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Biomedical subjects

M Fields

Publications and source records attributed to M Fields.

At least 55 records · Page 3Linked to original sources
PubMed1991

Anemia plays a major role in myocardial hypertrophy of copper deficiency.

The present study was undertaken to establish whether anemia plays a role in the cardiomegaly and myocardial pathology of copper deficiency. Fifteen weanling male rats were fed a copper-deficient (0.6 microgram Cu/g) diet for 5 weeks. Six rats were intraperitoneally injected once a week with packed red blood cells (RBC) that were obtained from copper-deficient rats fed starch. The remainder (n = 9) served as controls. The administration of RBC to copper-deficient rats fed fructose prevented the anemia. As a result, none of the injected rats exhibited heart hypertrophy or gross pathology and they all survived. In contrast, all other control, nontreated copper-deficient rats that were fed fructose were anemic and all exhibited severe signs of copper deficiency, which included heart hypertrophy with gross pathology, and four died of the deficiency. The data suggest that the anemia of copper deficiency contributes to heart pathology. Once the anemia is prevented, the copper-deficient rats should be protected against heart pathology and mortality.

Anemia↗
PubMed1991

The severity of copper deficiency can be ameliorated by deferoxamine.

The present study was undertaken in order to determine whether hepatic iron overload plays a role in the exacerbation of copper deficiency. Weanling male Sprague-Dawley rats were fed a copper-deficient (0.6 microgram Cu/g) diet containing 62% fructose for 5 weeks. Some of the copper-deficient rats were injected daily with deferoxamine (DFX), an iron chelator that has been widely used to reduce iron overload. DFX reduced hepatic iron concentrations, which in turn ameliorated the pathology of copper deficiency when compared with nontreated copper-deficient animals. It is suggested that hepatic iron overload in a reduced environment plays a major role in the exacerbation of copper deficiency. Once the concentration of hepatic iron is reduced, the severity of the deficiency should be improved.

Animals↗
PubMed1991

The role of the adrenals in copper deficiency.

The present study was undertaken in order to establish whether (1) a decrease in catecholamines will prevent the heart hypertrophy of copper deficient rats fed fructose, and (2) an increase in hepatic copper concentration will ameliorate the signs associated with copper deficiency when fructose-based diets are consumed. Adrenalectomy resulted in reduced plasma glucocorticoids and a threefold increase in hepatic copper concentration. The signs associated with the deficiency were not ameliorated in rats fed fructose. In addition, the reduction in catecholamine concentration did not protect the copper-deficient rats fed fructose against cardiomegaly and mortality. The data support the contention that the severity of copper deficiency in rats fed fructose is not solely dependent on hepatic copper concentration and/or levels of catecholamines.

Adrenal Glands↗
PubMed1990

Intravenous sedation: the risk to the dentist.

The risk of intravenous sedation to the patient is well documented. It now appears that there is also a risk to the dentist, not so much one of health but one of illegality, loss of career and personal esteem. Martyn Fields looks at some of the evidence, and gives advice on how to avoid a dangerous predicament.

Adolescent↗
PubMed1990

Consequences of copper deficiency are not differentially influenced by carbohydrate source in young pigs fed a dried skim milk-based diet.

Carbohydrates (CHO) such as fructose (FR) or sucrose, but not starch (ST), aggravate the consequences of dietary copper (Cu) deficiency in rats. To evaluate whether this Cu X CHO interaction is pertinent to human health, the pig was used as an animal model. In two studies, 66 weanling pigs were fed dried skim milk (DSM)-based diets for 10 wk with 20% of the total calories provided as either FR, glucose, or ST and containing either deficient (1.0-1.3 micrograms/g diet) or adequate (7.1 micrograms/g) levels of Cu. Plasma and tissue levels of Cu, the activities of plasma ceruloplasmin ferroxidase and erythrocyte Cu, Zn-superoxide dismutase, and hematocrits were lower (p less than 0.05) in animals fed Cu-deficient diets. The relative cardiac mass of all Cu-deficient groups was greater (p less than 0.05) than that of animals fed Cu-adequate diets. These effects were in general unaffected by type of CHO. For comparison, weaned male rats were also fed DSM-based containing diets ST or FR with adequate or deficient Cu for as long as 10 wk. Rats consuming the Cu-deficient diets were characterized by significantly lower hematocrits, decreased tissue Cu levels, and enlarged hearts, regardless of the CHO source. Together, these data demonstrate that DSM-based diets are not suitable for delineation of potential Cu X CHO interactions, and one or more components of DSM may exacerbate the consequences of dietary Cu deficiency.

