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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the pathogenesis of obesity in OZR is unknown, the association among hyperinsulinemia, insulin resistance, and hyperlipidemia suggests that investigations using OZR may help define how a number of vascular disease risk factors interact to cause end-organ damage. Like other rat strains, OZR do not develop atherosclerosis spontaneously. Nevertheless, in an endothelial injury model, atherosclerosis was worse in OZR than in LZR. Perhaps more intriguing is the fact that OZR develop spontaneous glomerular injury. Although the mechanisms important in the development and progression of glomerular injury in OZR remain to be clarified, both lipid abnormalities and glomerular hemodynamic alterations could play a role.
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PMID:The Zucker rat model of obesity, insulin resistance, hyperlipidemia, and renal injury. 173 Apr 47

Mandibuloacral dysplasia (MAD) is a syndrome with onset in midchildhood. The predominant characteristics of MAD include flexion contractures; mandibular hypoplasia; loss of body fat; atrophic, speckled skin; and progressive osteolysis of the clavicles. We studied three males with MAD. Each had lipodystrophy of the extremities, with sparing of the face and neck. All had moderate hyperlipidemia. In response to oral glucose, each had a diabetic response, with peak insulin levels between 2870 and 22,960 pmol/L. Insulin-stimulated glucose disposal was determined in two patients with MAD. At an insulin infusion rate of 120 mU/m2 per minute, glucose disposal was less than 25% of that measured at similar levels of insulinemia in nondiabetic control subjects, indicating marked insulin resistance in patients with MAD. The insulin resistance occurred without obesity, excessive levels of counterregulatory hormones, or anti-insulin-receptor antibodies. We suggest that MAD is a previously undescribed form of lipodystrophic insulin-resistant diabetes mellitus.
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PMID:Severe insulin resistance and diabetes mellitus in mandibuloacral dysplasia. 173 53

Corpulent male rats of the atherosclerosis prone JCR:LA-corpulent strain were fed diets supplemented with 10% by weight of olive oil or red fish oil. These rats are obese, with VLDL hyperlipidemia and marked insulin resistance. The diets were maintained to 9 months of age. Olive oil-fed rats had a 45% reduction in triglyceride concentrations with no significant changes in cholesterol or phospholipids. Red fish oil caused significant reduction in all lipid classes, with a 65% reduction in triglycerides and 35% reduction in cholesterol concentrations. Olive oil caused increases in the relative concentrations of oleic acid-containing triglycerides, while red fish oil preferentially enriched the longer chain fatty acids. There were no significant changes in insulin or glucose metabolism. The incidence of myocardial lesions, characteristic of the JCR:LA-cp strain, was unaltered by either oil-supplemented diet. These results, in a spontaneous animal model for cardiovascular disease, are consistent with other studies showing that diets rich in n-3 fatty acids do not, in themselves, confer protection against cardiovascular disease in animal models with genetically or experimentally induced lipid disorders.
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PMID:Effect of dietary n-3 fatty acids on atherosclerosis prone JCR:LA-corpulent rats. 174 17

Physical training is associated with lower plasma insulin concentrations and increased sensitivity to insulin in skeletal muscle and adipose tissue of individuals with non-insulin-dependent diabetes mellitus (NIDDM). The benefits of exercise to individuals with NIDDM in terms of increased insulin sensitivity could be applied to reversing the insulin resistance associated with gestational diabetes mellitus (GDM). Exercise may also benefit women with GDM by acting as an adjunct to diet in preventing excessive weight gain and preventing or decreasing the severity of hypertension and/or hyperlipidemia during pregnancy. Regular physical exercise should be considered as a potential approach to the prevention and treatment of GDM.
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PMID:Exercise in the treatment of NIDDM. Applications for GDM? 174 53

