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

A completely random design consisting of three replicates of 25 broiler chickens (Hubbard x Hubbard) at each of four treatments was used to evaluate the effects of low level, chronic aflatoxicosis on performance and various processing parameters. The treatments in Trial 1 were control, .075, .225, and .675 and in Trial 2 control, .3, .9, and 2.7 micrograms/g toxin in feed (ppm). The chickens were maintained on these treatments from day-old to 7 weeks of age with feed and water available ad libitum. All aflatoxin dose levels in Trial 1 significantly (P less than .05) decreased live, dressed, and chilled eviscerated weight, whereas only 2.7 ppm significantly (P less than .05) decreased live and dressed weight in Trial 2, with chilled eviscerated weight being significantly (P less than .05) decreased at .3 and 2.7 ppm in Trial 2. Parts weights and dimension measurements reflected the aflatoxin-induced decrease in dressed weight. Breast yield (%) was significantly (P less than .05) decreased by aflatoxin while back, wing, drum, and thigh yields were significantly increased by aflatoxin. No effect of aflatoxin was seen on the incidence of crooked keel, feather follicle infection, breast blisters, or conformation. A hypocarotenoidemia and hepatic hyperlipemia were clearly a result of chronic aflatoxicosis in these broiler chickens. These data demonstrate that the toxicity of aflatoxin is dependent on the environment in which broiler chickens are exposed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of low level chronic aflatoxicosis in broiler chickens. 663 79

Using a rabbit model, previous studies showed steroid-induced hyperlipidemia with subsequent fatty embolization of the subchondral arteries and hypertrophy of the marrow fat cells, followed by elevation of femoral head pressure from the normal level of 25 cm to nearly 60 cm H2O after eight weeks of treatment. This has led us to believe that pressure changes lead to decreased blood flow in the femoral head. In our study of 22 New Zealand white adult rabbits, weighing an average of 4.0 kg, 14 received a weekly dose of 12.45 mg of methylprednisolone (Depo-Medrol), and eight served as control. Femoral head blood flow was established using the radioactive microsphere technique. Control and cortisone-treated rabbits had femoral head blood flow measured 6, 8 and 10 weeks after treatment. The average blood flow in the control femoral heads averaged 0.2039 +/- 0.076 ml/min/gm, with no difference in the left side and the right side. In the treated group, the average blood flow at ten weeks was 0.162 +/- 0.039 ml/min/gm on the right and 0.164 +/- 0.037 ml/min/gm on the left, which was significantly different. This is parallel to unpredictable clinical findings in human beings.
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PMID:Femoral head blood flow in long-term steroid therapy: study of rabbit model. 664 15

Over the years, a variety of uses has been found of organic tin compounds as fungicides, as stabilizers in plastics and for other industrial uses. The purpose of this article is to summarize and review the results so far obtained as to the analytical method for organotins in biological samples, the toxicity, metabolism, and biochemical and health effects of organotin compounds. 1) Many methods have been developed for analysis of organotin compounds by spectrophotometry, polarography, gas- or liquid-chromatography, etc. These methods, however, are mainly for analysis of organotins in standard solutions or in water, and are not suitable for organotin compounds in biological samples. Recently, we have developed several methods for analysis of various kinds of organotin compounds in biological samples. These methods are able simultaneously to separate and determine trace amounts (at nanogram order) of organotin compounds and their metabolites in the same biological samples. 2) Acute toxicity of organotin compounds which appeared on the literature are summarized. Trialkyl and triaryl compounds seem to be more toxic than the tetra-, di-, or mono-compounds of the same chain length. With an increase in the number of C atoms the toxicity of alkyl compounds decreases. Aryltin compounds are less toxic than alkyltin compounds. 3) Intestinal absorption sites for tetra-alkyltins are jejunum and duodenum, and those for trialkyltins are ileum and jejunum. A considerable amount of orally administered tetra- and trialkyltins of low molecular weights are absorbed, but only very little of the other organotin compounds seems to be absorbed from the gastrointestinal tract. Absorbed organotin compounds rapidly undergo dealkylation by the microsomal mono-oxygenase system dependent on cytochrome P-450 in the liver, brain or other organs, and the compounds and their metabolites distribute to the whole body, ultimately being excreted into urine, bile and faeces. The biological half life of organotin compounds in mammals is usually short, a half of the amount of tributyl- and triphenyl-tins deposited in the body disappearing in several days. A part of organotin compounds excreted into bile is demonstrated to have been absorbed from the intestine and to circulate in the body via enterohepatic circulation. 4) Specific effects of organotin compounds on the biological systems and health include disturbance of the structure and function of the central nervous system (interstitial edema of white matter), inhibited oxidative phosphorylation in mitochondria of cells, atrophy of the thymus and thymus dependent lymphoid tissues resulting in the dysfunction of T cells for immunity, inhibited enzyme activity, lesions in the liver and bile ducts etc., although some specificity is observed among species of animals and organotin compounds. Recently we found that a single oral administration of triphenyltin fluoride to rabbits induces transient diabetes and diabetic lipemia by inhibiting insulin secretion from morphologically normal pancreatic B-cells...
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PMID:[Recent progress in the study of analytical methods, toxicity, metabolism and health effects of organotin compounds]. 675 93

