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)

Familial hypertriglyceridemia has been suggested to be an autosomal dominant condition with age-dependent penetrance, but so far the underlying defective gene has not been elucidated. LPL gene and apolipoprotein A-I/C-III/A-IV gene cluster might be involved in familial clustering of hypertriglyceridemia. Heterozygous LPL deficiencies caused by several types of gene mutation are known to result in a partial defect in catabolism of VLDL, occurring mild to moderate hypertriglyceridemia. However, although the mutation of LPL gene results in reduced lipolytic activity, this type of dyslipidemia appears to manifest only if VLDL-TG production is also increased. These suggest that overproduction of VLDL-TG is a more important cause of hypertriglyceridemia than is the LPL deficiency. Moreover, families with a clustering of hypertriglyceridemia are known to be at increased risk of hyperinsulinemia due to impaired insulin sensitivity. Impaired insulin sensitivity and hyperinsulinemia are the major determinants of excessive VLDL-TG synthesis and dyslipidemia. Taken together, abnormally high production of VLDL-TG seemed to be the major factor in causing familial hypertriglyceridemia, but clearance capacity can play an important role in determining the severity of the TG elevation.
Nihon Rinsho 1999 Dec
PMID:[Primary hypertriglyceridemia]. 1063 13

Demographic shifts, lifestyle changes, and adverse effects of childhood nutrition portend an epidemic of coronary heart disease in the Indian subcontinent, which is currently experiencing health transition. Indian susceptibility includes atherogenic blood lipid levels and a metabolic complex of central obesity, glucose intolerance, hyperinsulinemia, and dyslipidemia due to insulin resistance. These characteristics are demonstrated dramatically in urban Indians and in Indian migrants to the west. Prime targets for effective strategies of primordial prevention include children and families in lower socio-economic classes now in transition. There is the greatest urgency in India for medical, political, and social action to prevent high risk in the first place, combating the tobacco trade, enlisting food and agriculture agencies, and promoting physical activity in the population. An empowered community with an enlightened policy can prevent the threatened epidemic.
Prev Med 1999 Dec
PMID:Primordial prevention of coronary heart disease in India: challenges and opportunities. 1064 29

Serum mannose concentration increases in diabetic patients and correlates closely with blood glucose. In patients with glomerulonephritis, serum mannose and mannose/glucose ratio positively correlate with dyslipidemia and the extent of urinary protein excretion. We investigated whether changes in serum mannose mark subjects with features of metabolic syndrome, including obesity, hypertension, glucose intolerance, and dyslipidemia. The study comprised 20 patients with mean age of 68 (SD 11) years, body mass index 27.2 (SD 5.1) kg/m2, blood glucose 6.2 (SD 1.6) mmol/L, serum total cholesterol 6.3 (SD 1.2) mmol/L, triglyceride 2.0 (SD 0.08) mmol/L, uric acid 320 (SD 109) micromol/L, mannose 60.0 (SD 17) micromol/L, and mannose/glucose ratio 9.7 (SD 1.8) micromol/mmol. Serum mannose correlated with blood glucose (r=0.758, p=0.012), triglyceride (r=0.478, p=0.023), and HDL-cholesterol (r = approximately 0.427, p=0.022). Mannose/glucose ratio correlated with BMI (r=0.581, p=0.033), mannose (r=0.491, p=0.035), and uric acid (r=0.608, p=0.027). The rate of VLDL lipoprotein turnover may be instrumental in the regulation of serum mannose concentration. We conclude that an altered mannose metabolism is a novel consideration among the metabolic abnormalities in the metabolic syndrome.
Scand J Clin Lab Invest 1999 Dec
PMID:Metabolic syndrome is associated with changes in D-mannose metabolism. 1069 Oct 51

Dyslipidaemia, particularly increased triglycerides (TG) and low HDL-cholesterol (HDL-C), represents an important risk factor for Type 2 diabetes (T2DM) macrovascular complications. Our aim was to evaluate the effects of atorvastatin in a population of T2DM patients according to their cardiovascular risk: evidence of myocardial or coronary lesions (group A); evidence of familiar hypercholesterolaemia (group B); evidence of stable cardiovascular risk (group C). The mean age was 64+/-7 yr, mean disease duration 9.5+/-3 yr, the mean body mass index (BMI) 27.7+/-1.3 kg/m2, mean HbA1c 8+/-0.6%; total cholesterol 256+/-24 mg/dl in group A, 298+/-30 and 244+/-31 in groups B and C, respectively (p<0.05 B vs. A and C). Moreover, mean HDL-C values were about 45+/-7 mg/dl, TG 225+/-20 mg/dl, systolic and diastolic blood pressure 144+/-7 mm Hg and 84+/-8 mm Hg, respectively; fibrinogen values 330+/-23 mg/dl and microalbuminuria 58+/-9 mg/l. Lipid profile improved significantly during the treatment with personalised doses of atorvastatin (generally 10 mg/day) designed to achieve the therapeutic goals: the reduction of total cholesterol, TG (p<0.01), LDL-cholesterol (LDL-C) (p<0.01) and an increase of HDL-C were measured. The treatment with atorvastatin induced significant reduction of microalbuminuria and fibrinogen levels (p<0.01). Moreover, in the subgroup of patients with hypertension, diastolic blood pressure values were reduced without modification of antihypertensive treatment. This preliminary study suggests that the management of hypercholesterolaemia with atorvastatin in T2DM patients may be useful both for the primary and secondary prevention of chronic complications of T2DM.
Diabetes Nutr Metab 1999 Dec
PMID:Atorvastatin for the management of Type 2 diabetic patients with dyslipidaemia. A mid-term (9 months) treatment experience. 1078 62

