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Biomedical subjects

F H Nielsen

Publications and source records attributed to F H Nielsen.

At least 37 records · Page 2Linked to original sources
PubMed1994

Effects of germanium and silicon on bone mineralization.

The chemical properties of Ge are similar to Si. This study investigated whether Ge can substitute for, or is antagonistic to, Si in bone formation. Sixty male weanling Sprague-Dawley rats were randomly assigned to treatment groups of 12 and 6 in a 2 x 4 factorially arranged experiment. The independent variables were, per gram fresh diet, Si (as sodium metasilicate) at 0 or 25 micrograms and Ge (as sodium germanate) at 0, 5, 30, or 60 micrograms. Results confirmed that Ge does not enhance Si deprivation and provided evidence that Ge apparently can replace Si in functions that influence bone composition. When Si was lacking in the diet, calcium and magnesium concentrations of the femur were decreased; this was reversed by feeding either Ge and/or Si. Similar effects were found for zinc, sodium, iron, manganese, and potassium of vertebra. There were some responses to Si deprivation that Ge could not reverse; Ge did not increase femur copper, sodium, or phosphorus or decrease molybdenum of vertebra, effects that were evoked by Si supplementation. Additionally, some findings suggested that 60 micrograms Ge/g diet could be a toxic intake for the rat. On the other hand, some responses induced by Ge indicate that this element may be acting physiologically other than as a substitute for Si. Germanium itself affected bone composition. Germanium supplementation decreased Si and molybdenum in the femur and increased DNA in tibia. Regardless of the amount of Si fed, animals fed 30 micrograms Ge/g diet had increased tibial DNA compared to animals fed 0 or 60 micrograms Ge; however, tibial DNA of animals fed 30 micrograms Ge was not statistically different from those animals fed 5 micrograms Ge. Thus, Ge may be of nutritional importance.

Animals↗
PubMed1994

High dietary aluminum affects the response of rats to silicon deprivation.

Antagonistic interactions between silicon and aluminum occur in living organisms. Thus, an experiment was performed to ascertain whether high dietary aluminum would accentuate the signs of silicon deprivation in rats and conversely whether silicon deprivation would accentuate the response to high dietary aluminum. The experiment was factorially arranged with two variables: silicon as sodium metasilicate, 0 or 40 micrograms/g diet, and aluminum as aluminum citrate, 0 or 500 micrograms/g diet. After 9 wk, body weights and plasma urea nitrogen were higher and plasma concentrations of threonine, serine, glycine, cystine, and methionine were lower in silicon-adequate than silicon-deprived rats. High dietary aluminum significantly decreased plasma phenylalanine. An interaction between aluminum and silicon affected plasma triglyceride, cholesterol, and phosphorus concentrations. High dietary aluminum decreased these variables when silicon was absent from the diet, but increased them when silicon was present. Skull iron and silicon concentrations were decreased and iron and zinc concentrations in the femur were increased by the addition of 500 micrograms Al/g diet. High dietary aluminum decreased tibia density in silicon-adequate rats, but increased tibial density in silicon-deprived rats. The findings indicate that in rats, high dietary aluminum can affect the response to silicon deprivation and dietary silicon can affect the response to high dietary aluminum.

Aluminum↗
PubMed1994

Biochemical and physiologic consequences of boron deprivation in humans.

