Lipid Profile (lipid + profile)

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Lipid Profile

  • atherogenic lipid profile
  • blood lipid profile
  • plasma lipid profile
  • serum lipid profile


  • Selected Abstracts


    Ozonated Autohemotherapy in Patients on Maintenance Hemodialysis: Influence on Lipid Profile and Endothelium

    ARTIFICIAL ORGANS, Issue 2 2004
    Leszek Tylicki
    Abstract:, Ozonated autohemotherapy (O3-AHT) is used in the treatment of atherosclerotic ischemia of lower limbs (AILL). The impact of ozone on serum lipids and endothelium injury is of particular interest since these factors are important in the development of atherosclerotic lesions. To evaluate this issue, a prospective, placebo-controlled study was designed. Twelve hemodialyzed subjects with AILL received autohemotherapy with oxygen as a control followed by O3-AHT with ozone concentration of 50 µg/ml. Serum lipids and plasma activity of von Willebrand factor (vWF) were measured. After O3-AHT, total cholesterol significantly decreased compared to the baseline (,8.34%) [P < 0.01]. LDL cholesterol was also significantly lower than the initial value (,17.71%) [P < 0.001]. No significant changes in the activity of vWF were found after the first session of O3-AHT and after all nine sessions of O3-AHT. The study demonstrated that O3-AHT did not affect deleteriously the endothelium in patients with chronic renal failure on maintenance hemodialysis. It ,may stimulate beneficial changes in serum lipid profile manifesting as,,a, decrease ,in the total- and LDL-cholesterol ,levels. [source]


    Effects of Rutin on Lipid Profile in Hypercholesterolaemic Rats

    BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2009
    Amir Ziaee
    Rutin is found in many plants and is also an important dietary constituent of food and plant-based beverages. Rutin has several pharmacological properties including antioxidant and cardioprotective activities. Also, it was identified that rutin is the major low-density lipoprotein (LDL) antioxidant compound of mulberry in an in vitro study. The effects of rutin were tested by using it as a supplement in a high-cholesterol diet. Male rats were fed a high-cholesterol diet (1 ml/100 g) for 4 weeks with rutin (10 or 100 mg/kg) or rutin 100 mg/kg and lovastatin supplementation to study the hypocholesterolaemic effects of rutin on plasma lipid levels, hepatic enzyme activity, and liver tissue. Feeding the animals a high-cholesterol diet resulted in marked hypercholesterolaemia and increased the serum level of LDL cholesterol (LDL-C). Rutin (at 100 mg/kg) alone or in combination with lovastatin significantly reduced the levels of total cholesterol, and LDL-C and also markedly decreased liver enzymes and weight in animals with a high-cholesterol diet. Our findings show that 100 mg/kg of rutin alone or with lovastatin supplementation lowered liver weight and enzymes as well as plasma total cholesterol and LDL. The hepatic histopathological results reflect the correlation of rutin and lovastatin combination with both liver weight and the levels of plasma total cholesterol and LDL-C. These results indicate that rutin in combination with lovastatin has increased anti-hypercholesterolaemic effects in an animal model. [source]


    Epidemiological Association between Uric Acid Concentration in Plasma, Lipoprotein(a), and the Traditional Lipid Profile

    CLINICAL CARDIOLOGY, Issue 2 2010
    Giuseppe Lippi MD
    Abstract Background Elevated levels of uric acid in serum (SUA) or plasma (PUA) are increasingly related to cardiovascular disease. It is unclear whether they are independent risk factors or simply markers, reflecting association with other traditional risk factors. Methods We retrospectively assessed results of a lipid profile, including total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, total cholesterol to HDL-C ratio (TC/HDL-C), the atherogenic index of plasma (AIP), and lipoprotein(a) (Lp[a]), in a large cohort of unselected adult outpatients. Results Hyperuricemic men displayed significantly increased values of triglycerides and AIP when compared with men with normal PUA levels. In hyperuricemic women, significant differences were observed for HDL-C, triglycerides, TC/HDL-C, and AIP compared with women with normal PUA levels. The percentage of patients with unfavorable values was statistically higher for triglycerides and AIP in hyperuricemic men; for HDL-C, triglycerides, TC/HDL-C, and AIP in hyperuricemic women. In multivariable linear regression analysis triglycerides, AIP, and TC/HDL-C were independently associated with PUA in women, whereas no significant association was observed in men. Conclusion PUA measurement might be advisable in patients to identify those at increased risk of cardiovascular disease (CVD) who might benefit from further triage and intervention. Copyright © 2010 Wiley Periodicals, Inc. [source]


    Chinese Cabbage (Brassica campestris L.) does not Improve Glucose Tolerance, Serum Insulin, or Blood Lipid Profiles in a Rat Model of Type-2 Diabetes

    JOURNAL OF FOOD SCIENCE, Issue 9 2008
    M.S. Islam
    ABSTRACT:, The present study was conducted to investigate the effects of a low (0.5%) and a high (2.0%) dietary dose of freeze-dried Chinese cabbage (CC) (Brassica campestris L.) powder in a type-2 diabetes (T2D) model of rats. Five-week-old male Sprague,Dawley rats were fed a high fat (HF)-containing diet for 2 wk then randomly divided into 4 groups of 8 animals, namely: normal control (NC), diabetic control (DBC), Chinese cabbage low (CCL, 0.5%), and Chinese cabbage high (CCH, 2.0%) groups. Diabetes was induced by an intraperitoneal injection of streptozotocin (STZ; 40 mg/kg body weight) in all groups except the NC group. After 4 wk feeding of experimental diets, although food intake was not different among the DBC, CCL, and CCH groups, body weight gain was significantly (P < 0.05) higher in the CCH group compared to the DBC group. Relatively higher serum insulin concentrations and better glucose tolerance were observed in the CC-fed groups compared to the DBC group; however, the results were not significantly different. Fasting blood glucose, blood glycated hemoglobin (HbA1c), liver weight, and liver glycogen levels were not influenced by the CC-containing diets. Additionally, hypertriglyceridemic tendencies were observed in the CC-fed groups compared to the NC and DBC groups, while difference observed for total-, HDL-, and LDL-cholesterols between the groups were negligible. Results of this study suggest that up to 2% dietary dose of freeze-dried CC is not significantly effective to reduce diabetes-related symptoms in an HF diet-fed STZ-induced T2D model of rats. [source]