Adipose tissue lipoprotein lipase (LPL) activity is decreased in patients with poorly controlled diabetes, and this contributes to the dyslipidemia of diabetes. To study the mechanism of this decrease in LPL, we studied adipose tissue LPL expression in male rats with streptozotocin-induced diabetes. Heparin releasable and extractable LPL activity in the epididymal fat decreased by 75-80% in the diabetic group and treatment of the rats with insulin prior to sacrifice reversed this effect. Northern blot analysis indicated no corresponding change in LPL mRNA levels. However, LPL synthetic rate, measured using [(35)S]methionine pulse labeling, was decreased by 75% in the diabetic adipocytes, and insulin treatment reversed this effect. These results suggested regulation of LPL at the level of translation. Diabetic adipocytes demonstrated no change in the distribution of LPL mRNA associated with polysomes, suggesting no inhibition of translation initiation. Addition of cytoplasmic extracts from control and diabetic adipocytes to a reticulocyte lysate system demonstrated the inhibition of LPL translation in vitro. Using different LPL mRNA transcripts in this in vitro translation assay, we found that the 3'-untranslated region (UTR) of the LPL mRNA was important in controlling translation inhibition by the cytoplasmic extracts. To identify the specific region involved, gel shift analysis was performed. A specific shift in mobility was observed when diabetic cytoplasmic extract was added to a transcript containing nucleotides 1818-2000 of the LPL 3'-UTR. Thus, inhibition of translation is the predominant mechanism for the decreased adipose tissue LPL in this insulin-deficient model of diabetes. Translation inhibition involves the interaction of a cytoplasmic factor, probably an RNA-binding protein, with specific sequences of the LPL 3'-UTR.
J Biol Chem 2000 Dec 29
PMID:The translational regulation of lipoprotein lipase in diabetic rats involves the 3'-untranslated region of the lipoprotein lipase mRNA. 1102 42

New-onset diabetes mellitus, clinically similar to type 2 diabetes, will affect a small proportion (1%-6%) of patients infected with human immunodeficiency virus (HIV) who are treated with HIV-1 protease inhibitors (PIs). However, insulin resistance and impaired glucose tolerance will develop during PI treatment in a considerable proportion of patients. Dyslipidemia, abdominal obesity, and loss of peripheral fat frequently coexist with insulin resistance, but it is not clear whether all of these result from a common pathogenic mechanism. Recent data suggest that insulin resistance may also be associated with HIV infection in patients not receiving PI therapy. The long-term consequences of insulin resistance in this population are not known. The effect of switching to other antiretroviral therapies has not been fully determined. Treatment of established diabetes mellitus should generally follow existing guidelines. There is no clinically useful screening test that will determine the existence and degree of insulin resistance in individual patients. It is therefore reasonable to recommend general measures to increase insulin sensitivity in all patients infected with HIV, such as weight reduction for obese persons and regular aerobic exercise.
Clin Infect Dis 2000 Dec
PMID:Disorders of glucose metabolism in patients infected with human immunodeficiency virus. 1109 14

Cardiovascular illness is an important contributor to the morbidity of kidney disease. The spectrum of cardiovascular disease (CVD) in patients with chronic renal insufficiency (CRI) includes left ventricular hypertrophy (LVH) and dilatation, ischemic heart disease, and peripheral vascular disease. Both "traditional" and "uremia-specific" factors contribute to the occurrence and progression of cardiac disease in renal patients. A growing body of recent evidence indicates that the processes contributing to CVD commence early in CRI, leading to concentric LVH, left ventricular dilatation, congestive heart failure, and ischemic heart disease. Many of the coexisting conditions that have been identified consistently as contributing to the burden of cardiovascular illness in renal populations can be modified through medical interventions. Specific therapies exist for hypertension, anemia, hyperparathyroidism, and dyslipidemia. Studies to date have demonstrated that treatment of many of these factors-such as anemia and hypertension during end-stage renal disease-appear to benefit the cardiovascular system. Earlier intervention may offer the best opportunity to reduce the burden of illness in all groups of CRI patients. Identification of patients at the onset of kidney disease and attention to the known traditional and "uremic" risk factors are emerging as promising strategies. Long-term interventional studies are needed to determine costs, benefits, and risks of such strategies.
Am J Kidney Dis 2000 Dec
PMID:Cardiovascular disease in chronic renal insufficiency. 1111 55