Boron deprivation experiments with humans have yielded some persuasive findings for the hypothesis that boron is an essential nutrient. In the first nutritional study with humans involving boron, 12 postmenopausal women first were fed a diet that provided 0.25 mg boron/2000 kcal for 119 days, and then were fed the same diet with a boron supplement of 3 mg boron/day for 48 days. The boron supplementation reduced the total plasma concentration of calcium and the urinary excretions of calcium and magnesium, and elevated the serum concentrations of 17 beta-estradiol and testosterone. This study was followed by one in which five men over the age of 45, four postmenopausal women, and five postmenopausal women on estrogen therapy were fed a boron-low diet (0.23 mg/2000 kcal) for 63 days, then fed the same diet supplemented with 3 mg boron/day for 49 days. The diet was low in magnesium (115 mg/2000 kcal) and marginally adequate in copper (1.6 mg/2000 kcal) throughout the study. This experiment found higher erythrocyte superoxide dismutase, serum enzymatic ceruloplasmin, and plasma copper during boron repletion than boron depletion. The design of the most recent experiment was the same as the second study, except this time the diet was adequate in magnesium and copper. Estrogen therapy increased plasma copper and serum 17 beta-estradiol concentrations; the increases were depressed by boron deprivation. Estrogen ingestion also increased serum immunoreactive ceruloplasmin and erythrocyte superoxide dismutase; these variables also were higher during boron repletion than depletion for all subjects, not just those ingesting estrogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Density↗
PubMed1993

Dietary vitamin B12, sulfur amino acids, and odd-chain fatty acids affect the responses of rats to nickel deprivation.

An experiment was performed to ascertain whether changing the dietary intake of two substances, cystine and margaric acid (heptadecanoic acid), that affect the flux through pathways involving the two vitamin B12-dependent enzymes, methionine synthase and methylmalonyl-CoA mutase, would affect the interaction between nickel and vitamin B12. Rats were assigned to treatment groups of six in a fully crossed, four-factorial arrangement. The independent variables, or factors, were: per kg of fresh diet, nickel analyzed at 25 and 850 micrograms; vitamin B12 supplements of 0 and 50 micrograms; margaric acid supplements of 0 and 5 g; and L-cystine supplements of 0 and 12 g. The diet without cystine was marginally deficient in sulfur amino acids. Nickel affected growth, liver wt/body wt ratio (LB/BW), and a number of variables associated with iron, calcium, zinc, copper, and magnesium metabolism. Most of the effects of nickel were modified by the vitamin B12 status of the rat. In numerous cases, the interaction between nickel and vitamin B12 was dependent on, or altered by, the cystine or margaric acid content of the diet. Thus, the findings showed that the extent and the direction of changes in numerous variables in response to nickel deprivation varied greatly with changes in diet composition. These variables include those previously reported to be affected by nickel deprivation, including growth and the distribution or functioning of iron, calcium, zinc, copper, and magnesium. The findings also support the hypothesis that nickel has a biological function in a metabolic pathway in which vitamin B12 is important.

Animals↗
PubMed1993

AIN-93 purified diets for laboratory rodents: final report of the American Institute of Nutrition ad hoc writing committee on the reformulation of the AIN-76A rodent diet.

For sixteen years, the American Institute of Nutrition Rodent Diets, AIN-76 and AIN-76A, have been used extensively around the world. Because of numerous nutritional and technical problems encountered with the diet during this period, it was revised. Two new formulations were derived: AIN-93G for growth, pregnancy and lactation, and AIN-93M for adult maintenance. Some major differences in the new formulation of AIN-93G compared with AIN-76A are as follows: 7 g soybean oil/100 g diet was substituted for 5 g corn oil/100 g diet to increase the amount of linolenic acid; cornstarch was substituted for sucrose; the amount of phosphorus was reduced to help eliminate the problem of kidney calcification in female rats; L-cystine was substituted for DL-methionine as the amino acid supplement for casein, known to be deficient in the sulfur amino acids; manganese concentration was lowered to one-fifth the amount in the old diet; the amounts of vitamin E, vitamin K and vitamin B-12 were increased; and molybdenum, silicon, fluoride, nickel, boron, lithium and vanadium were added to the mineral mix. For the AIN-93M maintenance diet, the amount of fat was lowered to 40 g/kg diet from 70 g/kg diet, and the amount of casein to 140 g/kg from 200 g/kg in the AIN-93G diet. Because of a better balance of essential nutrients, the AIN-93 diets may prove to be a better choice than AIN-76A for long-term as well as short-term studies with laboratory rodents.