    The Long-Term Effects of Feeding Honey Compared with Sucrose and a Sugar-Free Diet on Weight Gain, Lipid Profiles, and DEXA Measurements in Rats

    JOURNAL OF FOOD SCIENCE, Issue 1 2008
    L. Chepulis
    ABSTRACT:, To determine whether honey and sucrose would have differential effects on weight gain during long-term feeding, 45 2-mo-old Sprague Dawley rats were fed a powdered diet that was either sugar-free or contained 7.9% sucrose or 10% honey ad libitum for 52 wk (honey is 21% water). Weight gain was assessed every 1 to 2 wk and food intake was measured every 2 mo. At the completion of the study blood samples were removed for measurement of blood sugar (HbA1c) and a fasting lipid profile. DEXA analyses were then performed to determine body composition and bone mineral densities. Overall weight gain and body fat levels were significantly higher in sucrose-fed rats and similar for those fed honey or a sugar-free diet. HbA1c levels were significantly reduced, and HDL-cholesterol significantly increased, in honey-fed compared with rats fed sucrose or a sugar free diet, but no other differences in lipid profiles were found. No differences in bone mineral density were observed between honey- and sucrose-fed rats, although it was significantly increased in honey-fed rats compared with those fed the sugar-free diet. [source]


    Effect of long-term treatment with rosiglitazone on arterial elasticity and metabolic parameters in patients with Type 2 diabetes mellitus: a 2-year follow-up study

    DIABETIC MEDICINE, Issue 11 2007
    M. Shargorodsky
    Abstract Aims, Thiazolidinediones may influence the atherogenic process by improving cardiovascular risk factors. The present study was designed to determine the long-term effect of rosiglitazone on arterial compliance and metabolic parameters in patients with Type 2 diabetes. Methods, In an open-label, prospective study, 65 diabetic patients received rosiglitazone orally (4,8 mg/day) for 6 months. After 6 months, the patients continued an open follow-up study and were divided into two groups: group 1 included patients continuing rosiglitazone for 2 years, group 2 included patients discontinuing rosiglitazone and receiving other oral glucose-lowering agents. Lipid profile, glycated haemoglobin (HbA1c), insulin, C-peptide, fibrinogen, high-sensitivity-CRP and homeostasis model assessment,insulin resistance were measured. Arterial elasticity was assessed using pulse wave contour analysis. Results, In patients treated with rosiglitazone for 2 years: the large artery elasticity index (LAEI) increased from 10.0 ± 4.6 to 13.9 ± 4.7 ml/mmHg × 100 after 2 years (P = 0.003). The small artery elasticity (SAEI) index increased significantly from 3.2 ± 1.2 to 5.1 ± 1.9 (P < 0.0001). In patients who discontinued rosiglitazone: LAEI did not change after 6 months, but decreased from 12.1 ± 5.4 to 8.9 ± 3.9 ml/mmHg × 10 (P < 0.0001) at the end of 2 years. SAEI increased during the first 6 months of treatment, from 3.9 ± 1.8 to 5.1 ± 1.5 ml/mmHg × 100 (P < 0.0001) and decreased after discontinuation of rosiglitazone (P = 0.042). Conclusions, Prolonged treatment with rosiglitazone improved arterial elasticity. However, significant deterioration in LAEI and SAEI was observed in patients who discontinued rosiglitazone. The beneficial vascular effect of rosiglitazone on arterial elasticity was independent of glycaemic control. [source]


    Association of the ,2 Allele of Apoe Gene to Hypertriglyceridemia and to Early-Onset Alcoholic Cirrhosis

    ALCOHOLISM, Issue 4 2008
    Zamira H. Hernández-Nazará
    Background:, The diverse incidence of alcoholic cirrhosis around the world and the fact that not all alcoholic drinkers develop liver disease indicates that genetic and environmental factors play an important role in the development of liver cirrhosis. Lipids participate in early stages of alcoholic cirrhosis. Therefore variations in the plasma lipid profile due to primary (genetic) or secondary (environmental) dyslipidemia could affect the development of liver disease. The aim of this study was to analyze the lipid profile and apolipoprotein E (APOE) polymorphism in patients with alcoholic liver cirrhosis (AC) and determine the risk associated with genotype polymorphism with the onset of alcoholic cirrhosis. Methods:, In a case and control study, 86 patients with AC divided into hyperlipidemic (H) and non-hyperlipidemic (non-H) groups, and 133 healthy individuals (C) matched by age and sex were studied. Lipid profile and liver function tests were measured by enzymatic methods. The APOE genotypes were identified by PCR-RFLP,s. Results:, A statistically significant increase of the APOE*2 allele and genotypes 2/2, 2/3, and 2/4 was present in AC patients compared to C group. A hyperlipidemic state characterized by increased levels of triglycerides and apolipoprotein B (APOB) and a decrease of high density lipoprotein-cholesterol (HDL-c) was detected in young-aged patients (31.2 ± 6.2 years old vs. 46.3 ± 12.5 years old). In this group, hypertriglyceridemia was closely associated to APOE*2 allele and to an early onset of liver cirrhosis. By contrast, APOE*4 allele was associated with a longer duration of alcohol intake (>20 years) in the non-H group. Conclusions:, This study shows the association of hypertriglyceridemia and APOE allele with the early onset of alcoholic liver cirrhosis, and the interaction between environmental factors, such as duration of alcohol abuse and amount of alcohol intake, and genetic factors (APOE*2 allele) on the hypertriglyceridemic process. [source]


