PubMed Health⌕ Search

Biomedical subjects

L M Klevay

Publications and source records attributed to L M Klevay.

At least 19 recordsLinked to original sources
PubMed1991

The effects of dietary copper deficiency and psychological stress on blood pressure in rats.

In each of two experiments, adult, male Sprague-Dawley rats were deprived of copper and were subjected to the chronic stress of close confinement. A 2 X 2 factorial design was used because both copper deficiency and stress have been implicated in the regulation of blood pressure and are implicated in a major consequence of human hypertension--ischemic heart disease. Copper deficiency was verified by a decrease in copper in several organs. Both copper deficiency and stress increased blood pressure; results were independent. Sodium in heart was increased by deficiency in both experiments, but was increased in brain in only the second experiment. The combination of stress and deficiency produced an increase in mortality in one of two experiments. A decrease in cholesterol in plasma due to stress is consistent with earlier data from rats but is in contrast to data from humans. Both stress and copper deficiency produce potentially adverse changes in cardiovascular physiology and the chemistry of brain, heart and other organs. These results may be germane to humans because stress is frequent and some diets are low in copper.

Animals↗
PubMed1990

Beer mitigates some effects of copper deficiency in rats.

Because of an epidemiologic association of decreased risk of death from ischemic heart disease with moderate use of alcoholic beverages, and because numerous abnormalities found in people with ischemic heart disease are also found in animals deficient in copper, rats were fed a diet deficient in copper and were given either beer or water to drink. Rats drinking beer lived nearly six times as long and had lower plasma cholesterol, less cardiac enlargement, and higher liver copper. Apparent absorption and biological half-life of oral radiocopper were increased by beer. The effects were not attributable to alcohol, chromium, or copper in beer. Beer intakes were similar to those of some people in the United States. Results may explain seasonal cycles in plasma cholesterol and may be germane to the epidemiology of ischemic heart disease because diets in the United States seem to be low in copper.

Animals↗
PubMed1990

Nutrition status and brain function in aging.

Biochemical indices of nutrition status assessed in 28 healthy persons aged greater than 60 y were related to cognitive performance and electroencephalographic (EEG) indices of neuropsychological function. Performance data were most frequently related to indices of nutrition status when tasks were demanding. Numerous correlations were also found between EEG indices and indices of thiamin, riboflavin, and iron nutriture. Certain observations, such as a decrement in alpha-wave activity in the EEG of subjects with low thiamin status, suggest that subtle neuropsychological impairment can occur in association with mild deficits in nutrition status. Other findings indicate that EEG frequency responses of older subjects with high iron status are similar to those of younger persons; however, these data are more difficult to interpret. The results suggest that further research on nutrition and neuropsychological function will lead to a better understanding of the role of nutrition in maintaining the functional integrity of the aging brain.

Aged↗
PubMed1989

Ischemic heart disease as copper deficiency.

Atherosclerosis is a complex process beginning early in life and often leading to death from ischemic heart disease in middle age. Hundreds of factors are said to contribute to this risk. More than 50 similarities between animals deficient in copper and people with ischemic heart disease have been identified. Some of the more important characteristics of this illness have been produced in experiments in which men and women were fed diets low in copper. Diets with similarly low amounts of copper are readily available to the population at large. More aspects of the anatomy, biochemistry, chemistry, epidemiology, pathogenesis and pathophysiology of ischemic heart disease can be explained by considering this illness to be a problem of copper deficiency than by considering any of several other explanations that have been offered.

Animals↗
PubMed1989

Composition of proteoglycans in the aortas of copper-deficient rats.

Copper deficiency adversely affects the extracellular matrix of the arterial wall, leading to cardiovascular lesions. To study the lesions resulting from copper deficiency, the composition of proteoglycans from aortas of copper-deficient rats was compared with proteoglycans of aortas from copper-supplemented rats. Copper deficiency in rats was verified by copper levels in adrenal glands (mean +/- SE, 0.37 +/- 0.07 vs 1.03 +/- 0.17 micrograms/g wet wt in supplemented rats). The proteoglycans were isolated from the aorta by extraction with 4 M guanidine-HCl and by digestion of the tissue with elastase. The proteoglycans were purified by CsCl isopycnic centrifugation and fractionated by gel filtration. The fractions were characterized for molecular size and glycosaminoglycan composition. Total uronate in the aortas from copper-deficient rats was 25% greater than in aortas from copper-supplemented rats, and the proteoglycans from copper-deficient rat aortas were of greater molecular size. Among the glycosaminoglycans the concentration (microgram/mg tissue) of isomeric chondroitin sulfates, particularly dermatan sulfate, was greater in copper-deficient animals than in copper-supplemented animals. These observations are similar to earlier findings in experimental atherosclerosis and to a response of cardiovascular connective tissue to injury.

Animals↗
PubMed1989

Comparison of metabolic responses and oxygen cost during maximal exercise using three treadmill protocols.

Sixteen healthy men aged 27.2 +/- 1.2 yr (mean +/- SEM) were tested to volitional exhaustion using the Balke, Bruce, and Ellestad treadmill protocols. Balke resulted in a greater (p less than 0.01) time to exhaustion and total work output, but a lower (p less than 0.05) peak oxygen consumption (ml.kg-1.min-1), and a lower (p less than 0.0001) cumulative net oxygen debt. Oxygen debt, expressed as a percent of total net oxygen cost, was smaller (p less than 0.001) on the Balke than the Bruce and Ellestad protocols (9.9 +/- 0.5, 18.7 +/- 0.6, and 19.3 +/- 0.6%, respectively). The rate of increase in oxygen consumption (p less than 0.0001) and blood lactate concentration (p less than 0.05) were lower on the Balke than on the Bruce and Ellestead protocols. Therefore, the observed differences in oxygen debt and lactate concentrations probably reflect differences in the rate of energy requirement, aerobic and anaerobic metabolism and physiological stress associated with each protocol.

