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)

A model of maternal lipemia without hyperglycemia, in the rat, produced by high-fat feedings, was developed to study the effects of and abnormal maternal lipid homeostasis on placental transport of nutrients and possible alterations of key enzymes of energy metabolism in the liver and brain of the fetuses. Pregnant rats fed lower concentrations of fat served as controls. All studies were carried out in dams and fetuses one day prior to delivery. The dietary treatment of the dams and fetuses produced in the fetuses ketonemia as well as lipemia. Following a bolus of 14C-3-0-methyl-D-glucose to the dams, the levels of the tracer remained higher in the blood and brain of lipemic than in control fetuses. By contrast, there was a decrease in the fluxes of 14C-alpha-amino-isobutyric acid in the fetuses of lipemic dams as compared to controls. Among enzymes of energy metabolism, fetal liver glucose-6-phosphatase and succinic dehydrogenase were enhanced by lipemia. Fetal brain glucose-6-phosphatase was depressed. Thus, lipemia, as occurring in poorly controlled maternal diabetes, may be a factor in determining the access to the fetus of essential, neutral amino acids and alter the normal activity of energy metabolism enzymes in the fetus.
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PMID:Placental permeability and energy metabolism enzymes in fetuses of lipemic rats. 710 47

Galactomannan currently seems to be a very promising auxiliary. The aim of the present work was to examine the applicability of this auxiliary in tablet-making. Galactomannan is a polysaccharide composed of galactose and mannose, which is distributed by the Swiss firm Meyhall under the name Meyprogat. The products are numbered according to their molecular weight and polymeric degree. Thus, Meyprogat 7, 30, 60, 90, 120 and 150 can be discriminated. It is used in many areas, for example in the food industry as a stabilizing agent, and in medical therapy to cure diabetes and hyperlipidaemia. In pharmaceutical technology, it is used in low concentration (5-10%) as a disintegrant agent and in high concentration (25%) as binding agent. It is able to form a hydrophilic matrix, which results in sustained release. Theophylline was chosen as model agent. After the preformulation examinations, granulations were made by a wet method, and after this tablets were formed. Examinations were made of the granulations, the physical parameters of the tablets were determined, and the release of the effective agent from the tablets was studied. The following conclusions were drawn: 1. Galactomannan yields tablets with very good hardness. 2. Galactomannan is suitable for the formation of hydrophilic matrix tablets. Through use of this macromolecular agent, the rate of dissolution can be influenced in accordance with the desired purpose.
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PMID:[Use of galactomannan to produce hydrophilic matrix tablets]. 802 83

Eighty five very low birth weight (VLBW) babies with birthweight less than 1250 g were randomly assigned such that 43 received parenteral nutrition (PN) with amino acid based glucose electrolyte solution (Vamin) and lipid emulsion (Intralipid) in the first 16 days of life. The other 42 (control group) received conventional intravenous dextrose with or without electrolytes plus enteral milk regimen. Baseline clinical parameters and neonatal problems encountered in the two groups were similar. There was no significant difference in the mortality rate in the two groups (48.9% in PN group and 42.9% in control group: X2 = 0.3, p > 0.05). The commonest cause of mortality in both the groups was septicemia (16.3% and 26.1% in PN and control groups, respectively). Local complications, sepsis and fluid electrolyte disturbances were similar in the two groups. Azotemia (25.6%), hyperlipidemia (9.3%), metabolic acidosis (9.3%) and prolonged cholestasis (14%) were commoner in the PN group but were reversible with early recognition. Time taken to regain birthweight was also similar in the two groups (X2 = 14.2 and 15.2 days for PN and control groups, respectively). Thus, PN failed to improve the survival or early weight gain in the routine management of the VLBW babies in our unit.
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PMID:Parenteral nutrition (PN) in the management of very low birth weight (VLBW) babies--a randomized controlled trial. 863 77