The aim of the present investigation was to study the effects of fish oil feeding in obese Zucker rats to establish its suitability as an animal model of hyperlipidaemia, and to understand the possible mechanism of fish oil-induced perturbations in cell metabolism. Lean and obese Zucker rats were fed on diets containing 180 g coconut, safflower, or menhaden oil/kg for 10 weeks. Body-weights and food intakes of lean coconut (LC), safflower (LS), and menhaden (LM) groups were similar. Obese menhaden (OM) rats had lower food intakes and body-weights compared with obese coconut (OC) and obese safflower (OS) groups, but values for all obese rats were higher than those for lean rats. Liver weights were higher in obese compared with lean rats, but on a percentage body-weight basis menhaden oil rats had higher values within genotype. Serum cholesterol and triacylglycerol levels were lower in the OM group compared with the OC and OS groups, and in the LM group compared with the LC group. Glucose and insulin levels were highest in OS rats followed by OC and OM rats and then the lean rats. Serum triiodothyronine and thyroxine were lower in OM rats compared with OC and OS rats. Liver mitochondrial state 3 rates with glutamate-malate and succinate were lower; mitochondrial beta-oxidation was unaffected and peroxisomal beta-oxidation was higher in menhaden oil rats compared with both coconut and safflower oil rats. In general, consumption of menhaden oil lowered hepatic malic enzyme (EC 1.1.1.38, 1.1.1.40), glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and glutathione peroxidase (EC 1.11.1.9) activities and elevated long-chain fatty acyl-CoA hydrolase (EC 3.1.2.2) activity when compared with the two other diets. It is concluded that obese Zucker rats do respond like human subjects to fish oil feeding but not to vegetable oils. The hypolipidaemic effect of fish oil appears to be mediated through a lowering of lipogenic enzymes, glucose-6-phosphate dehydrogenase and malic enzyme.
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PMID:Metabolic effects of coconut, safflower, or menhaden oil feeding in lean and obese Zucker rats. 176 Apr 46

Two main classes of oral hypoglycaemic drugs, the sulphonylureas and the biguanides, are currently used in the therapy of type II, non-insulin-dependent diabetes mellitus (NIDDM). The basic pharmacokinetic properties of these agents are discussed with a view to efficient and safe treatment. Both first- and second-generation sulphonylureas are rapidly absorbed from the gastrointestinal tract. In the plasma compartment, these drugs are strongly bound to serum proteins. All sulphonylureas are metabolised in the liver, and the metabolites and the parent drugs are eliminated mainly in the urine, but also (second-generation derivatives) in the faces. Rapid- and short-acting sulphonylureas may improve early insulin release and promote better postprandial glucose control. Long-acting derivatives may ensure better control of overnight glycaemia. The elderly are at risk of developing severe sulphonylurea-induced hypoglycaemia, and in this population the agent chosen should have a short or intermediate duration of action and no active metabolites. Caution is needed when prescribing any sulphonylurea in patients receiving drugs known to affect sulphonylurea action, and in those with impaired liver and/or kidney function. The bioavailability of the biguanides ranges from 40 to 60%. Binding to plasma proteins is absent or very low. Metformin and buformin are not metabolised and are excreted in the urine; phenformin undergoes hepatic hydroxylation and is excreted in both urine and faeces. Metformin is the only agent of this class currently recommended for clinical use. The main indications of metformin treatment are NIDDM associated with obesity and/or hyperlipidaemia, and in combination with sulphonylurea both as primary treatment and when secondary failure occurs with sulphonylurea alone. Lactic acidosis may develop in patients receiving therapy with biguanides, especially in the presence of a preexisting contraindication to their use.
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PMID:Pharmacokinetic optimisation of oral hypoglycaemic therapy. 176 Sep 2

When adipose tissue enlarges in obesity, as the result of an imbalance between caloric intake and caloric expenditure, many changes occur in the cellular components of the adipose mass. A combination of increased cell size and number underlies the accretion of the adipose mass, however, only a reduction in cell size is possible with weight loss. Several metabolic abnormalities accompany obesity--most important--hyperinsulinemia, hyperlipidemia, insulin resistance, and carbohydrate intolerance. Clinical consequences of obesity include hypertension, venous insufficiency, gallbladder disease, osteoarthritis, pulmonary and cardiovascular insufficiency, diabetes, and atherosclerotic cardiovascular disease, and all are dependent on the severity and duration of the obesity. Once established, obesity is difficult to correct because of the development of many adaptive mechanisms by which obesity defends itself.
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PMID:Cellular, metabolic, and clinical consequences of adipose mass enlargement in obesity. 180 21