    Lipid profile in patients with psoriasis in Zahedan, south-east Iran

    JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 4 2009
    M Hashemi
    [source]


    Effects of 10 years of growth hormone (GH) replacement therapy in adult GH-deficient men

    CLINICAL ENDOCRINOLOGY, Issue 3 2005
    Lucia I. Arwert
    Summary Objective, GH-deficient adults have changes in body composition, bone mineral density (BMD) and lipid profile that can be altered by GH substitution. However, long-term data on GH substitution (up to 10 years of follow-up) are limited. Design, The effects of 10 years of GH replacement therapy on BMD, body composition, bone parameters, serum lipids and glucose metabolism were studied. Patients, Twenty-three childhood-onset GH-deficient men (mean age at baseline 28·6 years) were studied during 10 years of GH substitution therapy. A group of 19 age-matched healthy men served as a control group for BMD measurements at baseline and after 10 years. Results, BMD of the lumbar spine increased during the 10 years of GH therapy. Bone markers and BMD in the hip increased during the first 5 years of GH therapy, but were not different from baseline after 10 years. BMD changes over time in the lumbar spine and femoral neck were significantly different in the patients compared to the controls. After 10 years the difference between the groups had decreased, but BMD was still higher in the controls than in the patients. Lipid profile had improved after 10 years of GH therapy, but body mass index (BMI), waist,hip ratio (WHR), fasting glucose and glycosylated haemoglobin (HbA1c) had increased compared to baseline. Conclusions, This long-term follow-up study found that 10 years of GH substitution in GH-deficient men causes sustained improvements in BMD in the lumbar spine and lipid profile but not in body composition. [source]


    High HDL-cholesterol in women with rheumatoid arthritis on low-dose glucocorticoid therapy

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2008
    C. García-Gómez
    ABSTRACT Background, Dyslipidaemia has been described in non-treated rheumatoid arthritis (RA), and improves after therapy with disease modifying anti-rheumatic drugs or glucocorticoids; however, it has generally been perceived that glucocorticoids adversely affect lipid metabolism. The association of low dose glucocorticoid therapy with plasma lipid levels was evaluated in female RA patients. Materials and methods, A cross-sectional study was conducted in 78 female RA patients [mean age: 60 (12) years; mean disease duration: 13 (9) years]. Sixty-five (83%) were on glucocorticoid therapy [total equivalent mean prednisone dose: 5·1 (1·7) mg d,1]. Each patient was assessed through a self-reported questionnaire, structured interview and physical examination. Blood samples were obtained for routine biochemistry, lipid profile and haematological tests. Lipid profiles of RA patients who were and were not on glucocorticoid therapy were compared. Results, Clinical and laboratory features of the two groups of patients were similar, except for the Health Assessment Questionnaire and body mass index, which were significantly higher in the patients on glucocorticoid therapy. These patients had 14·7% higher serum high-density lipoprotein cholesterol (HDL-c) levels than untreated patients (P = 0·043), mainly at the expense of HDL2 subfraction, which was 24·4% higher (P < 0·039), whereas HDL3-c was only 7·4% higher (P = 0·219). Serum levels of glucose and total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL -c), very low-density lipoprotein cholesterol, apolipoproteins A-I and B were not increased in patients on glucocorticoid therapy. Conclusions, Low dose glucocorticoid therapy in RA patients is associated with an increase in HDL-c, without increasing LDL-c or triglyceride. These lipid changes may overall be considered favourable. [source]


    The effects of soy protein containing isoflavones on lipids and indices of bone resorption in postmenopausal women

    CLINICAL ENDOCRINOLOGY, Issue 6 2003
    Fabien S. Dalais
    Summary objective To assess the effect of a dietary soy protein supplement containing isoflavones on lipids and indices of bone resorption in postmenopausal women. design Placebo-controlled, double-blind, randomized study. patients One hundred and six postmenopausal women were randomized to dietary soy supplementation (n = 51) or placebo (n = 55) for 3 months, of which 78 were included in the final analysis. measurements Lipid profiles including total, low-density lipoprotein (LDL) and HDL cholesterol as well as triacylglycerol were measured. Pyridinoline and deoxypyridinoline were used as markers of bone resorption. Urinary isoflavone excretion was measured to assess compliance. results There was a significantly greater increase in urinary isoflavone excretion detected in the soy group compared to placebo. Lipid profiles improved with significant decreases in LDL cholesterol (,0·60 ± 0·10 vs.,0·29 ± 0·09 mmol/l, P < 0·05), triacylglycerol (,0·22 ± 0·07 vs. +0·01 ± 0·05 mmol/l, P < 0·005) and the LDL : HDL ratio (,0·32 ± 0·10 vs. +0·20 ± 0·10, P < 0·005) in the soy group compared to placebo. There were no significant differences between the soy and placebo groups for urinary excretion of pyridinoline (,3·8 ± 3·1 vs.,0·8 ± 3·1 nmol/mmolCr, P = 0·4) or deoxypyridinoline (,0·8 ± 0·9 vs.,0·3 ± 0·7 nmol/mmolCr, P = 0·4). conclusions In postmenopausal women, dietary supplementation with soy protein containing isoflavones does not appear to have oestrogenic effects on markers of bone resorption. Soy protein favourably affected lipids; however, these effects (fall in triacylglycerol and no change in HDL) differ from those observed with oral oestrogen. These findings suggest that soy may not have biologically significant oestrogenic effects on bone resorption and we hypothesize that the lipid effects may be mediated, at least in part, through nonoestrogenic mechanisms. [source]


    Lipid profiles in untreated severe congenital isolated growth hormone deficiency through the lifespan