Animals↗
PubMed1992

Studies of the interaction between boron and calcium, and its modification by magnesium and potassium, in rats. Effects on growth, blood variables, and bone mineral composition.

Two experiments were performed to confirm that boron interacts with calcium, and that this interaction can be modified by dietary magnesium and potassium in the rat. Upon manipulating the dietary variables listed above, it was found that under certain conditions, boron and calcium deprivation similarly affected several variables; for example, they both could be made to elevate plasma alkaline phosphatase activity and to depress femur calcium concentration. Under some dietary conditions, both boron and calcium deprivation affected some variables related to blood or iron metabolism. However, the effects of dietary boron and calcium on spleen weight/body weight ratio, hematocrit, and femur iron concentration generally were not similar. Femur copper, magnesium, phosphorus, and zinc also were affected by an interaction between boron and calcium under some dietary conditions. The findings show that there is a relationship between boron and calcium, but they do not clearly indicate the nature of the relationship. However, the data suggest that boron and calcium act on similar systems in the rat.

Alkaline Phosphatase↗
PubMed1991

Ultratrace minerals mythical elixirs or nutrients of concern?

Demonstration of the nutritional significance of the ultratrace elements has resulted from studies indicating enhanced need in organisms exposed to various metabolic, hormonal, physiological and nutritional stresses. These studies indicate that some ultratrace elements, namely boron and silicon, will be found to be nutritionally important. The dietary lack of these elements may result in suboptimal function and composition of bone and brain.

Animals↗
PubMed1991

Nutritional requirements for boron, silicon, vanadium, nickel, and arsenic: current knowledge and speculation.

Definition of specific biochemical functions in higher animals (including humans) for the ultratrace elements boron, silicon, vanadium, nickel, and arsenic still has not been achieved although all of these elements have been described as being essential nutrients. Recently, many new findings from studies using molecular biology techniques, sophisticated equipment, unusual organisms, and newly defined enzymes have revealed possible sites of essential action for these five elements. Based on these findings and the response of animals and/or humans to low intakes of these elements, the following speculations have been presented: 1) Boron has a role that affects cell membrane characteristics and transmembrane signaling. 2) Silicon is necessary for the association between cells and one or more macromolecules such as osteonectin, which affects cartilage composition and ultimately cartilage calcification. 3) Vanadium reacts with hydrogen peroxide to form a pervanadate that is required to catalyze the oxidation of halide ions and/or stimulate the phosphorylation of receptor proteins. 4) Nickel is needed for the CO2-fixation to propionyl-CoA to form D-methylmalonyl-CoA. 5) Arsenic has an important role in the conversion of methionine to its metabolites taurine, labile methyl, and the polyamines. If any of these speculations are found to be true, the element involved will be firmly established as having a nutritional requirement because the body obviously cannot synthesize it. Based on animal findings, the dietary requirement is likely to be small; that is, expressed in micrograms per day.

Amino Acids↗
PubMed1990

Ascorbic acid: effect on ongoing iron absorption and status in iron-depleted young women.

The effect of ascorbic acid on iron retention from a diet with predicted low iron bioavailability (containing minimal meat and ascorbic acid) was investigated in iron-depleted premenopausal women. Eleven women were depleted of storage iron (indicated by serum ferritin) through a combination of diet (5.0 mg Fe/2000 kcal for 67-88 d) and phlebotomy. They then consumed a diet containing 13.7 mg Fe/2000 kcal, supplemented with placebo or ascorbic acid three times daily (1500 mg total) with meals for 5.5 wk. Ascorbic acid improved apparent iron absorption (balance method) [38 +/- 2% (means +/- SEM) vs 27 +/- 2%]. Ascorbic acid also improved hemoglobin, erythrocyte protoporphyrins, and serum iron but not hematocrit, serum ferritin, iron-binding capacity, or transferrin saturation. In iron-depleted women consuming a diet with predicted poor iron availability, ascorbic acid supplementation enhanced body iron retention for 5.5 wk.

