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Biomedical subjects

C G Lewis

Publications and source records attributed to C G Lewis.

At least 55 records · Page 3Linked to original sources
PubMed1992

Cardiomyopathy of copper deficiency: effect of vitamin E supplementation.

The present study was undertaken to determine whether the intraperitoneal injection of vitamin E to copper-(Cu) deficient rats fed fructose will protect the animals against the severity of Cu deficiency. Cu-deficient and adequate rats were fed a diet containing 62% carbohydrate as fructose. Half the Cu-deficient rats fed fructose were injected daily with vitamin E. Vitamin E treated rats were not protected against the lethal consequences of the interaction between Cu and fructose. These data provide evidence that the cardiomyopathy of Cu deficiency in rats consuming a fructose-based diet cannot be ameliorated by vitamin E supplementation.

Animals↗
PubMed1992

Garlic oil extract ameliorates the severity of copper deficiency.

This study was undertaken to determine whether a reduction in hepatic lipogenesis would be beneficial in the amelioration of copper (Cu) deficiency when fructose is fed. Garlic was chosen as the agent for reducing hepatic lipogenesis. Forty-eight weanling rats were fed Cu-deficient or adequate diets containing fructose or starch with or without garlic for 5 weeks. Garlic ameliorated the signs associated with Cu deficiency, although hepatic lipogenesis was not affected. Administration of garlic reduced the activity of the lipogenic enzyme glucose-6-phosphate dehydrogenase only in Cu-adequate rats. Consumption of garlic resulted in increased epididymal fat pad and pancrease sizes, and higher hematocrits, insulin and thyroxine concentrations. Mechanisms other than lipogenesis that could be responsible for this phenomenon are discussed.

Allyl Compounds↗
PubMed1992

Copper deficiency in rats: the effect of clofibrate.

This study was undertaken to determine whether hepatic lipogenesis plays a role in the exacerbation of copper (Cu) deficiency. Forty-eight male rats were fed from weaning a Cu-deficient or adequate diet containing 62% carbohydrate as either starch or fructose with or without clofibrate for 5 weeks. Clofibrate was fed since it had been shown to possess hypolipidemic properties. Administration of clofibrate reduced the activity of the lipogenic enzyme glucose-6-phosphate dehydrogenase. Total hepatic lipid, however, was not reduced. Clofibrate did not affect hepatic lipid concentration and the pathology associated with Cu deficiency when fructose was fed was not prevented by the consumption of clofibrate.

Animals↗
PubMed1992

Construction and characterization of Streptomyces coelicolor A3(2) mutants that are multiply deficient in the nonessential hrd-encoded RNA polymerase sigma factors.

Previous studies showed that Streptomyces coelicolor A3(2) has four genes (hrdA, hrdB, hrdC, and hrdD) that appear to encode RNA polymerase sigma factors very similar to the sigma 70 subunit of Escherichia coli and that hrdC and hrdD could be individually disrupted without causing obvious phenotypic defects. Here, hrdA was cloned and stable null hrdA and hrdD mutants were constructed by gene replacement. These two mutants and a previously constructed hrdC null mutant were used in crosses to generate hrdAC, hrdAD, hrdCD, and hrdACD strains. The inability to synthesize one, two, or all three of the nonessential hrd-encoded sigma factors had no obvious phenotypic consequences.

Alleles↗
PubMed1991

Characterization of a gene conferring bialaphos resistance in Streptomyces coelicolor A3(2).

A gene (bar) was identified adjacent to the hrdD sigma factor gene in Streptomyces coelicolor A3(2). The predicted bar product showed 32.2% and 30.4% identity to those of the pat and bar genes of the bialaphos (Bp) producers Streptomyces viridochromogenes and Streptomyces hygroscopicus, respectively; these genes encode phosphinothricin (PPT) N-acetyltransferases that function as enzymes in the Bp biosynthetic pathway and as resistance determinants. The S. coelicolor bar gene conferred high-level resistance to Bp when cloned in S. coelicolor on a high-copy-number vector. Enzymic assay showed that the S. coelicolor bar gene product inactivates PPT by transfer of acetyl groups from acetyl CoA. The S. coelicolor bar gene appears to be expressed from two promoters (p1 and p2) and is divergently transcribed with respect to hrdD. The downstream (barp2) transcript overlaps the hrdDp1 transcript and the upstream (barp1) transcript overlaps both the hrdDp1 and hrdDp2 transcripts. Inactivation of hrdD did not prevent transcription from either bar promoter, indicating that sigma hrdD is not essential for recognition of these sequences.