Marked changes in the plasma concentration of several non-glucose monosaccharides have been detected among patients++ with end-stage renal disease. To find changes specific to renal disease and not caused by a failing urinary excretion, we studied the plasma monosaccharide concentration in patients with early-stage glomerulonephritis whose renal function was normal or only mildly compromised. Plasma mannose, fructose and 1,5-anhydroglucitol (1,5-AG) concentrations were measured using gas chromatography/mass spectrometry and isotope-labelled sugar standard additions. The daily urinary protein excretion was positively correlated with the plasma cholesterol (r = 0.785), mannose (r = 0.550), triglyceride (r = 0.531 ) and fructose (r = 0.401) concentrations, while the correlation with 1,5-AG (r = -0.581) was inverse. The correlations were statistically significant. As previous studies have revealed a close positive correlation between the plasma mannose and glucose concentrations, we calculated the mannose/glucose concentration ratio to find out whether the increase in mannose concentration was or was not explained by ambient glucose. There was a strong correlation between the ratio and the urinary protein excretion (r = 0.704). It is inferred that the metabolic syndrome associated with glomerulonephritis and characterised by hyperlipidemia also involves a derangement in mannose and 1,5-AG metabolism.
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PMID:Proteinuria and plasma hexosugars in early-stage glomerulonephritis. 886 96

Why is it important to understand the mechanisms controlling intestinal adaptation? There are two major answers to this question. Firstly, in establishing the cellular and molecular events associated with intestinal adaptation, we will formulate a general framework that may be applied to the understanding of adaptation of other cell membranes. For example, alterations in the synthesis of glucose carriers and their subsequent insertion into membranes may alter sugar entry across the intestinal brush border membrane (BBM) using the sodium-dependent D-glucose transporter, SGLT1, or the BBM sodium-independent facultative fructose transporter, GLUT5, and may alter facilitated sugar exit across the basolateral membrane (BLM) using GLUT2. The precise role of transcriptional and translational processes in the up- or down-regulation of sugar transport requires further definition. Alterations in enterocyte microsomal lipid metabolic enzyme expression occurring during the course of intestinal adaptation will direct the synthesis of lipids destined for trafficking to the BBM and BLM domains of the enterocyte. This will subsequently alter the passive permeability properties of these membranes and ultimately influence lipid absorption. Therefore, establishing the physiological, cellular and molecular mechanisms of adaptation in the intestine will define principles that may be applied to other epithelia. Secondly, enterocyte membrane adaptation is subject to dietary modification, and these may be exploited as a means to enhance a beneficial or to reduce a detrimental aspect of the intestinal adaptive process in disease states. Alterations in membrane function occur in association with changes in dietary lipids, and these are observed in a variety of cells and tissues including lymphocytes, testes, liver, adipocytes, nerve tissue, nuclear envelope and mitochondria. Therefore, the elucidation of the mechanisms of intestinal adaptation and the manner whereby dietary manipulation modulates these processes affords the future possibility of dietary engineering aimed at using food as a therapeutic agent. It is hoped this approach will form the centerpiece for future investigation that would focus on disease prevention, as well as on the development of better therapeutic strategies to prevent the development or to treat the complications of conditions such as diabetes mellitus, obesity, hyperlipidemia and inflammatory bowel diseases. This review deals with the physiology of glucose transport with specific emphasis on transporters of the brush border membrane (BBM) and the basolateral membrane (BLM). On the BBM the sodium (Na)/glucose transporters (SGLT1 and SGLT2), the Na-independent transporter (GLUT5), and on the BLM the hexose transporter (GLUT2) are discussed. The molecular biology of these transporters is also reviewed.
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PMID:Adaptation of intestinal nutrient transport in health and disease. Part I. 907 26

