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R L Walzem

Publications and source records attributed to R L Walzem.

33 records · Page 2Linked to original sources
PubMed1998

Effect of dietary catechin and vitamin E on aortic fatty streak accumulation in hypercholesterolemic hamsters.

Male golden Syrian hamsters were fed for 16 weeks on a hypercholesterolemic diet containing, per kg, 150 g of lipids (90 g butterfat, 35 g vitamin E-stripped corn oil and 25 g fish oil), 2 g cholesterol and either 3 IU vitamin E (3 IU E), 3 IU vitamin E and 200 mg catechin hydrate (3 IU E-200 Cat) or 30 IU vitamin E (30 IU E). More fatty streaks, measured by Oil Red O staining, were deposited in aortas of hamsters fed 3 IU E than in those fed either 3 IU E-200 Cat or 30 IU E. Lipid staining increased with plasma low-density lipoprotein cholesterol (LDL-C) in all animals. At the same concentration of LDL-C, animals fed either 3 IU E-200 Cat or 30 IU E developed less fatty streaks than those fed 3 IU E. Plasma LDL-C and total cholesterol were highest in hamsters fed 3 IU E and LDL-C and total cholesterol in animals fed 3 IU-200 Cat were not different from those fed either 3 IU E or 30 IU E. This study showed the importance of circulating plasma LDL-C on atherogenesis and the inhibitory effect on this process of both dietary vitamin E and catechin.

Animals↗
PubMed1997

Susceptibility to atherosclerosis in mice expressing exclusively apolipoprotein B48 or apolipoprotein B100.

All classes of lipoproteins considered to be atherogenic contain apo-B100 or apo-B48. However, there is a distinct paucity of data regarding whether lipoproteins containing apo-B48 or apo-B100 differ in their intrinsic ability to promote the development of atherosclerosis. To address this issue, we compared the extent of atherosclerosis in three groups of animals: apo-E-deficient mice (apo-B+/+apo-E-/-) and apo-E-deficient mice that synthesize exclusively either apo-B48 (apo-B48/48apo-E-/-) or apo-B100 (apo-B100/100apo-E-/-). Mice (n = 25 in each group) were fed a chow diet for 200 days, and plasma lipid levels were assessed throughout the study. Compared with the levels in apo-B+/+apo-E-/- mice, the total plasma cholesterol levels were higher in the apo-B48/48apo-E-/- mice and were lower in the apo-B100/100apo-E-/- mice. However, the ranges of cholesterol levels in the three groups overlapped. Compared with those in the apo-B+/+apo-E-/- mice, atherosclerotic lesions were more extensive in the apo-B48/48apo-E-/- mice and less extensive in the apo-B100/100apo-E-/- mice. Once again, however, there was overlap among the three groups. The extent of atherosclerosis in each group of mice correlated significantly with plasma cholesterol levels. In mice from different groups that had similar cholesterol levels, the extent of atherosclerosis was quite similar. Thus, susceptibility to atherosclerosis was dependent on total cholesterol levels. Whether mice synthesized apo-B48 or apo-B100 did not appear to have an independent effect on susceptibility to atherosclerosis.

Animals↗
PubMed1997

Transfection of avian LMH-2A hepatoma cells with cationic lipids.