    CLINICAL ENDOCRINOLOGY, Issue 1 2002
    Helena K. Gleeson
    Summary objective Growth hormone deficiency (GHD) is associated with adverse changes in lipid profile. However, changes in lipids through life in a homogeneous group of GHD subjects have not been defined. patients and measurements We examined lipid levels in a group of untreated severely GHD patients with a mutation in the GHRH receptor gene from a rural community in North-east Brazil. Lipid profiles in 15 GHD subjects [eight children and adolescents (one male), age (median [range]) 13·2 (5·4,19·9) years; seven adults (one male), age 47 (33,66) years] were compared with those in 29 indigenous controls from the same extended kindred [17 children and adolescents (six male), age 10·2 (5·3,18·4) years; 12 adults (eight male), age 54·5 (33,80) years]. All GHD subjects had a peak GH response of < 0·5 ng/ml in response to an insulin tolerance test and extremely reduced IGF-1 levels (median 5·5 ng/ml). Data were compared between cohorts and with an age- and sex-matched white American reference population. results Abnormalities were confined to plasma total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels. More GHD children had levels of plasma TC and LDL-C above the 95th percentile for our reference population (3/8 and 4/7, respectively) compared to controls (0/17 and 1/15, respectively) (P < 0·05). In the adults, median TC and LDL-C levels were higher in the GHD than controls (P < 0·05) (6·3 vs. 4·1 mmol/l; 4·4 vs. 2·7 mmol/l, respectively). Median Z -scores, calculated using values from the reference population, were not different between GHD children and adults for both TC (+0·8 vs.+0·4) and LDL-C (+1·4 vs.+0·7). conclusions The lipid profile in children as well as in adults with very severe GHD is adversely modified. There would appear to be no significant worsening of the lipid abnormality with duration of GHD or achievement of adulthood. [source]


    Exenatide: a review from pharmacology to clinical practice

    DIABETES OBESITY & METABOLISM, Issue 6 2009
    R. Gentilella
    Background:, Exenatide is an incretin mimetic that activates glucagon-like-peptide-1 receptors. It blunts the postprandial rise of plasma glucose by increasing glucose-dependent insulin secretion, suppressing inappropriately high glucagon secretion and delaying gastric emptying. Methods:, In seven clinical trials performed in 2845 adult patients with type 2 diabetes mellitus who were inadequately controlled by a sulphonylurea and/or metformin (glycosylated haemoglobin, HbA1c ,11%), or by thiazolidinediones (with or without metformin) and treated for periods from 16 weeks to 3 years, exenatide (5 ,g b.i.d. s.c. for the first 4 weeks of treatment and 10 ,g b.i.d. s.c. thereafter) reduced HbA1c, fasting and postprandial glucose, and body weight dose dependently, and was similar to insulin glargine and biphasic insulin aspart in reducing HbA1c. Body weight diminished with exenatide, whereas it increased with both insulin preparations. Positive effects on the lipid profile and a reduction in C-reactive protein were also recorded with exenatide. Treatment extensions up to 3 years showed that benefits were maintained in the long term. Adverse events were usually mild to moderate in intensity, and generally the frequency decreased with continued therapy. The most common was nausea (whose incidence may be reduced by gradual dose escalation from 5 ,g b.i.d. to 10 ,g b.i.d.), vomiting, diarrhoea, headache and hypoglycaemia (almost exclusively in patients treated with a sulphonylurea). Results and conclusions:, Exenatide is a new, promising therapeutic option for type 2 diabetic patients inadequately controlled by oral agents, before insulin therapy, offering the added benefits of body weight reduction and tight postprandial glucose control. [source]


    Effects of cevoglitazar, a dual PPAR,/, agonist, on ectopic fat deposition in fatty Zucker rats

    DIABETES OBESITY & METABOLISM, Issue 6 2009
    D. Laurent
    Aim:, By acting as both insulin sensitizers and lipid-lowering agents, dual-acting peroxisome proliferator-activated receptors ,/, (PPAR,/,) agonists may be used to improve glucose tolerance in type 2 diabetic patients without inducing adiposity and body weight gain. Here, in an animal model of obesity and insulin resistance, the metabolic response to cevoglitazar, a dual PPAR,/,, was characterized using a combination of in vivo and ex vivo magnetic resonance methodologies and compared to treatment effects of fenofibrate, a PPAR, agonist, and pioglitazone, a PPAR, agonist. Methods:, Four groups of fatty Zucker rats: (i) Vehicle; (ii) fenofibrate 150 mg/kg; (iii) pioglitazone 30 mg/kg; and (iv) cevoglitazar 5 mg/kg were investigated before and after treatment. Animals were fed a fat-enriched (54% kcal fat) diet for 6 weeks, 2 weeks high of fat,exposure alone followed by a 4-week dosing period. Results and conclusions:, Cevoglitazar was as effective as pioglitazone at improving glucose tolerance. However, unlike pioglitazone, both fenofibrate and cevoglitazar reduced BW gain and adiposity, independent of food intake. All three treatment regimens normalized intramyocellular lipids. Metabolic profiling showed that in the muscle cevoglitazar improves the lipid profile via both PPAR,- and PPAR,-mediated mechanisms. Pioglitazone reduced hepatic lipid accumulation, while cevoglitazar and fenofibrate reduced hepatic lipid concentration below baseline levels (p < 0.05). Metabolic profiling showed that in the liver, cevoglitazar functions largely through PPAR, agonism resulting in increased ,-oxidation. Cevoglitazar only induced small changes to the lipid composition of visceral fat. In subcutaneous fat, however, cevoglitazar induced changes similar to those observed with fenofibrate suggesting export of fatty acids from this depot. [source]


    Elevated C-reactive protein in Native Canadian children: an ominous early complication of childhood obesity