Adult↗
PubMed1990

Effect of vanadium, iodine and their interaction on growth, blood variables, liver trace elements and thyroid status indices in rats.

A two-factor, two-by-three factorially arranged experiment was performed to ascertain whether iodine affects the response of rats to vanadium deprivation. Male weanling Wistar-Kyoto rats were fed a 16% casein 68% acid-washed ground corn diet for 8 weeks. The variables were supplemental vanadium at 0 or 1 microgram/g and supplemental iodine at 0, 0.33 or 25 micrograms/g. Vanadium deprivation increased thyroid weight and thyroid weight/body weight ratio and decreased the concentration of vanadium in liver. Vanadium and iodine interacted such that, as dietary iodine was increased, plasma glucose increased in the vanadium-deficient rats but decreased in the vanadium-supplemented rats. Also, as dietary iodine was increased, thyroid peroxidase activity decreased; the decrease was more marked in the vanadium-supplemented than the vanadium-deprived rats. The findings suggest that vanadium may have a physiological role affecting iodine metabolism and thyroid function.

Animals↗
PubMed1990

Studies on the relationship between boron and magnesium which possibly affects the formation and maintenance of bones.

Recent findings are reviewed indicating that changes in dietary boron and magnesium affect calcium, and thus bone, metabolism in animals and humans. In animals, the need for boron was found to be enhanced when they needed to respond to a nutritional stress which adversely affected calcium metabolism, including magnesium deficiency. A combined deficiency of boron and magnesium caused detrimental changes in the bones of animals. However, boron deprivation did not seem to enhance the requirement for magnesium. In two human studies, boron deprivation caused changes in variables associated with calcium metabolism in a manner that could be construed as being detrimental to bone formation and maintenance; these changes apparently were enhanced by low dietary magnesium. Changes caused by boron deprivation included depressed plasma ionized calcium and calcitonin as well as elevated plasma total calcium and urinary excretion of calcium. In one human study, magnesium deprivation depressed plasma ionized calcium and cholesterol. Because boron and/or magnesium deprivation causes changes similar to those seen in women with postmenopausal osteoporosis, these elements are apparently needed for optimal calcium metabolism and are thus needed to prevent the excessive bone loss which often occurs in postmenopausal women and older men.

Animals↗
PubMed1990

Thermogenesis and thermoregulatory function of iron-deficient women without anemia.

Physiological responses at 16 degrees C were studied in 11 women, age 28 +/- 2(mean +/- S.E.) years and 26 +/- 2% fat, after their body iron stores were depleted by diet (5.0 mg iron x 2,000 kcal-1 x d-1), phlebotomy and menstruation for about 80 d and were repleted by diet (13.7 mg iron x 2,000 kcal-1 x d-1) for about 100 d, including daily iron supplementation (50 mg of iron as ferrous sulfate) for the last 14 d of repletion. Iron depletion was characterized by a decline (p less than 0.05) in hemoglobin (12.0 +/- 0.2 g x dl-1), ferritin (5.5 +/- 0.5 ng x ml-1) and body iron balance (-9.1 +/- 2.6 mg x 6 d-1). Iron repletion, including supplementation, increased (p less than 0.05) hemoglobin (12.6 +/- 0.1 g x dl-1), ferritin (9.5 +/- 0.4 ng x ml-1) and iron balance (+67 +/- 6.7 mg x 6 d-1). Iron depletion reduced (p less than 0.05) metabolic heat production (49.6 +/- 1.1 vs 53.6 +/- 1.2 W x m-2) during acute cold exposure. The rates of cooling of the core and periphery were greater (p less than 0.05) during iron depletion than repletion. A shift in the lower core temperature threshold for shivering was paralleled by an earlier onset of shivering (p less than 0.05) in iron depletion indicating an adaptation in cold tolerance in an attempt to maintain core temperature. Iron depletion was associated with blunted post-exposure increases in plasma thyroid hormone concentrations and greater (p less than 0.05) increases in plasma norepinephrine concentrations as compared to iron repletion. In a subsample of the women, no significant effect of calcium or ascorbic acid supplementation was found on responses to cold exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1990

Response of various indices of iron status to acute iron depletion produced in menstruating women by low iron intake and phlebotomy.

