Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mechanisms responsible for the accumulation of low-density lipoprotein (LDL) were investigated in a new model, the perfused hamster aorta. To do this, we developed a method to study LDL flux in real time in individually perfused arteries; each artery served as its own control. Using quantitative fluorescence microscopy, the rates of LDL accumulation and efflux were separately determined. Perfusion of arteries with buffer plus lipoprotein lipase (LpL) increased LDL accumulation 5-fold (0.1 +/- 0.03 mV/min [control] versus 0.5 +/- 0.05 mV/min [LpL]) by increasing LDL retention in the artery wall. This effect was blocked by heparin and monoclonal antibodies directed against the amino-terminal region of apolipoprotein B (apo B). This suggests that specific regions of apo B are involved in LDL accumulation within arteries. Also, the effect of hydrolysis of triglyceride-rich lipoproteins on endothelial barrier function was studied. We compared endothelial layer permeability using a water-soluble reference molecule, fluorescently labeled dextran. When LpL was added to hypertriglyceridemic plasma, dextran accumulation within the artery wall increased > 4-fold (0.024 +/- 0.01 mV/min [control] versus 0.098 +/- 0.05 mV/min [LpL]). Under the same conditions, LpL increased LDL accumulation approximately 3-fold (0.016 +/- 0.003 mV/min [control] versus 0.047 +/- 0.013 mV/min [LpL]). Rapid efflux of LDL from the artery wall indicated that increased endothelial layer permeability was the primary mechanism during periods of increased lipolysis. Our data demonstrate two LpL-mediated effects that may increase the amount of LDL in the artery wall. These findings may pertain to the observed relationship between increased postprandial lipemia and atherosclerosis.
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PMID:Lipoprotein lipase increases lipoprotein binding to the artery wall and increases endothelial layer permeability by formation of lipolysis products. 916 84

Fibrinogen is an important risk factor for atherosclerosis, stroke and cardiovascular heart disease (CHD). This risk is increased when associated with a high serum cholesterol. Furthermore, it is also believed that not only fibrinogen concentration, but also the quality of fibrin networks may be an important risk factor for the development of CHD. CHD and stroke as a result of atherosclerosis, plus the related problems of hyperinsulinaemia, hyperlipidaemia and hypertension are strongly related to diet. The "western" diet, defined by low fibre and high fat, sucrose and animal protein intakes, appears to be a major factor leading to death. It has been established that the water-soluble dietary fibre, pectin, significantly decrease the concentration of serum cholesterol levels. Evidence is also accumulating that a diet rich in fibre may protect against diseases associated with raised clotting factors. This investigation studied the possible effects of pectin on fibrinogen levels and fibrin network architecture. Two groups of 10 male hyperlipidaemic volunteers each, received a pectin supplement (15 g/day) or placebo (15 g/day) for 4 weeks. Lipid and fibrin network structure variables were measured at baseline and the end of supplementation. Pectin supplementation caused significant decreases in total cholesterol, low-density lipoprotein cholesterol, apolipoprotein A & B and lipoprotein (a). Significant changes in the characteristics of fibrin networks developed in the plasma of the pectin supplemented group indicated that networks were more permeable and had lower tensile strength. These network structures are believed to be less atherogenic. It is suspected that pectin modified network characteristics by a combination of its effects on metabolism and altered fibrin conversion. This confirms the therapeutic possibilities of dietary intervention. Furthermore, this study also showed that changes in plasma fibrinogen need not be present to induce alterations in fibrin network architecture.
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PMID:Dietary pectin influences fibrin network structure in hypercholesterolaemic subjects. 917 40

Patients with chronic renal failure retain Na+ and H2O, and they retain K- and acid. This disordered homeostasis results in hypertension, edema, hyperkalemia and acidosis. Diuretics may be used to favorably modify these disturbances. However, because of the limited filtered load of water and electrolytes, and the low renal blood flow, measures need to be taken to maximize the response to diuretics. These measures include: (a) the use of the most bioavailable drug, torasemide, when using the oral route; (b) the use of the drug with the least hepatic elimination, furosemide, when using the intravenous route; (c) the use of combinations of loop- and distal tubule-acting diuretics; (d) the use of the maximum effective diuretic dose; and (e) the use of repeated doses or constant infusion. In benefiting hypertension, vascular congestion and hyperkalemia diuretics appear to exert their effects not only on the kidneys but also on extrarenal sites, such as the vascular tree and the gastrointestinal tract. The use of diuretics, however, is not without complications, which include: intravascular volume depletion and azotemia, ototoxicity (when using loop-acting diuretics), hyperlipidemia, acute pancreatitis, hyperkalemia (when using K(+)-sparing agents), and acidosis (when using carbonic anhydrase inhibitors).
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PMID:Use of diuretics in chronic renal failure. 918 1