    DIABETES OBESITY & METABOLISM, Issue 5 2006
    R. Retnakaran
    Aim:, Subclinical inflammation has been proposed as a pathophysiologic mechanism linking obesity with vascular and metabolic disease. Native North American populations are experiencing high prevalence rates of both (i) childhood obesity and (ii) adult cardiovascular disease (CVD) and type 2 diabetes. Thus, we sought to determine whether subclinical inflammation is an early complication of obesity in Native children. Methods:, Serum concentrations of the inflammatory biomarker C-reactive protein (CRP) were assessed in a population-based, cross-sectional study of the Sandy Lake Oji-Cree community of Northern Ontario, Canada, involving 228 children aged 10,19 years (mean age 14.8). Results:, Median CRP in this population was 0.5 mg/l (interquartile range 0.18,1.79 mg/l). CRP levels were higher than age-matched reference data from the Third National Health and Nutrition Examination Survey (NHANES III). Importantly, fully 15.8% of the children of this community had CRP concentrations between 3 and 10 mg/l, a range that identifies adults at high risk of CVD. Moreover, increasing CRP concentration in this paediatric population was associated with an enhanced CV risk profile, consisting of increased adiposity, higher insulin resistance, worsening lipid profile (higher total cholesterol, triglycerides, low-density lipoprotein cholesterol, apolipoprotein B and total cholesterol : high-density-lipoprotein cholesterol ratio), increased leptin and decreased adiponectin. On multivariate analysis, waist circumference and interleukin-6 (IL-6) emerged as independent determinants of CRP concentration. Conclusion:, Subclinical inflammation is an early complication of childhood obesity in Native children and may foreshadow an increased burden of CVD and type 2 diabetes in the future. [source]


    Insulin resistance , a common link between type 2 diabetes and cardiovascular disease

    DIABETES OBESITY & METABOLISM, Issue 3 2006
    Harold E. Lebovitz
    Evidence suggests that diabetes and cardiovascular disease (CVD) may share an underlying cause(s), a theory known as the ,common soil' hypothesis. Insulin resistance is central both to the progression from normal glucose tolerance to type 2 diabetes and to a constellation of cardiovascular risk factors known as the metabolic syndrome. These risk factors include visceral obesity and dyslipidaemia characterized by low levels of high-density lipoprotein cholesterol, hypertriglyceridaemia and raised small dense low-density lipoprotein particle levels. Changes in adipose tissue mass and metabolism may link insulin resistance and visceral obesity, a condition that is common in type 2 diabetes. Furthermore, weight reduction, increased physical activity, metformin and acarbose have been shown to reduce the development of type 2 diabetes in genetically predisposed subjects and may decrease the high cardiovascular risk of patients with diabetes. Some fatty acid derivatives can affect energy metabolism by activating peroxisome proliferator-activated receptors (PPARs), nuclear receptors that play a key role in energy homeostasis. These receptors represent an ideal therapeutic target for reducing cardiovascular risk, because they are involved in the regulation of both insulin action and lipid metabolism. In addition to lifestyle changes, PPAR, agonists such as thiazolidinediones are frequently beneficial and have been shown to ameliorate insulin resistance, while activation of PPAR, (e.g. by fibrates) can lead to improvements in free fatty acid oxidation and lipid profile, and a reduction in cardiovascular events. The development of agents with both PPAR, and PPAR, activity promises added benefits with amelioration of insulin resistance, delayed progression to and of type 2 diabetes and a reduction of CVD. [source]


    Effect of ABCA1 variant on atherogenic dyslipidaemia in patients with Type 2 diabetes treated with rosiglitazone

    DIABETIC MEDICINE, Issue 6 2009
    S. E. Park
    Abstract Aims, To investigate the effect of two common ATP-binding cassette transporter 1 (ABCA1) polymorphisms (rs4149263 and rs2020927) on atherogenic dyslipidaemia in Korean Type 2 diabetic patients who were treated with rosiglitazone. Patients and methods, Two hundred and fifty-six patients with Type 2 diabetes who had never previously received peroxisome proliferator-activated receptor gamma (PPAR-,) agonists or lipid-lowering treatment were treated with 4 mg of rosiglitazone daily for 12 weeks without any adjustment to their glucose-lowering regimen. The primary outcome was the change in atherogenic index of plasma (AIP), calculated as log [triglyceride (mmol/l)/high-density lipoprotein cholesterol (mmol/l)], before and after rosiglitazone treatment. The effect of rosiglitazone on the change in AIP was compared across the ABCA1 single nucleotide polymorphisms (SNPs) rs41429263 and rs2020927. Results, Before adjustment, the change in AIP at 12 weeks was significantly different across the rs4149263 genotypes [median (interquartile range): ,0.05 (,0.21, 0.09) for TT; 0.02 (,0.09, 0.17) for TC; and 0.11 (0.03, 0.25) for CC; P = 0.003], but not across the rs2020927 [,0.04 (,0.18, 0.10) for TT; 0.03 (,0.17, 0.15) for TC; and ,0.03 (,0.13, 0.10) for CC; P = 0.401]. After controlling for age, gender and duration of diabetes, the presence of the C-allele was significantly associated with an increase in AIP by 0.13 [95% confidence interval (CI), 0.04,0.21; P = 0.003]. This association did not change significantly when body mass index and pretreatment metabolic parameters were additionally controlled for (the change in AIP: 0.14; 95% CI, 0.04,0.24; P = 0.007). Conclusions, The ABCA1 SNP rs4149263 may be associated with the change in atherogenic lipid profile in Type 2 diabetes treated with rosiglitazone. [source]


    Growth and Lipid Metabolism in Girls and Young Women with Epilepsy during Pubertal Maturation

