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)

The transcription factor peroxisome proliferator-activated receptor (PPAR) alpha plays an important role in lipid homeostasis. In this study, we examined whether the down-regulation of PPAR-alpha gene expression is associated with dyslipidemia in a rat model of chronic renal failure (CRF). Rats with laboratory-induced uremia by 5/6 nephrectomy were bled at 2 weeks and 10 weeks after the nephrectomy to produce conditions. For the sake of convenience, the rats observed at postoperative week 2 were defined as acute renal failure (ARF) and those observed at week 10 were defined as CRF. Lipids in lipoprotein fractions were measured by high-performance liquid chromatography. The abundance of PPAR-alpha messenger RNA (mRNA) in the liver was measured by reverse transcriptase-polymerase chain reaction. Serum creatinine and blood urea nitrogen levels rose with the progression of renal failure, but the total protein levels remained constant. Serum triglyceride in ARF rats remained unchanged from the level in sham-operated control rats, whereas that in CRF rats was 66% higher than the control level. Serum cholesterol was elevated 1.5-fold in ARF rats and 2-fold in CRF rats compared with the sham-operated counterparts. As with triglyceride, very low-density lipoprotein remained unchanged in ARF rats but rose substantially in CRF rats. All of the major lipoprotein fractions were elevated in CRF rats. These lipid and lipoprotein changes were significantly associated with creatinine and blood urea nitrogen levels. The PPAR-alpha mRNA expression in the liver was unchanged in ARF rats but was 44% lower in CRF rats. The PPAR-alpha mRNA expression was inversely correlated with serum creatinine and lipids in the overall rats. Our results indicate that PPAR-alpha mRNA expression is down-regulated in the liver of CRF rats and that this down-regulation may play a crucial role in the development of dyslipidemia.
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PMID:Decreased peroxisome proliferator-activated receptor alpha gene expression is associated with dyslipidemia in a rat model of chronic renal failure. 1799 26

We examined the incidence of renal function deterioration (RFD) in a population of male gout patients and to identify associated risk factors. Subjects who had been regularly followed up for more than 2 years and had visited Chang Gung Memorial Hospital-Kaohsiung Medical Center Rheumatology Clinic between June 1, 2006 and January 31, 2007 were enrolled. Four subjects were excluded as secondary gout was suspected. Group I (Gr I) comprised subjects without RFD and group II (Gr II) comprised subjects with RFD during the follow-up period. RFD was defined as absolute increment in creatinine (Cr) levels over 0.4 mg/dl for subjects with baseline Cr levels <or=1.4 mg/dl or as more than 50% increment of baseline Cr level per 12-month interval in average for subjects with baseline Cr levels >1.4 mg/dl. Clinical parameters were analyzed to study the potential risk factors of RFD. Of 318 male gout patients, 296 (93.1%) were categorized as Gr I, and 22 (6.9%) were categorized as Gr II. The observation periods for Gr I and Gr II were 81.20+/-53.29 and 92.41+/-46.72 months, respectively (p=0.338). Initial Cr levels are similar between the two groups (1.25+/-0.51 vs 1.25+/-0.61, p=0.963). Multiple logistic regression analysis revealed that current age, age at disease onset, disease duration, treatment duration, body weight, height, family history of gout, tophi, urolithiasis, tobacco use, alcohol consumption, history of cerebral vascular accident, hypertension, diabetes mellitus, dyslipidemia, base-line and final Cr, blood urea nitrogen level, serum uric acid level, and body-mass index were not independent risk factors. However, history of ischemic heart disease [IHD; odds ratio (OR) 7.68, 95% confidence interval (CI) 1.99-29.70] and greater waist circumference (WC; OR 1.06, 95% CI 1.01-1.11) were two independent risk factors of RFD. Additionally, the Cox multivariable analysis disclosed that IHD (p<0.001) and greater WC (p=0.011) deteriorated kidney function in these patients. The incidence of RFD in male gout patients is 6.9%. History of IHD and greater WC are two independent risk factors for developing RFD.
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PMID:Ischemia heart disease and greater waist circumference are risk factors of renal function deterioration in male gout patients. 1803 May 16