The JCR:LA-cp rat exhibits the obesity/insulin resistance/hypertriglyceridemia syndrome in an extreme form. These normotensive rats spontaneously develop advanced atherosclerosis and ischemic myocardial lesions. The calcium channel antagonist, nisoldipine, was administered to obese rats of the JCR:LA-cp strain in drinking water at a dose of 1 mg/kg from age 6 weeks. Nisoldipine-treated rats showed no change in food consumption or body weight compared with control animals. Plasma glucose and insulin levels also were unchanged in the nisoldipine-treated rats. Insulin-mediated total glucose turnover, an index of insulin sensitivity as measured by euglycemic insulin clamp, was similarly not improved. Serum triglyceride levels in obese male rats were markedly reduced (57%; p < 0.001, at age 12 weeks), whereas obese female rats showed no significant change in triglyceride levels and an increase in esterified cholesterol in response to nisoldipine treatment. The impaired endothelium-dependent (nitric oxide-mediated) vascular relaxation of the male cp/cp rats was not improved by nisoldipine treatment. The severity of atherosclerotic raised lesions in the aortic arch of male cp/cp rats was significantly reduced (p < 0.01) by nisoldipine treatment, and this was accompanied by a major reduction in the incidence of ischemic myocardial lesions (85%; p < 0.01). Thus nisoldipine treatment ameliorates atherosclerotic damage and myocardial injury even in the presence of gross obesity, hyperinsulinemia, and significant hyperlipidemia. This effect appears to involve protection of the vascular wall from atherogenesis and probably antivasocontractile effects at the smooth muscle level as well.
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PMID:Cardioprotective and hypolipidemic effects of nisoldipine in the JCR:LA-cp rat. 921 99

In a series of studies on histaminergic functions in the hypothalamus, probes to manipulate activities of histaminergic neuron systems were applied to assess its physiologic and pathophysiologic implications using non-obese normal and Zucker obese rats, an animal model of genetic obesity. Food intake is suppressed by either activation of H1-receptor or inhibition of the H3-receptor in the ventromedial hypothalamus (VMH) or the paraventricular nucleus, each of which is involved in satiety regulation. Histamine neurons in the mesencephalic trigeminal sensory nucleus modulate masticatory functions, particularly eating speed through the mesencephalic trigeminal motor nucleus, and activation of the histamine neurons in the VMH suppress intake volume of feeding at meals. Energy deficiency in the brain, i.e., intraneuronal glucoprivation, activates neuronal histamine in the hypothalamus. Such low energy intake in turn accelerates glycogenolysis in the astrocytes to prevent the brain from energy deficit. Thus, both mastication and low energy intake act as afferent signals for activation of histaminergic nerve systems in the hypothalamus and result in enhancement of satiation. There is a rationale for efficacy of a very-low-calorie conventional Japanese diet as a therapeutic tool for weight reduction. Feeding circadian rhythm is modulated by manipulation of hypothalamic histamine neurons. Hypothalamic histamine neurons are activated by an increase in ambient temperature. Hypothalamic neuronal histamine controls adaptive behavior including a decrease in food intake and ambulation, and an increase in water intake to maintain body temperature to be normally constant. In addition, interleukin-1 beta, an endogenous pyrogen, enhanced turnover of neuronal histamine through prostaglandin E2 in the brain. Taken together, the histamine neuron system in the hypothalamus is essential for maintenance of thermoregulation through the direct and indirect control of adaptive behavior. Behavioral and metabolic abnormalities of obese Zucker rats including hyperphagia, disruption of feeding circadian rhythm, hyperlipidemia, hyperinsulinemia, and disturbance of thermoregulation are essentially derived from a defect in hypothalamic neuronal histamine. Abnormalities produced by depletion of neuronal histamine from the hypothalamus in normal rats mimic those of obese Zuckers. Grafting the lean Zucker fetal hypothalamus into the obese Zucker pups attenuates those abnormalities. These findings indicate that histamine nerve systems in the brain play a crucial role in maintaining homeostatic energy balance.
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PMID:Hypothalamic neuronal histamine: implications of its homeostatic control of energy metabolism. 922 31

We examined the effects of oyster (Ostrea gingas Thunb.) water extracts on hyperlipemia and liver injury produced in rats by feeding on peroxidized oil. The extracts of oyster were found to reduce the levels of serum free fatty acid, triglyceride, lipid peroxide and liver cholesterol in the peroxidized oil-treated rats. In addition, we found that the water extracts of oyster inhibited adrenaline-induced lipolysis, and that these extracts stimulated lipogenesis from glucose in isolated fat cells of rats. The active substance was isolated and identified as adenosine by direct comparison with an authentic sample.
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PMID:Effects of extract of oyster on lipid metabolism in rats. 950 94