    EPILEPSIA, Issue 7 2005
    Kirsi Mikkonen
    Summary:,Purpose: To assess growth and the serum lipid profile in girls with epilepsy receiving monotherapy at a mean age of 12.6 years and approximately 6 years later. Methods: A population-based cohort of 77 girls with epilepsy and 49 healthy controls participated in this follow-up study including two cross-sectional evaluations (age range, 8,18.5 years on the first evaluation, and 12.5,25.8 years on the second evaluation). Forty of the patients were initially taking valproate (VPA), 19, carbamazepine (CBZ), and 18, oxcarbazepine (OXC). Growth data were compiled, body mass index (BMI) was calculated, and serum total (TC), and high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) cholesterol and triglyceride concentrations were analyzed. Results: Linear growth and final height did not differ between the patients and the controls. At follow-up, the mean BMI of the patients who were off medication (61%) was similar to that of the controls, whereas the patients initially treated with VPA who were still taking any medication had a higher BMI. On the first evaluation, the patients taking VPA had low serum HDL-C, and those taking CBZ or OXC had high serum TC and LDL-C concentrations. At follow-up, serum lipid levels were similar in the patients off medication and the controls. Conclusions: Neither epilepsy nor antiepileptic therapy affects linear growth or final height, but they may have unfavorable effects on body weight and serum lipid concentrations. Lipid-profile impairment seems to be transient if the medication is discontinued. Overweight is common in patients treated with VPA during puberty if epilepsy and medication continue into adulthood. [source]


    Low-dose glucocorticoid therapy and lipid profile

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2009
    C. Garcia-Gómez
    No abstract is available for this article. [source]


    High HDL-cholesterol in women with rheumatoid arthritis on low-dose glucocorticoid therapy

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2008
    C. García-Gómez
    ABSTRACT Background, Dyslipidaemia has been described in non-treated rheumatoid arthritis (RA), and improves after therapy with disease modifying anti-rheumatic drugs or glucocorticoids; however, it has generally been perceived that glucocorticoids adversely affect lipid metabolism. The association of low dose glucocorticoid therapy with plasma lipid levels was evaluated in female RA patients. Materials and methods, A cross-sectional study was conducted in 78 female RA patients [mean age: 60 (12) years; mean disease duration: 13 (9) years]. Sixty-five (83%) were on glucocorticoid therapy [total equivalent mean prednisone dose: 5·1 (1·7) mg d,1]. Each patient was assessed through a self-reported questionnaire, structured interview and physical examination. Blood samples were obtained for routine biochemistry, lipid profile and haematological tests. Lipid profiles of RA patients who were and were not on glucocorticoid therapy were compared. Results, Clinical and laboratory features of the two groups of patients were similar, except for the Health Assessment Questionnaire and body mass index, which were significantly higher in the patients on glucocorticoid therapy. These patients had 14·7% higher serum high-density lipoprotein cholesterol (HDL-c) levels than untreated patients (P = 0·043), mainly at the expense of HDL2 subfraction, which was 24·4% higher (P < 0·039), whereas HDL3-c was only 7·4% higher (P = 0·219). Serum levels of glucose and total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL -c), very low-density lipoprotein cholesterol, apolipoproteins A-I and B were not increased in patients on glucocorticoid therapy. Conclusions, Low dose glucocorticoid therapy in RA patients is associated with an increase in HDL-c, without increasing LDL-c or triglyceride. These lipid changes may overall be considered favourable. [source]


    Genetic influence in antithrombotic actions of atorvastatin in hypercholesterolaemia

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2008
    L. Puccetti
    ABSTRACT Background, Recent data indicate that statins could offer coronary artery disease (CAD) benefit even by mechanisms beyond lipid lowering. Genetic influence has been shown for some antithrombotic actions of statins via oxidized-low-density lipoprotein cholesterol (ox-LDL) receptors and nitric oxide synthase (NOS) activity modulation. The present study was designed to evaluate the influence of ox-LDL lectin-like receptor-1 (LOX-1) and NOS polymorphisms in the incidence of cardiovascular events in pure hypercholesterolaemic subjects during statin treatment. Materials and methods, A prospective 4-year study involving 1039 event-free subjects (643 males, 396 females) treated with atorvastatin (10,40 mg day,1) to reach the appropriate Adult Treatment Panel-III LDL target of 3·36 mmol L,1. Enrolled subjects were evaluated every 6 months or at a clinical event. LOX-1 3,UTR/T-C and NOS G894T polymorphisms were detected by allelic discrimination assays (polymerase chain reaction), lipid profile by enzymatic-colorimetric method, ox-LDL by enzyme linked immunosorbent assay, platelet activation by P-selectin (P-sel) expression (FACScan), NOS activity (by intracellular citrullin recovery) and homocysteine (high performance liquid chromatography), C-reactive protein (CRP) by sensitive nephelometric technique. Results, LOX-1 3,UTR/T showed the strongest association with events in the whole cohort with respect to each other variable including LDL reduction and NOS G894T (OR 4·90, 95% CI 3·19,6·98, P < 0·00001). Smoking influenced events in LDL-targeted subjects (P < 0·0001). Ox-LDL and P-sel were better indicators than LDL or other variables according to 3,UTR/C genotype regardless of the magnitude of LDL reduction (OR 4·21, 95% CI 2·29,6·70 P < 0·0001). Conclusions, LOX-1 polymorphisms could influence statin effectiveness in CAD prevention by induction of sensitivity to antithrombotic mechanisms such as antiplatelet activity. [source]


    Fatty acid incorporation in endothelial cells and effects on endothelial nitric oxide synthase