In the last years, a plasmatic fibrinogen increase, a fibrinolytic system activity reduction and platelet activation, seemed to play a significant role on the genesis and progression of atheromatous plaques, especially when combined to a plasmatic lipoprotein increase. The results obtained in normolipidaemic patients (2000 asymptomatic subjects, 364 non-insulin diabetic patients randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 69 nifedipine-30 mg/daily-treated subjects, and 38 patients submitted to nifedipine-30 mg/daily-combined to indobufen-400 mg/daily-therapy), are reported. The results obtained in hyperlipidaemics (blood cholesterol level > 240 mg/dl; 356 patients, randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 56 patients with simvastatin 40 mg/daily and 85 with low saturated fat and low cholesterol diet), are also reported. Follow-up of all the patients was 4 years, but the simvastatin group followed-up only 1 year. An ultrasound examination of carotid and femoral arteries was performed in all the patients by means of a Duplex Scanner ATL Ultramark 5, with a high resolution probe (10 MHz). Subjects were graded into I-VI classes, according to the vessel progressive atherosclerotic impairment. In normolipidaemics, wall atheromatous changes were seen with increasing frequency with age, and a significant relationship among plaque progression rate and developed cerebrovascular symptoms, developed symptomatic peripheral symptoms, increased cardiovascular events and mortality rate, was evidenced. Non-insulin dependent diabetes, combined to normal levels of blood lipoproteins, appears an independent risk factor, superimposable to hyperlipidaemia. In this group of patients, bezafibrate therapy significantly reduced plaque progression, acting on blood coagulation factors and similar results were obtained in nifedipine and nifedipine plus indobufen groups. Also in hyperlipidaemics treated with diet, simvastatin and bezafibrate, the plaque progression was significantly reduced with respect to control group, especially when blood lipoproteins and coagulation were normalized. In conclusion, hyperlipidaemia, Ca++ and blood coagulation disorders, appear to be the main factors affecting the plaque progression, and the prevalence of each factor in the atheroma development must be well evaluated in the single patients to establish an adequate therapeutic strategies.
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PMID:[Modern trends in the therapy of arteriosclerosis in the light of new physiopathological findings]. 184 88

Renal disease is a frequent and serious complication of type I glycogen storage disease. A type I glycogen storage disease patient with focal segmental glomerulosclerosis and progressive renal insufficiency underwent a renal allograft transplantation. Despite the same cornstarch therapy, the post-transplantation course was complicated by worsening of the metabolic control manifested by exacerbated lactic acidaemia and hyperlipidaemia. This lactic acidaemia was remarkable for its association with hyperglycaemia. Hyperglycaemia accompanied by lactic acidaemia is strikingly unusual in type I glycogen storage disease, since this is a disease characterized by hypoglycaemia and an inverse relationship between blood glucose concentration and lactate levels. Both fasting insulin and C-peptide levels in the patient were greater than similar age-matched type I glycogen storage disease controls, indicating hyperinsulinaemia. The most likely mechanism responsible for the combined hyperglycaemia and lactic acidaemia was insulin resistance due to glucocorticoid treatment, instituted for immunosuppression. The hyperglycaemia associated with the lactic acidaemia was transient and resolved with steroid tapering. The exacerbated hyperlipidaemia, however, persisted after renal transplantation. Type I glycogen storage disease patients may be prone to glucocorticoid-induced insulin resistance, since the cellular metabolism in these patients may already be compromised with ineffective insulin action and/or reduced insulin output.
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PMID:Hyperglycaemia associated with lactic acidaemia in a renal allograft recipient with type I glycogen storage disease. 186 63

Dyslipidemia of chronic renal failure is of multifactorial origin. Decreased activity of lipoprotein lipase and hepatic triglyceride lipase, peripheral insulin resistance, hyperparathyroidism and L-carnitine deficiency are the contributing factors. This results in a disturbed catabolism of chylomicron, accumulation of very-low-density (VLDL) and intermediate-density (IDL) lipoproteins as well as incompletely cleared remnant particles, whereas low-density lipoprotein (LDL) levels are diminished. There is current debate as to whether cardiovascular disease is accelerated and whether hyperlipidemia should specifically be treated. In addition, there have been few means of influencing these metabolic alterations. Drug incompatibility and consequently side effects render treatment difficult. The drugs that have been most tested for lipid lowering in chronic renal failure are the fibric acids. By their mode of action, they are the logical choice. Dose reduction overcomes major side effects such as myopathy and rhabdomyolysis. The second generation of fibric acid derivatives (gemfibrozil and beclobrate) show several advantages over formerly used derivatives. Treatment with lovastatin and simvastatin appears to be safe and is recommended in a minority of patients with predominantly elevations of LDL. HMG-CoA reductase inhibitors also lower remnant particles effectively in hemodialysis (HD) patients. L-Carnitine and low-molecular-weight heparin have been shown to influence VLDL rich in triglycerides in a subset of patients on HD. In posttransplant hyperlipidemia, diet remains the first course of action in all patients. When this approach fails, the new lipid-lowering agents, especially fibric acids, appear to be safe in short-term studies in azathioprine- and ciclosporin-treated patients. Lovastatin has been shown to be safe in stable renal transplant patients. Its toxicity seems to depend mainly on high ciclosporin whole blood through or plasma levels.
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PMID:Hyperlipoproteinemia in chronic renal failure: pathophysiological and therapeutic aspects. 186 98


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