The clinical and laboratory data of a 5-year-old boy with the syndrome of essential hypernatremia are presented. In a four-year follow-up, no demonstrable hypothalamic structural lesion has been identified. Review of the literature has uncovered four similar cases, suggesting a distinct syndrome of altered hypothalamic function. The syndrome is characterized by: adipsia-hypodipsia (5/5 patients), recurrent hypernatremia (5/5), obesity (4/5), inability to excrete a water load (5/5), lack of growth hormone release in response to provocative stimuli (4/4), blunted thyrotropin releasing hormone responses (3/4), hypothyroidism (2/4), and hyperlipemia associated with hypernatremic crisis (1/1). In one of the patients the syndrome has been attributed to a disturbance of the opioid-peptide system.
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PMID:Hypothalamic adipsia without demonstrable structural lesion. 680 52

Hypernatremic states, often the result of hypothalamic osmoreceptor dysfunction in humans, are sometimes accompanied by hyperlipemia. To investigate whether hypernatremia could cause hyperlipemia we induced hypernatremia in three groups of rats with their respective controls: Group A rats received hypertonic saline alone intragastrically; group B animals were pair-fed and tap water was substituted for hypertonic saline in the treated group; in group C the rats were again fed intragastrically with a liquid diet mixed with hypertonic saline. Rats receiving excess salt had mean serum Na+ concentrations exceeding 159 mmoles/l. While the serum triglyceride values were significantly higher in all hypernatremic rats, hepatic triglyceride content was greater only in group C rats (p less than .01). Serum free fatty acids and ketone bodies were also higher in group C rats (p less than .01) as compared to controls. These data suggest that hypernatremia by itself leads to hyperlipemia and a fatty liver.
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PMID:Hypernatremia induces hyperlipemia and a fatty liver. 684 93

When deoxycorticosterone acetate (DOCA)-loaded uninephrectomized rats were fed on standard laboratory pellet diet and 1% saline for 5 weeks, caloric homeostasis became abnormal resulting in (a) hyperlipidemia, (b) cholesterol deposit in the heart, (c) significant reduction of triglycerides in the aorta, heart and liver and (d) a 60% increase in the cardiac free fatty acids (FFA) on one hand and a 50% reduction of the hepatic FFA on the other. These facts suggest that the hypertension severely reduces hepatic lipogenesis, whereas the cardiovascular system depends much more on FFA as a metabolic fuel than on glucose. This idea is supported by the deficiency in total body potassium (K) and decrease in serum immunoreactive insulin (IRI) which occur in the hypertension. These alterations were attenuated by the fungal prenylphenols, 4-0-methylascochlorin (MAC) and ascofuranone (AF). The protective effect seems to be partly attributable to the counteraction to DOCA. In addition, the agents caused a specific increase of renal water reabsorption. MAC treatment resulted in a particularly marked reduction of saline intake and excretion of unusually thick urine with 2.8 times higher sodium (Na) concentration than in the DOCA/saline control rats.
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PMID:Unusual concentration of urine and prevention of polydipsia by fungal prenylphenols in DOCA hypertensive rats. 701 11

Chromium deficiency may cause insulin resistance, hyperinsulinemia, impaired glucose tolerance, and hyperlipidemia, recovered by chromium supplementation. The effect of chromium supplementation on serum lipids and glucose tolerance was tested in a double-blind 12-wk study of 23 healthy adult men aged 31 to 60 yr. Either 200 micrograms trivalent chromium in 5 ml water (Cr) or 5 ml plain water (W) was ingested daily 5 days each week. Half the subjects volunteered for glucose tolerance tests with insulin levels. At 12 wk high-density lipoprotein cholesterol increased in the Cr group from 35 to 39 mg/dl (p less than 0.05) but did not change in the water group (34 mg/dl). The largest increase in high-density lipoprotein cholesterol and decreases in insulin and glucose were found in those subjects having normal glucose levels together with elevated insulin levels at base-line. The data are thus consistent with the hypothesis that Cr supplementation raises high-density lipoprotein cholesterol and improves insulin sensitivity in those with evidence of insulin resistance but normal glucose tolerance.
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PMID:Effect of chromium chloride supplementation on glucose tolerance and serum lipids including high-density lipoprotein of adult men. 703 73