Animal Feed↗
PubMed1990

Oxytocin and vasopressin binding sites in human and bovine ovaries.

Human ovarian tissue and bovine ovarian stroma and follicles bound tritiated oxytocin and tritiated arginine vasopressin with similar affinity, whereas bovine corpora lutea bound tritiated oxytocin only. Competition for the binding of tritiated oxytocin by various agonists and antagonists was suggestive of receptor function. The number of oxytocin binding sites varied cyclically in all tissues. In bovine ovarian stroma and corpora lutea the concentrations were lowest on day 14 and highest on days 17, 19, and 21 after ovulation, with a striking peak in the luteal concentration on day 19. In human ovarian tissues the concentrations also were highest in samples obtained in late luteal phase. In large follicles the concentration of oxytocin binding sites was highest on the day of estrus and lowest on day 7. In bovine ovary the number of arginine vasopressin binding sites was approximately 50% lower than oxytocin binding sites and the cyclic variations were not significant. Human ovarian tissue had similar numbers of oxytocin and arginine vasopressin binding sites. Because bovine ovaries produce oxytocin and arginine vasopressin the results suggest a paracrine or autocrine role for these neuropeptides in luteolysis and ovulation. Although their synthesis in human ovaries is still controversial the presence of binding sites suggests a physiologic role in the regulation of human ovarian function as well.

Analysis of Variance↗
PubMed1990

Copper deficiency in pregnancy: effect on maternal and fetal polyol metabolites.

The present study was undertaken to determine whether the mortality of the fetus and the neonate of copper-deficient rats consuming fructose during pregnancy is associated with an aberration in carbohydrate metabolism. A total of 84 Sprague-Dawley rats were fed a copper-deficient or a copper-adequate diet containing fructose or starch for 19 or 21 days after conception. The consumption of a fructose-based diet during pregnancy resulted in higher concentrations of maternal blood fructose, sorbitol, triglyceride, and uric acid when compared with a starch diet. The placenta contained more than 10-fold the concentration of glucose and more than double the concentrations of fructose, triglycerides, and sorbitol when fructose was the dietary carbohydrate compared with starch. The livers of fetuses belonging to the fructose dietary group exhibited high concentrations of glucose and sorbitol. In addition, fetal blood contained higher concentrations of glucose, fructose, sorbitol, and triglycerides than the corresponding values from the starch dietary group. The consumption of a copper-deficient diet containing fructose during pregnancy resulted in massive subcutaneous hemorrhages of the fetus. In contrast, this pathology was rare in other dietary groups. The combination of copper deficiency with fructose feeding resulted in more than double the concentration of sorbitol in fetal liver, and higher concentrations of insulin and dopamine of fetal blood compared with the consumption of a copper-deficient diet containing starch.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Alcohol consumption aggravates copper deficiency.

Male weanling Sprague-Dawley rats were fed a copper-deficient (0.6 microgram Cu/g) diet containing either fructose or starch. Half of the animals fed the starch diet drank a 20% solution of ethanol in water. Ethanol was chosen as an agent to mimic fructose metabolism with the intention that ethanol will exacerbate the signs of copper deficiency and will negate the protective effect of dietary starch. The consumption of a 20% ethanol drink for 6 weeks by copper-deficient rats fed starch resulted in the exacerbation of the deficiency similar to that exerted by fructose. The signs associated with the deficiency in both alcohol and fructose consumption included anemia, heart hypertrophy with gross abnormalities, and mortality. In contrast, none of the copper-deficient control rats that drank water exhibited anemia or heart abnormalities, and none died of the deficiency. In addition, sorbitol pathway in the kidney and liver was stimulated by the consumption of alcohol and fructose. The data support the contention that the combination of certain metabolic pathways of carbohydrate metabolism with copper deficiency are responsible for the exacerbation of the deficiency.

Alcohol Drinking↗
PubMed1990

Dietary copper, simple sugars, and metabolic changes in pigs.

