factor in the patients who developed microalbuminuria. Total cholesterol did not change, but a significant decrease in high density lipoprotein cholesterol was observed in patients who developed microalbuminuria. In conclusion, the study demonstrated coincidence of microalbuminuria and decreasing high density lipoprotein cholesterol, but no coincidence between onset of microalbuminuria and endothelial dysfunction assessed by von Willebrand factor.
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PMID:Endothelial function and serum lipids in the course of developing microalbuminuria in insulin-dependent diabetes mellitus. 766 35

Clinical factors associated with urinary albumin excretion (UAE) in type II diabetes are less well known than in type I diabetes. To examine the factors associated with UAE in type II diabetes, 933 Appropriate Blood Pressure Control in Diabetes Trial patients were classified according to UAE status: normoalbuminuria (< 20 micrograms/min), microalbuminuria (20 to 200 micrograms/min), and macroalbuminuria (> 200 micrograms/min). The class of UAE was then correlated with various clinical factors. Using univariate analyses, Hispanic ethnicity, African-American race, male gender, poor glycemic control, insulin use, long duration of diabetes, dyslipidemia, diastolic and systolic hypertension, smoking, and obesity were significantly correlated with microalbuminuria and macroalbuminuria. Using multivariate logistic regression analyses controlling for diabetes duration, glycosylated hemoglobin, gender, and race, the most significant predictors of microalbuminuria and macroalbuminuria were systolic hypertension, body mass index, high-density lipoprotein cholesterol, insulin use, and smoking pack-years. Of these factors, several are potentially reversible with aggressive intervention.
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PMID:Clinical factors associated with urinary albumin excretion in type II diabetes. 777 79

Fibric acid derivatives may interact with other drugs and the interactions can be of clinical relevance. The pharmacological properties and effects of these drugs which pertain to their potential for drug interactions, are: (a) a very high binding affinity to plasma proteins, especially albumin; (b) the changes produced in vitamin K kinetics; (c) endoplasmic reticulum hyperplasia; (d) induction of cytochrome P450; (e) changes in xenobiotic-metabolizing enzymes; (f) their capability to have a direct effect on carbohydrate metabolism and/or regulation; and (g) potential pharmacokinetic interactions with antidiabetic drugs. Other types of interactions may affect the safety and/or the therapeutic efficacy of fibrates. These interactions are not necessarily risky, but may be important in the long term. Other clinically relevant interactions with less commonly used drugs have been described. Fibrates will continue to be used because they have proved to be safe and effective in correcting many types of dyslipidemia by reducing serum levels of total cholesterol and triglycerides and by increasing high density lipoprotein cholesterol. Furthermore, they have been proven to decrease morbidity and morality from coronary heart disease. Therefore, awareness of their potential drug interactions is most relevant to their safe clinical therapeutic use.
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PMID:Drug interactions with fibric acids. 780 77

The concept of microalbuminuria is reviewed. Measuring the urinary albumin excretion rate and testing for microalbuminuria is well established in the control and treatment of patients with insulin-dependent diabetes mellitus. Microalbuminuria predicts nephropathy and early cardiovascular death. In the presence of microalbuminuria frequent examinations are warranted for early detection of retinopathy, blood-pressure rise, and for optimizing the glycemic control. In patients with non-insulin-dependent diabetes, the independent value of microalbuminuria as a cardiovascular risk factor is not yet clarified. The urinary albumin excretion rate should be measured at diagnosis, because the indications are that presence of microalbuminuria reinforces the urge to intervene against other well-documented cardiovascular risk factors (hypertension, dyslipidemia, tobacco, and obesity). In the nondiabetic population, there is accumulating evidence that an elevated urinary albumin excretion rate is associated with early cardiovascular morbidity and mortality. Large scale cross-sectional and prospective studies are needed in order to clarify further the role of microalbuminuria as an independent risk factor in the background population.
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PMID:Microalbuminuria: an important diagnostic tool. 808 48

Twenty-nine patients with insulin-dependent diabetes mellitus with similarly manifest renal involvement were examined to elucidate the role of dyslipidemia in diabetic nephropathy progress. Clinico-laboratory parameters (urinary albumin excretion, blood serum levels of total cholesterol, triglycerides, low, very low, and high density lipoprotein cholesterol) and morphologic changes in renal tissue biopsy specimens were analyzed. An increment of the number of large lipid incorporations was observed in various cells of renal glomeruli and interstitium, as well as a high prevalence of low density lipoprotein deposition in glomerular basal membranes and canaliculi as the renal process augmented in severity. Since lipids accumulating in glomerular structures may stimulate mesangial cell proliferation and mesangial matrix hyperproduction, the authors believe that dyslipidemia in diabetes mellitus may be conducive to a more rapid progress of renal disease.
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PMID:[Hyperlipidemia as a factor in the development and progress of diabetic nephropathy]. 810 57