The effects of chitosan-coated dialdehyde cellulose (Chitosan DAC), a newly developed oral adsorbent of urea and ammonia, were examined in rats with progressive chronic renal failure (CRF) induced by adriamycin. CRF rats induced by repeated injections of adriamycin were fed a diet containing chitosan DAC (5% content) or Kremezin (5% content), an oral charcoal adsorbent (AST-120) under strict paired-feeding for four months. CRF rats that received both a normal diet and Kremezin showed progressive azotemia, hyperphosphatemia, hyperlipidemia, proteinuria, and anemia, and began to die from 9 weeks after feeding started. In contrast, chitosan DAC-treatment showed marked prolongation of the survival period and decreases in blood urea nitrogen, serum creatinine, and serum phosphate. In addition, chitosan DAC-treatment ameliorated anemia in CRF rats, although hyperlipidemia and proteinuria were not improved. Furthermore, fecal weight, fecal water content, fecal nitrogen and fecal sodium were markedly increased, and the apparent protein ratio was decreased in CRF rats fed a diet containing chitosan DAC for 9 weeks. In contrast, none of these effects were observed in CRF rats receiving Kremezin. These observations suggest the further possibility of using oral adsorbent therapy for CRF patients.
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PMID:[Pharmacological properties of chitosan-coated dialdehyde cellulose (chitosan DAC), a newly developed oral adsorbent (II). Effect of chitosan DAC on rats with chronic renal failure induced by adriamycin]. 755 38

Left ventricular hypertrophy with diffuse intermyocardiocytic fibrosis is a feature of uremia. The role of blood pressure and/or other cardiovascular uremic risk factors in cardiac remodeling is still uncertain. To determine the extent to which improvement of kidney function and the control of uremia-related risk factors are associated with a reduction of myocardial injury, we evaluated the effect of dietary protein restriction or the angiotensin-converting enzyme inhibitor lisinopril on cardiac structure in remnant kidney rats. One week after subtotal nephrectomy, Wistar rats were allocated to receive drinking water solution (group 1), 5 mg/kg per day lisinopril (group 2), or a low-protein diet (6%) (group 3) for 12 weeks. Group 2 and 3 showed a comparable efficacy in preventing the expected rise in creatininemia, urinary protein excretion, and glomerulosclerosis. However, hypertension development was prevented only in group 2. Groups 1 and 3 developed a significant (P < .01) increase in left ventricular weight (2.45 +/- 0.1 and 2.5 +/- 0.5 mg/g body wt, respectively) compared with group 2 (1.9 +/- 0.06 mg/g body wt). Cardiac hydroxyporline concentration was also lower in group 2 compared with group 1 (2.07 +/- 0.16 versus 2.73 +/- 0.17 mg/g left ventricular weight, P < .05) but not compared with group 3 (2.59 +/- 0.19 mg/g left ventricular weight). The effect of angiotensin-converting enzyme inhibition on left ventricular mass and intracardiac collagen content appeared to be dissociated from anemia, sympathetic activity, and hyperlipidemia. There was a close relationship between systolic pressure and left ventricular mass; however, no relationship between the degree of cardiac fibrosis and systolic pressure could be determined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of systemic blood pressure to myocardial remodeling in uremic rats. 763 42

The present study investigated the effects of ascorbic acid (AA) supplementation on the cardiac performance and the plasma levels of glucose, insulin, triglycerides, cholesterol and free fatty acid in diabetic and non-diabetic rats. Diabetes was induced by intravenous injection of streptozotocin (STZ) 55 mg/kg. AA was given in drinking water in concentrations of 1 g/l or 2 g/l for 8 weeks after STZ injection. Myocardial performance was determined using the isolated perfused working heart preparations. Following AA supplementation, there were no significant changes in any of the parameters measured in non-diabetic rats; however, the occurrence of polydipsia, hyperphagia, hyperlipidemia and myocardial dysfunction in STZ-diabetic rats was significantly alleviated in a dose-dependent manner. Nevertheless, the decreased body weight gain, hypoinsulinemia and hyperglycemia in diabetic animals were not affected. The data show that AA supplementation in STZ-diabetic rats improves both hyperlipidemia and cardiac function. However, the mechanisms of these effects and the correlation between these improvements are not clear.
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PMID:Ascorbic acid supplementation prevents hyperlipidemia and improves myocardial performance in streptozotocin-diabetic rats. 778 89


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