Hyperlipidemia has been well recognized as a striking feature of nephrotic syndrome and other renal diseases. However, the underlying pathophysiological mechanisms still have not yet been elucidated. In this study, we evaluated acylation-stimulating protein (ASP) and complement component 3 (C3) in children (n=48) with various forms of proteinuric renal disease [nephrotic syndrome, acute poststreptococcal infection glomerulonephritis (APSGN), and lupus nephritis (LN)] in comparison with age- and gender-matched controls (n=279). In children with proteinuric renal disease, various aberrations in plasma lipids were noted, including increased triglyceride, cholesterol, and low-density lipoprotein cholesterol (LDL-C) (all p<0.0001). Whereas C3 was not altered in children with nephrotic syndrome (1.05+/-0.05 g/L vs. 1.29+/-0.04 controls), the decrease was pronounced in children with LN and APSGN (0.42+/-0.11, p<0.05 and 0.30+/-0.06, p<0.001, respectively). Plasma C3 correlated positively with lipid parameters [triglyceride, cholesterol, LDL-C, apolipoprotein B (apoB), high-density lipoprotein cholesterol (HDL-C) and apoA1] and inversely with total protein, blood urea nitrogen, and creatinine. By contrast, plasma ASP was significantly elevated in all proteinuric renal diseases (101.4+/-7.1 nmol/L nephrotic syndrome, 90.9+/-14.1 LN, and 81.8+/-7.2 APSGN vs. 44.3+/-1.5 controls, p<0.05 to p<0.001), and this increase was correlated with changes in lipid parameters (triglycerides and apoA1). In summary, these results demonstrate alterations in C3 and ASP that may contribute to or compensate for dyslipidemia.
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PMID:Increased plasma acylation-stimulating protein in pediatric proteinuric renal disease. 1825 59

Dunnigan-type familial partial lipodystrophy (FPLD) is a rare monogenic adipose tissue disorder in which the affected subjects have increased predisposition to insulin resistance and related metabolic complications, such as glucose intolerance, diabetes, dyslipidemia, and hepatic steatosis. Our patient was a 35-year-old female who had been receiving insulin injection therapy for diabetes mellitus and was transferred to our hospital. She was diagnosed with FPLD on the basis of the following symptoms: increase in subcutaneous fat in the face, neck, and upper trunk; loss of subcutaneous fat in the lower limbs and the gluteal region. We found a heterozygous CGG to CAG transition in codon 482 of exon 8 in the gene encoding lamin A/C (LMNA), which leads to an arginine to glutamine substitution (R482Q). At the time of admission, her serum creatinine level was 8.4 mg/dl, and her blood urea nitrogen (BUN) level was 81 mg/dl. Her serum creatinine level was elevated and hemodialysis was performed twice every week. However, she died of cerebral hemorrhage 9 months after hemodialysis. Although it is uncommon for patients with FPLD to exhibit renal dysfunction and require hemodialysis, this case suggests the need for careful analysis of renal function in a patient with FPLD.
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PMID:A case of Dunnigan-type familial partial lipodystrophy (FPLD) due to lamin A/C (LMNA) mutations complicated by end-stage renal disease. 1901 97

The aim of this study was to investigate the modulating effect of atorvastatin on serum paraoxonase 1 enzyme (PON1) activity in type 2 diabetic Egyptian patients with or without nephropathy. The present study was carried out on the following groups: control group, which consisted of 30 healthy persons; Group I, which consisted of 20 type 2 diabetic patients without nephropathy; and Group II, which consisted of 20 type 2 diabetic patients with nephropathy. All the patients selected were under an antidiabetic regimen of insulin, and patients receiving antihypertensive agents were excluded from the follow-up study to avoid drug interaction fallacies. Twenty-two patients (15 without nephropathy and seven with nephropathy) received atorvastatin in individually adjusted oral dosage (range 10-20 mg) once per day for 12 weeks. All cases were subjected to thorough clinical examination and history taking and measurement of serum levels of PON1 activity, malondialdehyde (MDA), glutathione reductase activity, fasting glucose, total cholesterol, triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), urea, and creatinine. Urine samples were collected for determination of proteinuria. The obtained results showed that PON1 activity and HDL significantly decreased and fasting glucose significantly increased in Group I and Group II when compared to the control group, with significant difference in their levels between Group II and Group I. MDA, total cholesterol, and LDL levels significantly increased and glutathione reductase activity significantly decreased in Group I and Group II when compared to the control group. Urea, creatinine, and proteinuria levels showed significant increase in Group II when compared to the control group and Group I, with nonsignificant difference between control group and Group I. Atorvastatin therapy caused a significant increase in PON1 activity, and serum levels of MDA and glutathione reductase activity were significantly decreased and increased, respectively. Also, total cholesterol, triglyceride and LDL-cholesterol levels were significantly reduced with a significant increase in HDL-cholesterol levels. There was a significant modest reduction in serum urea and creatinine levels as well as in proteinuria level. Fasting glucose level was significantly reduced under the antidiabetic regimen of insulin through the follow-up period. PON1 activity showed a significant negative correlation with glucose and LDL, and a significant positive correlation with HDL in all the studied groups. It could be concluded that atorvastatin with its pleiotropic effects could provide optimal therapeutic intervention to control not only dyslipidemia, but also oxidative stress status with consequent improvement in the course of type 2 diabetes and diabetic nephropathy. More specifically, restoration of PON1 activity by atorvastatin opens a window to investigate other drugs that could provide a new adjuvant therapeutic line for better control of diabetes and diabetic nephropathy. Further research is also recommended to study the distribution of PON1 genetic polymorphism among the Egyptian population to explain the variability in its activity and its relationship with other factors that associate diabetes and its complications.
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PMID:Modulating effect of atorvastatin on paraoxonase 1 activity in type 2 diabetic Egyptian patients with or without nephropathy. 1955 42