The less rigorous attention to the management of the complications of chronic renal insufficiency (CRI) and its comorbid conditions has potentially tragic consequences. In fact, with early recognition and intervention, many of the complications of CRI and its comorbid conditions can be ameliorated or prevented. We review here the most prevalent, troublesome, and potentially preventable complications and comorbidities of CRI with a view toward developing high-quality, cost-effective strategies for delivering early interventional care. Complications of CRI include malnutrition, anemia, disorders of divalent ion metabolism and osteodystrophy, metabolic acidosis, and dyslipidemia. Important comorbid conditions of CRI are hypertension, diabetes mellitus, and cardiovascular disease. Clinical intuition suggests that early intervention will avert morbidity related to the hypoalbuminemia and other nutritional disorders of CRI, the metabolic acidosis, and the dyslipidemias, but prospective data are lacking at present. Correction of anemia, usually with recombinant human erythropoietin, may be key to the prevention of cardiac disease and other comorbidities of CRI. Incipient disorders of bone and mineral metabolism are managed prospectively using such measures as protein restriction to reduce phosphorus intake, phosphate binders, calcium supplementation, and vitamin D analogues. Hypertension, whatever its original etiology, is clearly an important risk factor for the progression of kidney failure and for the development of diffuse vascular disease; appropriate and aggressive treatment is essential. In patients with diabetic nephropathy, the principles of both primary and secondary prevention have been validated in several large trials of glycemic and blood pressure control. The seeds of these insidious, challenging, and costly comorbid conditions are sown very early in CRI, at a time when they are-in theory-most amenable to intervention. We therefore must be as proactive as possible in the timely implementation of relatively simple therapies that have the potential to prevent some of these adverse outcomes of CRI.
Am J Kidney Dis 2000 Dec
PMID:Complications of chronic renal insufficiency: beyond cardiovascular disease. 1111 56

Recent research has emphasized the importance of the metabolic cluster, which includes glucose intolerance, dyslipidemia, and high blood pressure, as a strong predictor of the obesity-related morbidities and premature mortality. Fundamental to this association, commonly referred to as the metabolic syndrome, is the close interaction between abdominal fat patterning, total body adiposity, and insulin resistance. As the initial step in identifying major genetic loci influencing these phenotypes, we performed a genomewide scan by using a 10-centiMorgan map in 2,209 individuals distributed over 507 nuclear Caucasian families. Pedigree-based analysis using a variance components linkage model demonstrated a quantitative trait locus (QTL) on chromosome 3 (3q27) strongly linked to six traits representing these fundamental phenotypes [logarithm of odds (lod) scores ranged from 2.4 to 3.5]. This QTL exhibited possible epistatic interaction with a second QTL on chromosome 17 (17p12) strongly linked to plasma leptin levels (lod = 5.0). Situated at these epistatic QTLs are candidate genes likely to influence two biologic precursor pathways of the metabolic syndrome.
Proc Natl Acad Sci U S A 2000 Dec 19
PMID:Quantitative trait loci on chromosomes 3 and 17 influence phenotypes of the metabolic syndrome. 1112 Oct 50

We examined the impact of ambulatory care clinical pharmacist interventions on clinical and economic outcomes of 208 patients with dyslipidemia and 229 controls treated at nine Veterans Affairs medical centers. This was a randomized, controlled trial involving patients at high risk of drug-related problems. Only those with dyslipidemia are reported here. In addition to usual medical care, clinical pharmacists were responsible for providing pharmaceutical care for patients in the intervention group. The control group did not receive pharmaceutical care. Seventy-two percent of the intervention group and 70% of controls required secondary prevention according to the National Cholesterol Education Program guidelines. Significantly more patients in the intervention group had a fasting lipid profile compared with controls (p=0.021). The absolute change in total cholesterol (17.7 vs 7.4 mg/dl, p=0.028) and low-density lipoprotein (23.4 vs 12.8 mg/dl, p=0.042) was greater in the intervention than in the control group. There were no differences in patients achieving goal lipid values or in overall costs despite increased visits to pharmacists. Ambulatory care clinical pharmacists can significantly improve dyslipidemia in a practice setting designed to manage many medical and drug-related problems.
Pharmacotherapy 2000 Dec
PMID:Clinical and economic impact of ambulatory care clinical pharmacists in management of dyslipidemia in older adults: the IMPROVE study. Impact of Managed Pharmaceutical Care on Resource Utilization and Outcomes in Veterans Affairs Medical Centers. 1113 Feb 23


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