Insulin resistance is of pathogenic importance in several common human disorders including type 2 diabetes, hypertension, obesity and hyperlipidemia, but the underlying mechanisms are unknown. The spontaneously hypertensive rat (SHR) is a model of these human insulin resistance syndromes. Quantitative trait loci (QTLs) for SHR defects in glucose and fatty acid metabolism, hypertriglyceridemia, and hypertension map to a single region on rat chromosome 4. Genetic analysis of an SHR derived from a National Institutes of Health colony led to the identification of a causative mutation in the SHR Cd36. We have investigated glucose and fatty acid metabolism in the stroke-prone SHR (SHRSP). We demonstrate defects in insulin action on 2-deoxy-D-glucose transport (SHRSP 3.3 +/- 1.5 vs. 21.0 +/- 7.4 pmol x min(-1) x [20 microl packed cells](-1), SHRSP vs. WKY, respectively, P = 0.01) and inhibition of catecholamine-stimulated lipolysis (P < 0.05 at all concentrations of insulin) in adipocytes isolated from SHRSP. In contrast, basal levels of catecholamine-stimulated nonesterified free fatty acid (NEFA) release and plasma levels of NEFA are similar in SHRSP and WKY. These results are in agreement with the data on the SHR.4 congenic strain, which suggested that the QTL containing Cd36 mutations accounted for the entire defect in basal catecholamine action but only for approximately 40% of the SHR defect in insulin action. In the SHR, both abnormalities appear consequent of defective Cd36 expression. Because Cd36 sequence and expression are apparently normal in SHRSP, it is likely that the molecular mechanism for defective insulin action in this strain is caused by a gene(s) different than Cd36.
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PMID:Cd36 and molecular mechanisms of insulin resistance in the stroke-prone spontaneously hypertensive rat. 1111 30

This study was designed to monitor the metabolic differences after feeding starch, galactose and fructose diets with adequate or marginal copper levels to normal male rats over a period of 9-21 months. Two hundred and forty-five weanling male Sprague-Dawley rats weighing approximately 50-60 g were randomly divided into one of the eight dietary groups. All diets were either Cu marginal (1.5 &mgr;g/g diet) or adequate (5-6 &mgr;g/g) with 627 carbohydrate (g/kg diet) as starch; 500 galactose and 127 starch; 500 fructose and 127 starch; or 400 galactose and 227 fructose. Glycated hemoglobin, ceruloplasmin oxidase activity, hematocrit, and plasma glucose, cholesterol, and triglyceride were measured in 72 rats after nine months. Galactose-fed rats had the lowest (P < 0.0001) body weights. Severe mortality rates were found in galactose-fructose-marginal Cu-fed rats. Marginal Cu deficiency significantly (P < 0.0001) reduced hepatic copper and increased hepatic Fe in all carbohydrate groups. Ceruloplasmin activity of the rats fed the marginal Cu and fructose-containing diets declined to undetectable levels and plasma cholesterol levels increased. Glycated hemoglobin was significantly (P < 0.001) increased in the galactose-fed rats compared to fructose or starch-fed rats regardless of dietary copper concentration. The data suggest that dietary galactose and fructose exacerbate effects of long term marginal Cu intake including hypertrophy of liver, heart and kidney, hyperlipidemia, and increased mortality.
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PMID:Effects of dietary galactose and fructose on rats fed diets marginal or adequate in copper for 9-21 months. 1144 91

One new flavonoide was isolated from Vicia amoena Fisch. On the basis of spectral (UV, MS, NMR) and chemical reactions, it was elucidated to be kaempferol-3-O-beta-D-mannoside, named amoenin(A3). Moreover, five known compounds have been isolated and identified as quercetin, kaempferol, quercetin-3-O-alpha-L-rhamoside, quercetin-3-O-beta-D-glucoside, kaempferol-3, 7-O-alpha-L-dirhamoside. The total flavonoides showed significant effects on inducing hyperlipidemia and increasing micro-blood vessel elasticity.
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PMID:[Studies on the chemical constitutens of Vicia amoena Fisch]. 1159 20