Inadequate dietary copper is known to result in undesirable metabolic changes in rats and humans. Abnormal cardiac function, leading to sudden death, is a common finding when copper deficient rats are fed a 62% fructose diet. To further study the apparent mineral-carbohydrate relationship to cardiac physiology, 3 male and 3 female swine were randomly assigned to four groups (6 pigs per group) which were fed low copper (1.5 ppm) or copper supplemented (40 ppm) diets with 20% of calories from either fructose or glucose for 10 weeks. In agreement with results from other animal studies, copper deficient swine exhibited decreased plasma ceruloplasmin, erythrocyte superoxide dismutase and plasma lysyl oxidase activities and lowered serum copper. The copper deficient fructose group had the lowest aortic lysyl oxidase activity and hematocrit when compared to the other groups. The relative heart weight in the copper deficient fructose group was 93% greater than the other three dietary groups. The livers of copper deficient fructose fed pigs were also significantly larger. Two enzymes related to cardiac and hepatic function, aspartate and alanine aminotransferase were also measured. Copper deficiency significantly lowered alanine aminotransferase but there was no dietary effect on aspartate amino-transferase. The results of this project indicate that the pig is a sensitive model for the study of cardiovascular abnormalities which occur when fructose is consumed with a low copper diet.

Journal Article↗
PubMed1990

Effect of changing the type of dietary carbohydrate or copper level of copper-deficient, fructose-fed rats on tissue sorbitol concentrations.

This study was designed to examine the relationship between the fructose-copper interaction and tissue sorbitol concentrations. Weanling male rats were provided with a diet which contained 62.7% fructose and 0.6 microg copper/g (F-Cu) for 4 weeks. At this time, rats were changed to either a fructose diet which contained 6.0 microg copper/g or to a starch diet with or without copper for 2 weeks. When compared with the other dietary groups, it was found that rats fed the F-Cu diet grew poorly; had altered relative liver, pancreatic, heart, and kidney sizes; were anemic; and had higher tissue concentrations of pancreatic and heart glucose, liver, pancreatic, heart, and kidney fructose, and liver, pancreatic, and kidney sorbitol. When rats were changed from the F-Cu diet to one containing copper or to a starch diet with or without copper, weight gain, relative liver, pancreatic and heart sizes, and hematocrit improved significantly. In general, there was a reduction in pancreatic and heart glucose; liver, pancreatic, heart, and kidney fructose; and pancreatic and kidney sorbitol concentrations when rats were changed from the F-Cu diet to any of the other diets. We conclude that the fructose-copper interaction may have a common biochemical basis related to the metabolism of glucose, fructose, and sorbitol.

Journal Article↗
PubMed1990

The effect of vitamin E on lipid peroxidation in the copper-deficient rat.

The present study was designed to determine whether the supplementation of vitamin E in the copper-deficient diet would ameliorate the severity of copper deficiency in fructose-fed rats. Lipid peroxidation was measured in the livers and hearts of rats fed a copper-deficient diet (0.6 microg Cu/g) containing 62% fructose with adequate vitamin E (0.1 g/kg diet) or supplemented with vitamin E (1.0 g/kg diet). Hepatic lipid peroxidation was significantly reduced by vitamin E supplementation compared with the unsupplemented adequate rats. In contrast, myocardial lipid peroxidation was unaffected by the level of vitamin E. Regardless of vitamin E supplementation, all copper-deficient rats exhibited severe signs of copper deficiency, and some of the vitamin E-supplemented rats died of this deficiency. These findings suggest that although vitamin E provided protection against peroxidation in the liver, it did not protect the animals against the severity of copper deficiency induced by fructose consumption.

Journal Article↗
PubMed1990

The effect of various levels of fructose in a copper-deficient diet on Cu deficiency in male rats.

The present study was designed to examine the effects of various levels of fructose in a copper-deficient diet on some of the signs of Cu deficiency in the rat. Weanling male rats were randomly assigned to one of five diets which contained 0.6 micrograms Cu/g diet and 627 g carbohydrate/kg which was (g/kg): 627 fructose (diet 100); 470 fructose, 157 starch (diet 75); 313.5 fructose, 313.5 starch (diet 50); 157 fructose, 470 starch (diet 25); or 627 starch (diet 0). Rats ate their respective diets for either 2 or 5 weeks. There was a significant linear inverse response of body-weight (P less than 0.0001), packed cell volume (P less than 0.0001) and erythrocyte superoxide dismutase (EC 1.15.1.1) activity (P less than 0.008) to increasing levels of dietary fructose and a direct linear response of plasma cholesterol (P less than 0.05) and blood urea nitrogen concentrations (P less than 0.001) to increasing levels of dietary fructose. Liver, kidney and pancreatic Cu concentrations decreased in a dose-response manner as the level of dietary fructose increased. In general, if fructose was included in the diet the signs of Cu deficiency were exacerbated in a dose-response manner.