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2007
    S. Couloubaly
    Abstract Background The nature of fatty acids provided by the diet as well as plasma lipid metabolism can modify the composition and properties of plasma membrane and thus the activity of membrane proteins. In humans, as well as in experimental models, diabetes is associated with both an alteration in serum lipid profile and a documented endothelial dysfunction. This in vitro study investigated on an immortalized human endothelial cell line (EA.hy 926) the specific effects of several free fatty acids (FFAs) on the composition of cellular membranes and the regulation of endothelial nitric oxide synthase (eNOS). Materials and methods 0·1% of lipid deprived serum was added to the incubation medium with 25 mm glucose in order to study the effects of individual fatty acids: myristic acid, palmitic acid, stearic acid, oleic acid or linoleic acid at 100 µm bound with albumin. The effects of the FFAs on the endothelial nitric oxide synthase were investigated on mRNA level by quantitative PCR, on protein level and Ser1177 phosphorylation by Western blot and on enzymatic activity on living cells using radiolabelled arginine. Results Free linoleic acid increased the membrane content in n-6 fatty acids (mainly C18: n-6 and its metabolites) with a decrease in saturated and monounsaturated fatty acids. These conditions decreased the basal eNOS activity and reduced the phosphorylation of eNOS-Ser1177 due to activation by histamine. Free palmitic acid enriched the membranes with 16 : 0 with a slight decrease in monounsaturated fatty acids. These conditions increased eNOS activation without increasing Ser1177 phosphorylation upon histamine activation. The addition of the other FFAs also resulted in modifications of membrane composition, which did not to affect eNOS-Ser1177 phosphorylation. Conclusion Among the fatty acids used, only modification of the membrane composition due to linoleic acid supply disturbed the basal enzymatic activity and Ser1177 phosphorylation of eNOS in a way that limited the role of histamine activation. Linoleic acid might involve the dysfunction of both eNOS basal activity and its phosphorylation status and may then contribute to an impaired vasodilatation in vivo. [source]


    Association of serum sialic acid and MMP-9 with lipids and inflammatory markers

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2000
    Kalela
    Background Inflammation of the arterial wall has emerged to be an important contributor to the process of atherosclerosis, the major cause of coronary heart disease. Several factors are currently under investigation as inflammatory markers of atherosclerosis. Serum sialic acid and matrix metalloproteinase-9 may provide such markers. We studied their association with the lipid profile and with the inflammatory markers C-reactive protein and leukocyte count in a clinically healthy population of men. Materials and methods Cardiovascular risk-related laboratory tests were carried out in 65 consecutive male employees in connection with an occupational health survey in 1996. The subjects were divided into tertiles on the basis of serum sialic acid or matrix metalloproteinase-9 concentration. Results In a stepwise polychotomous logistic regression model adjusting for coronary heart disease risk factors, serum sialic acid concentration was not associated with markers of inflammation but rather with the lipid risk factors of atherosclerosis: inversely with HDL cholesterol (OR = 0.081, 95% CI 0.0068,0.97) and positively with total cholesterol (OR = 2.4, 95% CI 1,5.6). Matrix metalloproteinase-9 levels had a significant positive correlation with the leukocyte count (OR = 2.3, 95% CI 1.4,4). Conclusions Serum sialic acid does not appear to be an indicator of inflammation but is somehow connected with the level of total and HDL cholesterol. Serum matrix metalloproteinase-9 may provide a useful marker of inflammation because it correlates with the leukocyte count and is not associated with the lipid profile. [source]


    Migraine, lipid profile, and cardiovascular disease

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2010
    M. E. Bigal
    No abstract is available for this article. [source]


    Turner syndrome and the evolution of human sexual dimorphism

    EVOLUTIONARY APPLICATIONS (ELECTRONIC), Issue 3 2008
    Bernard Crespi
    Abstract Turner syndrome is caused by loss of all or part of an X chromosome in females. A series of recent studies has characterized phenotypic differences between Turner females retaining the intact maternally inherited versus paternally inherited X chromosome, which have been interpreted as evidence for effects of X-linked imprinted genes. In this study I demonstrate that the differences between Turner females with a maternal X and a paternal X broadly parallel the differences between males and normal females for a large suite of traits, including lipid profile and visceral fat, response to growth hormone, sensorineural hearing loss, congenital heart and kidney malformations, neuroanatomy (sizes of the cerebellum, hippocampus, caudate nuclei and superior temporal gyrus), and aspects of cognition. This pattern indicates that diverse aspects of human sex differences are mediated in part by X-linked genes, via genomic imprinting of such genes, higher rates of mosaicism in Turner females with an intact X chromosome of paternal origin, karyotypic differences between Turner females with a maternal versus paternal X chromosome, or some combination of these phenomena. Determining the relative contributions of genomic imprinting, karyotype and mosaicism to variation in Turner syndrome phenotypes has important implications for both clinical treatment of individuals with this syndrome, and hypotheses for the evolution and development of human sexual dimorphism. [source]


    Thiazolidinedione derivatives in diabetes and cardiovascular disease: an update

    FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2008
    Pantelis A. Sarafidis
    Abstract As the incidence and the public health impact of type 2 diabetes are constantly rising, treatment of hyperglycemia, prevention of diabetes-related complications are currently top medical priorities. Within the last decade several new classes of oral hypoglycemic agents were added to our armamentarium against diabetes. Among these new classes, the group of thiazolidinediones, which act through reduction of insulin resistance is perhaps the most widely used. For about 20 years, numerous background and clinical studies have evaluated the beneficial and adverse effects of these compounds. Current knowledge suggests that thiazolidinediones are as effective as metformin or sulfonylurea derivatives in improving glycemic control and exert several other beneficial metabolic and vascular effects, such as improvement in lipid profile, blood pressure lowering, redistribution of body fat away from the central compartment, microalbuminuria regression, reduction in subclinical vascular inflammation and others. On the other hand, currently used thiazolidinediones have well-established side effects, most important of which are fluid retention leading to weight gain and heart failure deterioration. Further, in the expectance of proper outcome studies to clarify the effects of these agents in cardiovascular morbidity and mortality, data from recent meta-analyses suggest that rosiglitazone may increase the risk for some cardiovascular outcomes. This article will discuss all the above issues attempting to provide an updated overview of this expanding field. [source]