This study included the following experiments: (1) effects of dextrose solution (250 mL of water containing 75 g of dextrose) or honey solution (250 mL of water containing 75 g of natural honey) on plasma glucose level (PGL), plasma insulin, and plasma C-peptide (eight subjects); (2) effects of dextrose, honey, or artificial honey (250 mL of water containing 35 g of dextrose and 40 g of fructose) on cholesterol and triglycerides (TG) (nine subjects); (3) effects of honey solution, administered for 15 days, on PGL, blood lipids, C-reactive protein (CRP), and homocysteine (eight subjects); (4) effects of honey or artificial honey on cholesterol and TG in six patients with hypercholesterolemia and five patients with hypertriglyceridemia; (5) effects of honey for 15 days on blood lipid and CRP in five patients with elevated cholesterol and CRP; (6) effects of 70 g of dextrose or 90 g of honey on PGL in seven patients with type 2 diabetes mellitus; and (7) effects of 30 g of sucrose or 30 g of honey on PGL, plasma insulin, and plasma C-peptide in five diabetic patients. In healthy subjects, dextrose elevated PGL at 1 (53%) and 2 (3%) hours, and decreased PGL after 3 hours (20%). Honey elevated PGL after 1 hour (14%) and decreased it after 3 hours (10%). Elevation of insulin and C-peptide was significantly higher after dextrose than after honey. Dextrose slightly reduced cholesterol and low-density lipoprotein-cholesterol (LDL-C) after 1 hour and significantly after 2 hours, and increased TG after 1, 2, and 3 hours. Artificial honey slightly decreased cholesterol and LDL-C and elevated TG. Honey reduced cholesterol, LDL-C, and TG and slightly elevated high-density lipoprotein-cholesterol (HDL-C). Honey consumed for 15 days decreased cholesterol (7%), LDL-C (1%), TG (2%), CRP (7%), homocysteine (6%), and PGL (6%), and increased HDL-C (2%). In patients with hypertriglyceridemia, artificial honey increased TG, while honey decreased TG. In patients with hyperlipidemia, artificial honey increased LDL-C, while honey decreased LDL-C. Honey decreased cholesterol (8%), LDL-C (11%), and CRP (75%) after 15 days. In diabetic patients, honey compared with dextrose caused a significantly lower rise of PGL. Elevation of PGL was greater after honey than after sucrose at 30 minutes, and was lower after honey than it was after sucrose at 60, 120, and 180 minutes. Honey caused greater elevation of insulin than sucrose did after 30, 120, and 180 minutes. Honey reduces blood lipids, homocysteine, and CRP in normal and hyperlipidemic subjects. Honey compared with dextrose and sucrose caused lower elevation of PGL in diabetics.
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PMID:Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose. 1511 61

In the present study, the effect of mangiferin (a xanthone glucoside, isolated from the leaves of Mangifera indica) on the atherogenic potential of streptozotocin (STZ)-diabetes was investigated. In addition, the effect of mangiferin on oral glucose tolerance in glucose-loaded normal rats was also determined. The chronic intraperitoneal (i.p.) administration of mangiferin (10 and 20 mg/kg) once daily (o.d.) for 28 days exhibited antidiabetic activity by significantly lowering fasting plasma glucose level at different time intervals in STZ-diabetic rats. Further, mangiferin (10 and 20 mg/kg, i.p.) showed significant antihyperlipidemic and antiatherogenic activities as evidenced by significant decrease in plasma total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C) levels coupled together with elevation of high-density lipoprotein cholesterol (HDL-C) level and diminution of atherogenic index in diabetic rats. In addition, the chronic administration of mangiferin (10 and 20 mg/kg, i.p.) for 14 days significantly as well as markedly improved oral glucose tolerance in glucose-loaded normal rats suggesting its potent antihyperglycemic activity. The accumulating evidences suggest that both pancreatic and extrapancreatic mechanisms might be involved in its antidiabetic or antihyperglycemic action. In conclusion, the present study demonstrates that mangiferin possesses significant antidiabetic, antihyperlipidemic and antiatherogenic properties thus suggesting its beneficial effect in the treatment of diabetes mellitus associated with hyperlipidemia and related cardiovascular complications.
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PMID:Effect of mangiferin on hyperglycemia and atherogenicity in streptozotocin diabetic rats. 1574 Aug 86


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