Animals↗
PubMed1989

Exocrine pancreatic function of rats consuming a high-fructose, low-copper diet.

This study was designed to examine changes in exocrine pancreatic function in male rats consuming a diet containing either 62% starch or fructose with either 6.0 ppm or copper for 39 days. Copper deficiency significantly lowered pancreatic weight, copper concentration, and amylase and lipase specific activities in the pancreas and in washings from the small intestine. Significantly lower values were observed in copper deficient rats consuming fructose when compared to those consuming starch. In addition, chymotrypsin and trypsin specific activities in the pancreas and trypsin specific activity in the small intestine were lower in copper deficient rats consuming fructose when compared to all other dietary groups. Low dietary copper in combination with the consumption of high dietary fructose lead to an interaction which severely affected exocrine pancreatic function in ways which cannot be explained either by copper deficiency or dietary fructose consumption alone.

Animals↗
PubMed1989

Accumulation of sorbitol in copper deficiency: dependency on gender and type of dietary carbohydrate.

The present study was designed to examine tissue sorbitol levels in copper-deficient rats consuming dietary fructose as the only source of carbohydrate and to determine if any changes in tissue sorbitol levels are influenced by the sex of the rat. Tissue levels of glucose, sorbitol, fructose, and glyceraldehyde were measured along with the activities of aldose reductase and sorbitol dehydrogenase of male and female rats consuming copper-deficient or adequate diets containing either fructose or starch for 3 weeks. Regardless of copper status, sorbitol accumulated in the livers of males consuming fructose compared to females and to males eating starch. The greatest sorbitol accumulation in the kidney occurred in the copper-deficient male rat consuming the fructose diet. These results strongly suggest that the pathology and complications of copper deficiency in the male rat fed fructose may be due to the increased sorbitol contents of tissues.

Aldehyde Reductase↗
PubMed1989

Day-long glucose, insulin, and fructose responses of hyperinsulinemic and nonhyperinsulinemic men adapted to diets containing either fructose or high-amylose cornstarch.

Ten hyperinsulinemic and 11 nonhyperinsulinemic men consumed a typical American diet containing 20% of calories either as fructose or as high-amylose cornstarch for 5 wk in a crossover design to determine their effects on indices of glucose tolerance. Blood glucose, insulin, and fructose were determined before and 30, 60, 90, 120 and 180 min after breakfast, lunch, and dinner. Glucose responses were significantly lower 60 and 120 min and the insulin response lower 60 min after the meals containing fructose. Hyperinsulinemic men showed a tendency toward decreased insulin sensitivity after consuming fructose on the basis of an increased insulin-to-glucose ratio and decreased insulin binding to erythrocytes. These results generally show a beneficial effect of fructose on glucose tolerance; however, recommendations for including large amounts of fructose in the diet should also be based on a complete evaluation of the effect on other metabolic risk factors.

Adult↗
PubMed1989

Copper status in the rat is affected by modes of copper delivery.

The purpose of this study was to determine whether the interaction between fructose and copper status can be affected by the mode of copper administration. Male Sprague-Dawley rats (n = 94) were fed from weaning diets that contained 0.65-0.85 mg copper/kg diet for 42 d. The experimental design of the study was a 2 x 2 x 3 analysis of variance: two types of carbohydrate (fructose, corn starch), two modes of copper delivery (orally or subcutaneously) and three different extrinsic copper levels (0, 1.5 or 3 mg/kg diet or 0, 11.25 or 22.5 micrograms Cu/d by injection). In the rats fed fructose, direct indicators of copper status such as plasma copper and tissue superoxide dismutase activity were increased to a much greater extent when copper was supplied subcutaneously rather than orally as part of the diet. In the starch-fed rats the effect of the mode of copper delivery on the levels of these indices was usually not significantly different. As a result, the feeding of fructose as compared to starch produced lower levels of direct indicators of copper status when copper was supplied in the diet but not subcutaneously. It appears that ingestion of fructose as compared to starch increases the requirement for copper and that the mode of copper administration that circumvents the gastrointestinal tract attenuates the fructose-copper interaction. Thus, the fructose-copper interaction occurs either during intestinal digestion and absorption, hepatic uptake of copper via the portal blood or its hepatic utilization.

Administration, Oral↗