Insulin resistance, obesity, hypertension, and dyslipidemia are strongly associated with metabolic syndrome (MeSy), which is considered to be a reversible clinical stage before its evolution to coronary heart disease and diabetes. Currently, the antihypertensive and hypolipidemic properties of aqueous Hibiscus sabdariffa extracts (HSE) have been demonstrated in clinical trials and in vivo experiments. The aim of the present study was to evaluate the effects of a Hibiscus sabdariffa extract powder (HSEP) and a recognized preventive treatment (diet) on the lipid profiles of individuals with and without MeSy according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) criteria. The protocol was a follow-up study carried out in a factorial, randomized design (T1=preventive treatment comprises Diet, T2=HSEP, T3=HSEP+preventive treatment (Diet) X MeSy, non-MeSy individuals). A total daily dose of 100 mg HSEP was orally administered in capsules for one month. The preventive treatment (diet) was selected according to NCEP-ATP III recommendations and adjusted individually. Total cholesterol, LDL-c, HDL-c, VLDL-c, triglycerides, glucose, urea, creatinine, AST, and ALT levels in the blood were determined in all individuals pre- and post-treatment. The MeSy patients treated with HSEP had significantly reduced glucose and total cholesterol levels, increased HDL-c levels, and an improved TAG/HDL-c ratio, a marker of insulin resistance (t-test p<0.05). Additionally, a triglyceride-lowering effect was observed in MeSy patients treated with HSEP plus diet, and in individuals without MeSy treated with HSEP. Significant differences in total cholesterol, HDL-c, and the TAG/HDL-c ratio were found when the means of absolute differences among treatments were compared (ANOVA p<0.02). Therefore, in addition to the well documented hypotensive effects of Hibiscus sabdariffa, we suggest the use of HSEP in individuals with dyslipidemia associated with MeSy.
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PMID:Effects of Hibiscus sabdariffa extract powder and preventive treatment (diet) on the lipid profiles of patients with metabolic syndrome (MeSy). 1996 89

Aldehydes such as acrolein are ubiquitous pollutants present in automobile exhaust, cigarette, wood, and coal smoke. Such aldehydes are also constituents of several food substances and are present in drinking water, irrigation canals, and effluents from manufacturing plants. Oral intake represents the most significant source of exposure to acrolein and related aldehydes. To study the effects of short-term oral exposure to acrolein on lipoprotein levels and metabolism, adult mice were gavage-fed 0.1 to 5 mg acrolein/kg bwt and changes in plasma lipoproteins were assessed. Changes in hepatic gene expression related to lipid metabolism and cytokines were examined by qRT-PCR analysis. Acrolein feeding did not affect body weight, blood urea nitrogen, plasma creatinine, electrolytes, cytokines or liver enzymes, but increased plasma cholesterol and triglycerides. Similar results were obtained with apoE-null mice. Plasma lipoproteins from acrolein-fed mice showed altered electrophoretic mobility on agarose gels. Chromatographic analysis revealed elevated VLDL cholesterol, phospholipids, and triglycerides levels with little change in LDL or HDL. NMR analysis indicated shifts from small to large VLDL and from large to medium-small LDL with no change in the size of HDL particles. Increased plasma VLDL was associated with a significant decrease in post-heparin plasma hepatic lipase activity and a decrease in hepatic expression of hepatic lipase. These observations suggest that oral exposure to acrolein could induce or exacerbate systemic dyslipidemia and thereby contribute to cardiovascular disease risk.
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PMID:Acrolein consumption induces systemic dyslipidemia and lipoprotein modification. 2003 6

