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

Serum lipids were studied in iron-deficient and control rats during suckling and after weaning at 21, 30, and 60 days of age. Diets providing 5 or 307 ppm iron were fed to dams and their offspring during gestation, lactation, and after weaning. Rats on the deficient diet throughout the experimental period developed a hyperlipidemia characterized by elevated triglycerides, cholesterol, and phospholipids which was present at 21, 30, and 60 days. Control pups weaned to the deficient diet developed anemia at 30 days of age and hypertriglyceridemia at 60 days of age. Repletion of deficient rats with iron after weaning caused a rapid decline in serum lipid levels after only 9 days on the control diet. The hyperlipidemia of iron deficiency thus appears to be reversible with iron supplementation. The time required to develop hypertriglyceridemia in iron deficiency is longer postweaning than during suckling.
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PMID:Serum lipids in suckling and post-weanling iron-deficient rats. 51 75

Three levels of iron (5, 29, 307 ppm iron) were fed to rats from conception through the 18th day of lactation. Dams in the 5 ppm iron group and pups in the 5 and 29 ppm iron groups developed anemia characterized by lower hemoglobin and hematocrit values than control animals. Liver and spleen levels of iron in dams and pups in the 5 and 29 ppm iron groups were lower than in the 307 ppm iron groups. Milk iron was lower in the 5 ppm iron group than in the 29 and 307 ppm iron groups. Pups in the 5 ppm iron group had hyperlipidemia characterized by elevated serum triglycerides, cholesterol, and phospholipids. Milk lipids and post-heparin plasma lipoprotein lipase levels in pups did not differ among experimental groups. Triglyceride and CO2 production from [U-14C]glucose were significantly greater in the iron-deficient pups than in control pups. Hyperlipidemia in 18-day-old iron-deficient rat pups appears to be related to increased endogenous production of triglycerides.
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PMID:Iron deficiency hyperlipidemia in 18-day-old rat pups: effects of milk lipids, lipoprotein lipase, and triglyceride synthesis. 61 36

Nutrient requirements do not change markedly with advancing age, but life style, socioeconomic status, psychologic changes, and the presence of chronic disease alter nutrient intake in the elderly. It is important to recognize and deal with these factors in attempting to correct malnutrition and in prescribing dietary treatment. Malnutrition includes a variety of disorders: undernutrition, nutrient deficiencies and imbalances, and obesity. Frequent small feedings, with nutritional supplements for patients with profound weight loss, are the initial treatment for undernutrition. Iron supplements and a diet of foods rich in iron and in promoting iron absorption are required in treating iron deficiency anemia. Management of macrocytic anemia should include specific nutrient therapy plus improvement of diet to include leafy vegetables and animal foodstuffs. Diet is an important adjunct in treating chronic diseases. Maturity-onset diabetes mellitus often can be managed by diet alone, with attention to correct proportions of fat, carbohydrate, and protein and to the decreased caloric requirements of elderly patients. The importance of continuing dietary modifications in hyperlipidemia and hypertension is well known. Although dietary manipulation in osteoporosis is not curative, a diet high in calcium and containing adequate floride and vitamin D affords maximum dietary protection against progress of the disease.
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PMID:Guidelines for maintaining adequate nutrition in old age. 64 78

The aim of this paper was o study the long-term changes induced in the rat as a consequence of a 90% resection of small intestine. At 6 months after operation the surviving rats were stable and showed: hypoproteinemia, hyperlipemia, and a decrease of bile flow, total lipids, and cholesterol of bile. What residual intestine concern there was an increase in length and size, and decreased transit time; stomach, duodenum and colon too showed increase size. Histologically there was hypertrophy of villi, regressive changes of pancreas and kidney, as well as deposit of iron in the kidney. The reasons for these changes are discussed.
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PMID:[Metabolic and histological changes induced in the rat by massive resection of the small intestine]. 89 Aug 74

An improved method for analysis of serum iron is described which is simple, rapid, precise and convenient for routine use in clinical laboratories. Serum proteins are precipitated with trichloroacetic acid-hydrochloric acid solution, with simultaneous release of Fe(III) from transferrin. Fe(III) is reduced to Fe(II) by sodium ascorbate, and Fe(II) is reacted with ferrozine to form a lavender complex, which is measured by spectrophotometry at 562 nm. Measurements of iron in 183 serum samples by this method were compared with measurements by a "direct" spectrophotometric method without without deproteinization, as previously described. Close agreement was obtained in 171 of these 183 pairs of analyses (93.5 percent). Discrepancies (greater than 12 mug per dl) were noted in the remaining 12 serums, which were attributed to interference in direct spectrophotometric analyses of iron, owing to (1) hemolysis, (2) lipemia, (3) jaundice, (4) protracted storage or (5) repeated freezing and thawing of the serums.
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PMID:Modified method for analysis of serum iron. 116 95

We developed a direct, simple, and sensitive procedure for the simultaneous colorimetric assay of iron and copper in serum, using sodium dodecyl sulfate-ascorbic acid to dissociate iron and copper from transferrin and ceruloplasmin, respectively. We also use a new water-soluble reagent, 2-(5-nitro-2-pyridylazo)-5-(N-propyl-N-sulfopropylamino)phenol disodium salt (nitro-PAPS) and thioglycolic acid to eliminate interference from copper in the measurement of iron. Within- and between-run precisions of the present method were 2.5-2.8% for iron and 1.8-4.6% for copper. The proposed method is susceptible to interference by hemoglobin and lipemia, especially for the iron assay. Linear-regression analyses of results of the proposed method with those of the bathophenanthroline method for iron and of the atomic absorption spectroscopic method for copper correlated well (r = 0.996, Sy/x = 0.73 and r = 0.959, Sy/x = 1.11, respectively).
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PMID:Sensitive, direct procedures for simultaneous determinations of iron and copper in serum, with use of 2-(5-nitro-2-pyridylazo)-5-(N-propyl-N-sulfopropylamino)phenol (nitro-PAPS) as ligand. 162 8