We investigated response sensitivities of indices of iron status to controlled iron depletion and repletion in 11 premenopausal women. The women were depleted of storage iron (as reflected by serum ferritin) through a combination of a low-iron diet and phlebotomy. They then consumed a diet containing 13.7 mg of iron per 2000 kcal, supplemented with either ascorbic acid or placebo (for 5 1/2 weeks) and a daily 50-mg iron supplement (for the subsequent 17 days). The relative sensitivities of different indices for detecting iron depletion were as follows: ferritin greater than % transferrin saturation greater than plasma iron greater than hemoglobin greater than hematocrit greater than zinc protoporphyrin (ZnPP) and erythrocyte protoporphyrin (EP). Ascorbic acid treatment during repletion, before iron supplementation, significantly (P less than 0.05) affected changes in hemoglobin, ZnPP, ZnPP/heme, and EP/heme. Changes in heme synthesis evidently do not occur until iron stores are depleted and, conversely, during iron repletion hematopoiesis must be satisfied before iron stores, as reflected by ferritin, increase. Thus, the use of only one index of iron status is of limited value for detecting iron depletion.

Adult↗
PubMed1989

Selected ultratrace elements in total parenteral nutrition solutions.

Ultratrace elements are potentially essential (eg. boron, molybdenum, nickel, and vanadium) or toxic (eg, aluminum and cadmium) in humans. Long-term total parenteral nutrition (TPN) patients can inadvertently receive significant amounts of ultratrace elements present as contaminants in TPN solutions. We determined the intake of selected ultratrace elements from a standard TPN solution and compared it with the amount reported to be absorbed from food in normal subjects. Contamination of TPN solutions with ultratrace elements was widespread and variable. The daily intakes of Mo, Ni, V. and Cd from this contamination were comparable to the amounts reported to be absorbed through the gastrointestinal tract in normal subjects. Al intake was high; B intake was low, approximately 10% of the amount absorbed by normal subjects. Thus, TPN solutions are contaminated with significant amounts of ultratrace elements. The biological significance of the intravenous infusion of these ultratrace elements is unclear and requires further investigation, particularly in home TPN patients.

Aluminum↗
PubMed1988

Effects in rats of iron on lead deprivation.

In two fully crossed, two-factor experiments, F1 generation male rats were fed a basal diet supplemented with lead (lead acetate) at 0 or 2 micrograms/g and iron (ferric sulfate) at 50 or 250 micrograms/g (Experiment 1). Supplements in Experiment 2 were lead at 0 or 1 micrograms/g and iron at 50, 250, or 1000 micrograms/g. After 28 or 50 d in Experiment 1, and 35 d in Experiment 2, a relationship between lead and iron was found. Body weight was lower in low-lead than lead-supplemented 28-d-old rats regardless of dietary iron, whereas hematocrit and hemoglobin were lower in low-lead than lead-supplemented rats fed 50 micrograms iron/g diet. A similar finding was obtained with hematocrit and hemoglobin in 35-d-old rats. Dietary lead did not affect rats fed 250 or 1000 micrograms iron/g diet. Also, feeding low dietary lead did not affect 50-d-old rats regardless of dietary iron. Liver and bone concentrations of lead were markedly affected by dietary lead and iron. The concentration of lead in liver and bone was lower in low-lead than lead-supplemented rats. Compared to rats fed 50 micrograms iron/g diet, rats fed 250 micrograms iron/g diet exhibited a decreased lead concentration in liver and bone. This decrease was accentuated by lead supplementation. The findings suggest that lead acted pharmacologically to affect iron metabolism in rats.

Aging↗