Increased Very Low Density Lipoprotein (VLDL) production is a major feature of diabetic dyslipidemia with consequences on the metabolism of other lipoproteins such as Low Density Lipoproteins (LDL) and High Density Lipoproteins (HDL). More precisely, we observe, in patients with type 2 diabetes, an increased production of VLDL(1) particles that is potentially detrimental by generating atherogenic remnants, small dense LDL particles and triglyceride-rich HDL particles. Several pathophysiological factors are responsible for increased VLDL production, in type 2 diabetes. Among those, insulin resistance plays an important role. Indeed, defective activation of PI3-kinase, secondary to insulin resistance, is associated with a reduction of apoB degradation in the hepatocytes, a rise in MTP expression (by increasing nuclear transcription factors Fox01 and Foxa2) and an increased activity of phospholipase D1 and ARF-1, which are involved in VLDL(1) formation. Moreover, peripheral insulin resistance is responsible for increased lipolysis of adipose tissue leading to augmented portal flux of FFA to the liver and, as a consequence, activation of VLDL production. In addition, increased de novo lipogenesis is observed in type 2 diabetes. This is secondary to increased activation of SREBP-1c (Sterol Regulatory Element-Binding Protein-1c), mainly by Endoplasmic Reticulum stress, and of ChREBP (Carbohydrate Responsive Element Binding Protein), mainly by hyperglycemia. Furthermore, decreased plasma adiponectin observed in type 2 diabetes, may also play a role in increased VLDL production by decreasing liver AMP-kinase activation and by increasing plasma FFA levels as a consequence of reduced muscle FFA oxidation.
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PMID:Abnormal hepatic apolipoprotein B metabolism in type 2 diabetes. 2018 75

The present study was designed to investigate the effects of angiotensin(1-7) (Ang(1-7)) a Mas receptor agonist, and A-779, a Mas receptor antagonist, in streptozotocin-induced diabetic nephropathy (DN). A single administration of streptozotocin (STZ) (50 mg/kg i.p.) to rats produced diabetes, and diabetic nephropathy developed after 8 weeks of STZ administration. The extent of DN was assessed biochemically and morphologically by measuring serum creatinine, creatinine clearance, blood urea nitrogen (BUN), proteinuria, urinary N-acetyl-beta-D glucosaminadase activity, renal collagen contents, lipid profile, serum nitrite/nitrate concentration and kidney weight/body weight (%). Treatments with Ang(1-7) (576 microg/kg/day i.p. for 4 weeks) and Ang(1-7) plus A-779 (744 microg/kg/day i.p. for 4 weeks) were started after 4 weeks of STZ administration. The treatment with Ang(1-7) attenuated STZ-induced nephropathy in rats by decreasing proteinuria, renal collagen content and by improving endothelial functions without preventing tubular damage. It has been shown for the first time that treatment with Ang(1-7) decreases dyslipidemia and BUN in diabetic rats, implying a renoprotective effect of the peptide. However, serum creatinine, creatinine clearance and kidney weight/body weight (%) remained unaffected with Ang(1-7) treatment. It may be concluded that activation by specific agonists of the Mas receptor may be useful in combating glomerular damage in DN.
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PMID:Ameliorative potential of angiotensin1-7/Mas receptor axis in streptozotocin-induced diabetic nephropathy in rats. 2038 42

Urine acidification is induced by metabolic acidosis which is associated with a high intake of protein-rich diet. The purpose of this study was to investigate the relationship of urine acidification with visceral obesity and the metabolic syndrome. We recruited 1,051 male subjects who underwent health examinations at the Health Care Center in Kinki Central Hospital. Subjects who were treated for hypertension, dyslipidemia, diabetes mellitus, and hyperuricemia and had the past history of chronic liver disease, chronic kidney disease and cancer, were excluded in this study. All subjects were administered to urine pH, blood and physical examinations. Lower urine pH was associated with higher serum urea nitrogen which reflects high intake of protein-rich diet, whereas it had no relation to serum creatinine. Lower urine pH was also associated with an increase in waist circumference, homeostasis model assessment-R, fasting plasma glucose, HbA1c, serum triglyceride, serum uric acid and with a decrease in high density lipoprotein cholesterol. Urine pH was not associated with mean blood pressure. Urine acidification is a characteristic of visceral obesity and the metabolic syndrome. High intake of protein-rich diet may contribute urine acidification, which is associated with various metabolic abnormalities in visceral obesity.
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PMID:Association of urine acidification with visceral obesity and the metabolic syndrome. 2144 1


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