Acetyltransferases↗
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↗
PubMed1991

Cobalt in periprosthetic soft tissue. Observations in 6 revision cases.

Cobalt (Co) was analyzed in sera obtained before surgery and in biopsies of periarticular soft tissue from 7 control patients undergoing primary total hip arthroplasty and from 6 Co-exposed patients who developed aseptic loosening of the femoral component after hip arthroplasty (CoCrMo alloy, greater than 59 percent Co, metal-on-plastic type). Serum-Co concentrations were not elevated in the Co-exposed patients compared with control patients or healthy adults. In 5 of the 6 Co-exposed patients, Co concentrations were greatly increased in periprosthetic tissue sections 0-1 mm from the synovial surface (median 2.4 [2.1-27] micrograms Co/g) compared with corresponding sections from the control patients (median 0.4 [0.1-0.6] microgram Co/g). Co concentrations diminished in tissue sections at successive distances of 2-3 and 4-5 mm from the synovial surfaces. In the Co-exposed patients, Co concentrations in sera and periprosthetic soft tissues were not correlated, indicating that serum Co concentration is not a reliable index of the Co burden in periprosthetic soft tissue.

Adult↗
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

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

Failure of body mass index or body weight to influence markedly the response to ovarian hyperstimulation in normal cycling women.

A retrospective analysis was performed of 368 normally cycling women treated with a single cycle of a standard ovarian hyperstimulation regime (CC 100 mg days 5 to 9 and hMG 150 IU days 6, 8, and 10) associated with either an IVF or GIFT program. Neither the peak serum E2 level attained nor the number of days of stimulation required bore a relationship to the BMI or the total body weight of these women. Whereas the mean number of oocytes aspirated from women with BMI less than 19.1 was higher (6.4 +/- 3.2) compared with obese women (BMI greater than 27.6, 4.8 +/- 2.6), the rate of fertilization was not different for both BMI extremes. It is concluded that factors other than BMI or total body weight have more important influences on the response to hyperstimulation in normal women.

Body Mass Index↗
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

Enzyme-specific activities and mineral concentrations of the exocrine pancreas from female SHR/N-corpulent (cp) rats.

A new rodent model, SHR/N-cp, for study of non-insulin-dependent diabetes mellitus (NIDDM) has recently been developed. The present study reports exocrine pancreatic enzyme activities and mineral concentrations in female corpulent (cp/cp) and lean (+/?) rats fed a diet containing carbohydrate as cooked corn starch or sucrose for 7 months to determine the potential of the model for studies of diet and pancreatic function in NIDDM. Although corpulent female rats weighed 2.5 times more than their lean littermates, they consumed less calories when expressed per 100 g body weight than lean rats. Corpulent rats had a significantly smaller relative pancreatic weight than lean rats (p less than 0.0001), but had greater total pancreatic DNA content and concentration (p less than 0.003) and higher pancreatic amylase (p less than 0.0001), lipase (p less than 0.0011), and chymotrypsinogen (p less than 0.0208) specific activities. Corpulent rats had a significantly lower pancreatic copper concentration than their lean littermates (p less than 0.0193). Corpulent rats consuming starch had a higher pancreatic iron concentration than all other experimental groups (p less than 0.05). The corpulent female rats were only mildly diabetic based upon serum and urine indices. The data suggest that the female SHR/N-corpulent rat may be a useful model for studying exocrine pancreatic function of mild cases of non-insulin-dependent diabetes.

Amylases↗