Several studies have indicated that insulin resistance, elevated blood pressure (BP), and dyslipidemia precede the onset of non-insulin-dependent diabetes mellitus (NIDDM). Little data, however, exist on the presence of renal disease in prediabetic subjects. We measured albumin excretion in a cross-sectional population study in subjects 65-74 years of age living in eastern Finland in relation to the risk of developing diabetes 3.5 years later. The prevalence of microalbuminuria (urinary albumin-to-urinary creatinine ratio > or = 2 mg/mmol) was 1.3-, 1.8-, and 2.0-fold higher among subjects with impaired glucose tolerance (n = 242), newly diagnosed NIDDM subjects (n = 92), and previously diagnosed NIDDM subjects (n = 136), respectively, compared with subjects with normal glucose tolerance (n = 826). Nondiabetic subjects with microalbuminuria had multiple abnormalities in cardiovascular risk factors including elevated BP, high triglyceride concentration, high insulin concentration, and a low high-density lipoprotein cholesterol concentration, a cluster of risk factors typical for prediabetic individuals. The relationship between microalbuminuria and the incidence of NIDDM over the 3.5-year follow-up was studied in 891 subjects who were free of diabetes at baseline. Converters to diabetes (n = 69) had a higher prevalence of hypertension (68.1 vs. 54.4%, P < 0.05) and a higher prevalence of microalbuminuria (43.5 vs. 30.4%, P < 0.05) than nonconverters (n = 822). In logistic regression analysis, microalbuminuria predicted the development of NIDDM independently of BP level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microalbuminuria precedes the development of NIDDM. 813 60

Hyperinsulinemia, insulin resistance, or both have been described in patients with essential hypertension. Previous work from our laboratory has shown that in hypertensive patients with microalbuminuria, dyslipidemia and abnormal patterns in the diurnal variations of blood pressure are frequently associated. Whether hyperinsulinemia and microalbuminuria are directly related has not been determined. To test this possibility, we measured the plasma insulin response to an oral glucose load in 25 patients with or without microalbuminuria and 20 normotensive control subjects. Serum lipid profile and 24-hour ambulatory blood pressure were obtained. In the hypertensive patients as a group, the plasma insulin response to glucose (evaluated as the insulin area under the curve) was significantly enhanced compared with a group of 20 normotensive healthy control subjects (46,311 +/- 3745 and 27,557 +/- 2563 pmol/L x 2 hours, P < .01). When the hypertensive patients were subdivided according to their albumin excretion rate, the microalbuminuric patients had significantly higher plasma glucose (969 +/- 45.2 versus 762 +/- 28.7 mmol/L x 2 hours, P < .01) and insulin (59,172 +/- 5964 versus 37,737 +/- 3422 pmol/L x 2 hours, P < .01) area under the curve values. In addition, a significant direct correlation was found to exist between insulin area under the curve and the urinary albumin excretion rate (r = .63, P < .001). Serum levels of lipoprotein(a) were significantly greater (P < .01) in patients with than in those without microalbuminuria and in control subjects. Furthermore, daytime diastolic blood pressure and nighttime systolic and diastolic blood pressure values were greater in patients with than in those without microalbuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated serum insulin levels in patients with essential hypertension and microalbuminuria. 820 63

The concept of microalbuminuria is reviewed. Measuring the urinary albumin excretion rate and testing for microalbuminuria is well established in the control and treatment of patients with insulin-dependent diabetes mellitus. Microalbuminuria predicts nephropathy and early cardiovascular death. In the presence of microalbuminuria, frequent examinations are warranted for early detection of retinopathy, hypertension and for optimizing the glycaemic control. In patients with non-insulin dependent diabetes, the independent value of microalbuminuria as a cardiovascular risk factor is not yet clarified. The urinary albumin excretion rate should be measured at diagnosis, because the indications are that presence of microalbuminuria reinforces the urge to intervene against other well-documented cardiovascular risk-factors (hypertension, dyslipidemia, tobacco and obesity). In the non-diabetic population there is accumulating evidence that an elevated urinary albumin excretion rate is associated with early cardiovascular morbidity and mortality. Large scale cross-sectional and prospective studies are needed in order to further clarify the role of microalbuminuria as an independent risk factor in the background population.
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PMID:[Microalbuminuria--a valuable diagnostic parameter]. 827 36

Dyslipidemia is an important risk factor for atherosclerotic vascular disease. Serum lipoprotein (a) [Lp(a)] has been implicated as an independent atherogenic risk factor. We measured serum (Lp(a) levels in our patients and studied its correlations with other lipoproteins and clinical parameters. All stable patients on continuous ambulatory peritoneal dialysis (CAPD) for more than one month were enrolled in the study. Fasting serum Lp(a), total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol, apolipoprotein-A and apolipoprotein-B levels were measured on entering the CAPD program and at 3 monthly intervals. One hundred and nine patients (M/F: 65/44, mean age +/- SD: 59.5 +/- 12.0 years) were studied. Fifty-two patients had diabetes mellitus. Age- and sex-matched normals were used as controls. Serum Lp(a) levels were raised in 54.5% of CAPD patients compared to 18.6% of controls (p < 0.01). There was no significant change in Lp(a) levels over time. Serum Lp(a) levels showed positive and negative correlations with LDL-cholesterol and triglycerides, respectively, but not with age, sex, diabetic status, and serum total cholesterol and albumin levels. Thirty-six of 54 (66.7%) patients with serum Lp(a) levels greater than 30 mg/dL had either coronary, cerebral, and/or peripheral vascular disease compared to 30/55 (54.5%) of patients with serum Lp(a) levels less than 30 mg/dL (p = NS). In conclusion, serum Lp(a) levels were raised in a significant proportion of CAPD patients, but there was no significant association with vascular disease.
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PMID:Lipoprotein (a) levels and clinical correlations in CAPD patients. 853 86


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