Adult↗
PubMed1989

Acute renal failure and fluid retention and kidney damage in copper-deficient rats fed a high-NaCl diet.

The effect of an interaction between Cu status and dietary NaCl level on kidney structure, water balance, and the plasma renin-angiotensin-aldosterone system (RAAS) was examined in 64 male Sprague-Dawley rats (178 gm) fed a copper-supplemented diet (CuS) (10 micrograms Cu per gram) or a copper-deficient diet (CuD) (less than 0.7 micrograms Cu per gram), with (CuSNa, CuDNa) or without 3% NaCl for 42 days. NaCl did not affect growth, fluid retention, or kidney ultrastructure in Cu-supplemented rats. Cu deficiency decreased growth rate and kidney Cu, increased plasma cholesterol concentration, and suppressed plasma RAAS. NaCl increased the magnitude of these changes in Cu-deficient rats. The mortality rate was higher in CuDNa (8/16) than in Cu-deficient (2/16) rats. An acute renal failure syndrome characterized by tissue edema, pleural effusion, and ascites occurred in rats fed CuDNa. Bioelectric impedence analysis indicated that body water content was similar in rats fed CuS, CuSNa, and CuD but was higher in edematous and nonedematous rats fed CuDNa. Transmission electron microscopy indicated that glomeruli from Cu-deficient rats were poorly perfused and often occluded by expanded mesangium and contained numerous lysozome-like bodies. Fusion of podocyte foot processes, derangement of glomerular basement membrane, and hypertrophy and lipid accumulation by glomerular capillary endothelium were present in tissue from rats fed CuDNa. These results indicate that Cu deficiency reduces NaCl tolerance in rats. Ultrastructural changes in kidney tissue and the suppression of RAAS in rats fed CuDNa suggest that the edema and ascites result from acute renal failure and not from increased fluid and electrolyte reabsorption.

Acute Kidney Injury↗
PubMed1988

Dietary cholesterol lowers liver copper in rabbits.

Atherosclerosis and hypercholesterolemia have been produced in rabbits since 1913 by feeding them cholesterol. These experiments have a great influence on current thinking about the etiology and possible prevention of ischemic heart disease. Male, New Zealand White rabbits were fed 0.5% dietary cholesterol. Cholesterol and copper in plasma increased sixty-fold and 50%, respectively. Liver copper decreased 74% and hematocrit decreased 26%. Iron was unchanged in heart and liver, but was increased in kidney. Zinc was decreased in heart, but was unchanged in liver or kidney. Changes in organ iron and zinc were smaller than the decrease in liver copper. Similar experiments with higher doses of dietary cholesterol may have resulted in copper deficiency. It may be appropriate to revise interpretations of data from these experiments and to reformulate hypothesis based on the data. Results are consonant with the theoretical implication of copper metabolism and copper deficiency in the etiology and pathogenesis of ischemic heart disease.

Animals↗
PubMed1985

Alteration of the connective tissue network of striated muscle in copper deficient rats.

The connective tissue network in striated muscle, consisting principally of collagen is arranged in a three dimensional network and is intimately associated with muscle function. Previous studies have shown that animals maintained on a copper-deficient diet undergo myocardial hypertrophy and exhibit cardiovascular lesions such as ventricular aneurysms that eventually rupture. A deficiency of copper in the diet is known to inhibit lysyl oxidase, a metalloenzyme requiring copper as a cofactor and which is also responsible for collagen and elastin crosslinking. Examination by scanning and transmission electron microscopy of skeletal and cardiac muscle from rats maintained on copper-deficient diets showed both gross and microscopic lesions to the connective tissue network. Immunohistochemical staining by light microscopy with antibodies against lysyl oxidase showed that the enzyme was equally present in both control and experimental animals. Fluorescent staining for antibodies against collagen types I and III showed similar results. From these studies we concluded that the collagen secreted during hypertrophy was not crosslinked by lysyl oxidase due to the absence of the copper cofactor. This resulted in the failure of the connective tissue network to transmit and distribute the increased force associated with myocardial hypertrophy and resulted in myocardial aneurysms.

Animals↗
PubMed1979

Evidence of dietary copper and zinc deficiencies.

The mean daily amounts of copper and zinc found in hospital diets by atomic absorption spectrometry were 0.76 and 9.4 mg, respectively. Comparison of these diets with published data showed median daily amounts of copper and zinc to be 0.78 and 12.0 mg, respectively, for 20 diets made from conventional foods. These amounts of copper and zinc are less than the 2 mg of copper and 13 mg of zinc thought to be required daily by adults. Hospital diets and perhaps diets in general seem to be low in copper and zinc; the amounts of copper are lower than those of zinc in comparison with respective requirements. Common dietary amounts of these elements may cause health problems.

Adult↗
PubMed1979

Diets deficient in copper and zinc?

Hospital diets, and, perhaps, diets in general may be low in copper and zinc, with the diets being lower in copper than zinc in comparison to requirements. Several human diseases or pathologic conditions of unknown etiology have similarities to findings in deficient animals. Thus nutritional status and metabolism of copper may be important in anemia, ischemic heart disease, rheumatoid arthritis, osteoporosis, multiple sclerosis and seborrheic dermatitis. Zinc may be involved in growth failure, acne, difficulties of labor, congenital abnormalities and wound healing. Whether or not dietary amounts of copper and zinc are involved in the etiology or the pathogenesis of these conditions can be determined by clinical investigation.

Acne Vulgaris↗