We evaluated the analytical performance of two clinical chemistry slides developed recently by Eastman Kodak Company for the analysis of lactate and iron with the Kodak Ektachem 700 XR analyzer. Tested with supplemented serum pool materials we found imprecisions of the lactate analysis between 0.7% and 1.3% (within-run), resp., 1.0% and 1.5% (between-run). The imprecision of the iron analysis was between 1.0% and 2.2%, resp., 1.2% and 2.7%. Linearity of the methods was proven between 0.7 mmol/L and 13.0 mmol/L (lactate analysis) and between 5.4 mumol/L and 82.4 mummol/L (iron analysis), respectively. We found no significant interferences by hemolysis, lipemia, or bilirubin. The Kodak lactate results (x) correlated well with those of enzymatic methods (y) of Boehringer Mannheim (r = 0.995; y = 1.095x - 0.128) and of DuPont (r = 0.990; y = 1.015x - 0.242). The Kodak iron analysis (x) was correlated with the FerroZine methods (y) of Boehringer Mannheim (r = 0.988; y = 0.868x + 1.111), Hoffman LaRoche (r = 0.989; y = 0.868x + 3.416). and with atomic absorption (y) (r = 0.960; y = 0.826x + 3.416). We conclude that the newly developed methods for the analysis of lactate and iron with the Kodak Ektachem analyzer are acceptable alternatives to other common methods.
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PMID:Evaluation of the Kodak Ektachem slide assays for iron and lactate. 202 63

The manual Reference Method of the Centers for Disease Control for serum iron (CDC/RM/Fe) and a semiautomated adaptation of it were used to evaluate two working methods: one, a detergent solubilization procedure for the Roche Cobas-Bio analyzer, the other, the Kodak Ektachem 700 procedure, based on dry-film technology. The CDC/RM/Fe and its semiautomated version gave essentially the same results for 40 sera from hospital patients. This semiautomated version was in turn compared with the two working procedures in a study involving 200 patients. Each of the working methods correlated well with the semiautomated CDC/RM/Fe method. Separate recovery and interference studies indicated satisfactory analytical recovery of iron in all cases, but the detergent solubilization method was found to be susceptible to interference by hemoglobin, lipemia, and bilirubin.
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PMID:Proposed reference method for iron in serum used to evaluate two automated iron methods. 217 60

In this paper, we studied the effect of elastase on aminonucleoside (AN) nephrosis which is considered a model of focal glomerular sclerosis (FGS). Elastase is an enzyme which disintegrates elastin, discovered by Balo, and used in the treatment of arteriosclerosis and hyperlipidemia. It has also been known to improve metabolism of acid mucopolysaccharides, so, this study focused on metabolic improvement. Three groups of male Sprague-Dawley rats were studied and observed at regular intervals; 30, 60, 90 days. The ANE group (AN + elastase) was administered one shot of AN (10 mg/100 g B.W.) during the test interval, while elastase (5 mg/kg B.W.) was injected 5 days/week for the entire test interval. The AN group was administered one shot of AN only. The third group was a control (C). The following results were observed: (1) Focal segmental hyalinosis and sclerosis (FSHS); ANE group was weaker than AN group. (2) Other significant qualifying glomerular changes (vacuolar change and hyaline droplets of the epithelial cells, adhesion, and foam cells); ANE group was weaker than AN group. (3) Anion loss in GBM was shown by a lack of colloidal iron staining under light microscopy, and by a lack of PEI particles under electron microscopy; there was significantly less anion loss with ANE group, than with AN group. The findings suggest that elastase has an affect on the metabolism of acid mucopolysaccharide and collagen in sclerotic lesion, and may restrain the progress of amino-nucleoside nephrosis.
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PMID:[The effect of the elastase on aminonucleoside nephrosis]. 253 42

The effects of chronic ethanol feeding on hepatic lipid peroxidation, ascorbic acid, glutathione and vitamin E levels were investigated in rats fed low or adequate amounts of dietary vitamin E. Hepatic lipid peroxidation was significantly increased after chronic ethanol feeding in rats receiving a low-vitamin E diet, indicating that dietary vitamin E is an important determinant of hepatic lipid peroxidation induced by chronic ethanol feeding. No significant change was observed in hepatic non-heme iron content, but hepatic content of ascorbic acid and glutathione was increased by ethanol feeding. Both low dietary vitamin E and ethanol feeding significantly reduced hepatic alpha-tocopherol content, and the lowest hepatic alpha-tocopherol was found in rats receiving a combination of low vitamin E and ethanol. Plasma alpha-tocopherol was elevated after ethanol feeding, probably because of the associated hyperlipemia. Both the ratio of plasma alpha-tocopherol/plasma lipid and the red blood cell alpha-tocopherol were reduced by ethanol feeding. Furthermore, ethanol feeding caused a marked increase of hepatic alpha-tocopheryl quinone, a metabolite of alpha-tocopherol by free radical reactions. Ethanol feeding caused little changes of alpha-tocopherol and alpha-tocopheryl quinone content in mitochondria, whereas a striking increase in alpha-tocopheryl quinone was observed in microsomes. These data suggest that ethanol feeding causes a marked alteration of vitamin E metabolism in the liver and that the combination of ethanol with a low-vitamin E intake results in a decrease of hepatic alpha-tocopherol content which renders the liver more susceptible to free radical attack.
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PMID:Lipid peroxidation and antioxidant defense systems in rat liver after chronic ethanol feeding. 280 60


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