    Endothelial Function in Patients With Migraine During the Interictal Period

    HEADACHE, Issue 1 2007
    Federico A. Silva MD
    Objectives.,The aim of this study is to evaluate endothelial function in migraineur subjects during the asymptomatic period. Background.,Migraine has been proposed as a risk factor for cerebrovascular events. The underlying mechanisms that relate these 2 pathologies are unknown. Nitric oxide (NO) has been proposed as the final causative molecule of migraine. Increased NO metabolites concentrations have been reported in migraineur subjects during acute migraine attacks, but there is no evidence indicating alterations in endothelial NO release during the symptom free period in theses subjects. Design and Methods.,Fifty migraineur subjects and 25 healthy subjects matched by gender and age were included. Every subject underwent a complete examination that included medical history, physical examination, resting electrocardiogram, forearm flow-mediated vasodilation (FMD), blood determinations of fasting nitrates and nitrites (NO2,+ NO3,), glucose, lipid profile, creatinine, C-reactive protein, and blood cell count. Results.,No differences in FMD or NO2,+ NO3, were detected among groups. The only difference between migraineurs and control subjects was a higher mean blood pressure 92.1 (8.8) mmHg versus 86.7 (8.2) mmHg P= .01. Conclusion.,The endothelial function is not altered during the interictal period in migraineur subjects. [source]


    Effect of recombinant human erythropoietin on insulin resistance in hemodialysis patients

    HEMODIALYSIS INTERNATIONAL, Issue 3 2009
    Essam KHEDR
    Abstract Insulin resistance is a characteristic feature of uremia. Insulin resistance and concomitant hyperinsulinemia are present irrespective of the type of renal disease. Treatment with recombinant human erythropoietin (rHuEPO) was said to be associated with improvement in insulin sensitivity in uremic patients. The aim of this study was to compare insulin resistance in adult uremic hemodialysis (HD) patients including diabetic patients treated with or without rHuEPO. A total of 59 HD patients were studied, patients were divided into 2 groups of subjects: 30 HD patients on regular rHuEPO treatment (group A), and 29 HD patients not receiving rHuEPO (group B) diabetic patients were not excluded. Full medical history and clinical examination, hematological parameters, lipid profile, serum albumin, parathyroid horomone, Kt/V, fasting glucose, and insulin levels were measured in all subjects. Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) was used to compare insulin resistance. The results of this study showed that the mean insulin level of HD patients treated with rHuEPO (group A) (17.5 ± 10.6 ,U/mL) was significantly lower than patients without rHuEPO (group B) (28.8 ± 7.7 ,U/mL), (P<0.001). Homeostasis Model Assessment of Insulin Resistance levels in group A were significantly lower than in group B (3.8 ± 2.97, 7.98 ± 4.9, respectively, P<0.001). Insulin resistance reflected by HOMA-IR levels among diabetic patients in group A was significantly lower than among diabetic patients in group B (3.9 ± 3.2, 9.4 ± 7.2, respectively, P<0.001). Also, HOMA-IR levels among nondiabetic patients in group A were significantly lower than among nondiabetic patients in group B (3.7 ± 2.85, 6.9 ± 1.43, respectively, P<0.01). We found a statistically significant negative correlation between duration of erythropoietin treatment, fasting blood glucose, insulin levels, and insulin resistance (r=,0.62, ,0.71, and ,0.57, P<0.001). Patients treated with rHuEPO showed less insulin resistance compared with patients not treated with rHuEPO in diabetic and nondiabetic patients and, duration of erythropoietin treatment is negatively correlated with insulin levels and insulin resistance in HD patients. [source]


    Low cholesterol along with inflammation predicts morbidity and mortality in hemodialysis patients

    HEMODIALYSIS INTERNATIONAL, Issue 2 2009
    George TSIRPANLIS
    Abstract Low and not high cholesterol seems to predict high mortality in hemodialysis (HD) patients. The confirmation of this reverse epidemiology as well as its possible interconnection with the increased inflammatory activity observed in this population is being explored in the present study. A group of 136 HD patients was prospectively studied for 2 years, and cardiovascular disease (CVD) as well as all-cause mortality and morbidity were recorded. Baseline lipid profile, inflammatory status, and patients' characteristics were studied as potential survival and hospitalization predictors. During the 24-month follow-up, 21 deaths (52.4% due to CVD) and 38 hospitalizations (55.3% due to CVD) were recorded. In multivariate Cox regression analysis, decreased interleukin-10 (IL-10) and decreased total serum cholesterol (TChol) were the only independent predictors of CVD mortality while C-reactive protein and decreased TChol predicted all-cause mortality. Interleukin-10 at baseline was 11.29 ± 21.49 vs. 5.51 ± 4.57 pg/mL (P<0.018) and TChol 167.37 ± 47.84 vs.122.04 ± 26.48 mg/dL (P<0.000) in survivors vs. nonsurvivors from CVD, while C-reactive protein at baseline was 9.37 ± 11.54 vs. 23.15 ± 18.76 mg/L (P<0.000) and TChol 169.26 ± 46.42 vs. 133.26 ± 46.33 mg/dL (P<0.003) in survivors vs. nonsurvivors from any cause of death. Using the same method of statistical analysis, IL-6 and decreased soluble gp130 (sgp130),an antagonist of IL-6 action,were found to be the only independent prognostic factors for hospitalization due to CVD while decreased soluble gp130 remained the sole predictor of hospitalization due to any cause. In conclusion, reverse epidemiology regarding cholesterol is confirmed in the present study. Furthermore, inflammatory activity also predicts, independently of or in conjunction with low-cholesterol, CVD and all-cause morbidity and mortality in HD patients. [source]


    Mechanisms of dyslipidemia of chronic renal failure

    HEMODIALYSIS INTERNATIONAL, Issue 1 2006
    Nosratola D. VAZIRI
    Abstract Chronic renal failure is associated with profound dysregulation of lipid metabolism and marked abnormalities of plasma lipid profile. This review is intended to provide an overview of the molecular basis of lipid disorders in chronic renal failure and explore their potential impact on cardiovascular disease and energy metabolism. [source]