The serum sodium concentration reflects the osmolality of the extracellular fluid and provides no direct information about total body sodium content. Patients with hyponatremia may have decreased, normal, or increased total body sodium content. The first step in the approach to the patient with hyponatremia is measurement of plasma osmolality. Hyponatremia with normal plasma osmolality results from hyperlipemia or hyperproteinemia, whereas hyponatremia with increased plasma osmolality results from hyperglycemia or mannitol infusion. Patients with hyponatremia and decreased plasma osmolality may be hypovolemic, hypervolemic, or normovolemic. The volume status of the patient is best determined by history, physical examination, and a few ancillary tests (e.g., total plasma protein concentration, hematocrit, blood pressure, central venous pressure). The clinical signs of hyponatremia are related more to the rapidity of onset than to the severity of the associated plasma hypoosmolality and reflect influx of water into the central nervous system. The main goals of treatment in hyponatremia are to diagnose and manage the underlying disease and, if necessary, to increase serum sodium concentration and plasma osmolality.
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PMID:Hyponatremia. 959 12

The aim of the present study was to evaluate the effects of three fibres (sugar-beet fibre, guar gum and inulin) incorporated in the basal diet of healthy dogs at 7 per cent of dry matter (DM). Parameters examined included stool output, water consumption, nutrient digestibility and fasting and postprandial plasma metabolites. All fibres increased wet faecal output; an increase in faecal DM output being observed with sugar-beet fibre only. Sugar-beet fibre and inulin increased daily water consumption. Sugar-beet fibre and guar gum decreased DM digestibility. The three fibres diminished organic matter and crude protein digestibility while ether extract digestibility was decreased by guar gum and inulin. Guar gum induced lower postprandial insulin, alpha-amino-nitrogen and urea plasma concentrations. Guar gum also lowered fasting cholesterolaemia. Sugar-beet fibre and inulin showed no metabolic effects. These physiological properties suggest that guar gum would be a suitable ingredient for dietary therapy of chronic diseases such as diabetes mellitus or hyperlipidaemia in the dog.
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PMID:The influence of sugar-beet fibre, guar gum and inulin on nutrient digestibility, water consumption and plasma metabolites in healthy Beagle dogs. 962 62

This article reviews the nutritional requirements of puberty and the clinical assessment of nutritional status, and discusses the nutritional risks imposed by vegetarian diets, pregnancy, and athletic involvement. Energy (calories) and protein are essential in pubertal development. Adolescent females require approximately 2200 calories/day, whereas male adolescents require 2500-3000 calories/day. Additional intake requirements include fat, calcium, iron, zinc, vitamins, and fiber. The clinical assessment of nutritional status begins with obtaining a good diet history of the patient and this could be offered by the body mass index. Nutritional deficiencies and poor eating habits established during adolescence can have long-term consequences, including delayed sexual maturation, loss of final adult height, osteoporosis, hyperlipidemia, and obesity. As for vegetarian adolescents, nutritional risks include lack of iodine, vitamin B12, vitamin D, and some essential fatty acids. In addition, substances in some grains reduce gut absorption, thus increasing mineral deficiencies. Pregnancy may also be a risk factor for poor nutrition during adolescence. A pregnant adolescent has different nutritional needs because she is still growing. Among adolescent athletes many are turning to nutritional supplements in an attempt to improve athletic performance. A balanced, varied diet provides adequate calories and nutrition to meet the needs of most adolescents. They also have greater water needs than do adult athletes. Details on adolescent health concerns are further discussed in this article.
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PMID:Nutrition in the adolescent. 1003 86

This is a preliminary study in which both acute and chronic oral administration of bis(maltolato)oxovanadium (IV) (BMOV) was examined in the Zucker diabetic fatty (ZDF) rat, an animal model that develops overt hyperglycemia in the presence of hyperinsulinemia followed by beta-cell depletion. At 9-10 weeks of age, in the presence of hyperglycemia, hyperinsulinemia and hyperlipidemia, an acute oral gavage dose response was conducted to determine glucose-lowering properties of BMOV, time of response and effect of BMOV on plasma insulin levels. Doses of BMOV greater than 0.2 mmol/kg resulted in plasma glucose levels of less than 9 mmol/l. The highest dose administered (0.8 mmol/kg) significantly reduced plasma insulin (initial: 2.83+/-0.2, final: 1.23+/-0.09 nmol/l, P<0.05) and plasma triglyceride (initial: 4.94+/-0.33, final: 1.55+/-0.07 mmol/l, P<0.05) levels. At 15 weeks of age, in the presence of hyperglycemia, hyperlipidemia and normal insulin levels, BMOV was administered orally in the drinking water for a 10-week period to determine the effect of treatment on glucose, insulin and lipid levels. BMOV treatment significantly reduced plasma glucose levels (final BMOV-treated: 13.25+/-1.43, untreated: 28.71+/-0.6 mmol/l, P<0.05) and effectively preserved pancreatic beta-cell function. These data suggest a role for BMOV as a therapeutic agent in non-insulin-dependent diabetes mellitus through improvement in glucose homeostasis and preservation of insulin reserves.
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PMID:Acute and chronic oral administration of bis(maltolato)oxovanadium(IV) in Zucker diabetic fatty (ZDF) rats. 1019 84


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