LMH-2A is an estrogen-responsive avian hepatoma cell line whose susceptibility to cationic-lipid-mediated transfection is poorly described. 3 beta[N-N',N'-dimethylaminoethane)-carbamoyl] cholesterol (DCC) requires a one-step synthesis, and can be used to formulate transfection-grade liposomes when combined with dioleoylphosphatidyl-ethanolamine (DOPE) 1/1 (wt/wt). Luciferase activities in LMH-2A cells were 8.5-fold and 87.5-fold greater than those in HepG2 and FTO2B cells, respectively, following DCC-liposome-mediated transfection with a reporter consisting of the human cytomegalovirus immediate-early promoter (CMV), joined to Photinus pyralis luciferase (L) cDNA, designated pCMVL. Using pCMVL, N-(2-bromoethyl)-N,N-dimethyl-2,3-bis(9-octadecenyloxy)-propana minimun bromide) (BMOP)/DOPE 1/1 (wt/wt), at a 7.5:1 ratio with DNA, produced luciferase activities that were 2.9-fold higher than those of DCC-liposomes, at an optimal 10:1 lipid:DNA ratio. At optimal lipid:DNA ratios, commercially available liposomes, Transfectam, Lipofectamine, and Lipofectin, produced luciferase activities that were 1.39, 1.03, and 0.47-fold those of DCC-liposomes. The effect of 0, 10, 100, or 500 nM/L 17 beta-estradiol on the expression of pCMVL and a second luciferase reporter containing the -593/+48 promoter region of the estrogen-responsive avian apo VLDL-II gene, designated pApoL, was tested in cells cultured in the presence or absence of 10% chicken serum. The CMV promoter supported a high level of expression in LMH-2A cells that was unaffected by serum alone, but was weakly responsive to estrogen. Estrogen responses of both reporters reached a plateau at 10 nM/L. Estrogen increased the expression of pApoL 24-fold and 79-fold in the absence and presence of serum, respectively. The -593/+48 region of the apo VLDL-II promoter may not contain previously reported negative insulin response elements, but chicken serum contains factors that enhance estrogen responsiveness of this region.

Analysis of Variance↗
PubMed1996

Polylysine enhances cationic liposome-mediated transfection of the hepatoblastoma cell line Hep G2.

Plasmid DNA condensed by polylysine enhanced cationic-liposome-mediated transfection of Hep G2 cells. The luciferase expression plasmid pCMVL was complexed with the polycation poly-L-lysine and mixed with liposomes that contained a 1:1 molar ratio of the cationic lipid 1,2-dioleoyloxy-3-trimethyl-ammoniumpropane, with the neutral phospholipid 1,2-di-(cis-9-octadecenoyl)-sn-glycero-3-phosphoethanolamine. Polylysine enhanced cationic-liposome-mediated transfection of the hepatoblastoma cell line Hep G2 9-fold compared with pCMVL complexed alone with liposomes. The ratio of cationic to anionic charge of the polylysine-pCMVL complexes, and the quantity of cationic liposomes, are important determinants for optimal transfection of Hep G2 cells.

Cations↗
PubMed1995

Older plasma lipoproteins are more susceptible to oxidation: a linking mechanism for the lipid and oxidation theories of atherosclerotic cardiovascular disease.

Increases in plasma cholesterol are associated with progressive increases in the risk of atherosclerotic cardiovascular disease. In humans plasma cholesterol is contained primarily in apolipoprotein B-based low density lipoprotein (LDL). Cells stop making the high-affinity receptor responsible for LDL removal as they become cholesterol replete; this slows removal of LDL from plasma and elevates plasma LDL. As a result of this delayed uptake, hypercholesterolemic individuals not only have more LDL but have significantly older LDL. Oxidative modification of LDL enhances their atherogenicity. This study sought to determine whether increased time spent in circulation, or aging, by lipoprotein particles altered their susceptibility to oxidative modification. Controlled synchronous production of distinctive apolipoprotein B lipoproteins (yolk-specific very low density lipoproteins; VLDLy) with a single estrogen injection into young turkeys was used to model LDL aging in vivo. VLDLy remained in circulation for at least 10 days. Susceptibility to oxidation in vitro was highly dependent on lipoprotein age in vivo. Oxidation, measured as hexanal release from n-6 fatty acids in VLDLy, increased from 13.3 +/- 5.5 nmol of 2-day-old VLDLy per ml, to 108 +/- 17 nmol of 7-day-old VLDLy per ml. Oxidative instability was not due to tocopherol depletion or conversion to a more unsaturated fatty acid composition. These findings establish mathematically describable linkages between the variables of LDL concentration and LDL oxidation. The proposed mathematical models suggest a unified investigative approach to determine the mechanisms for acceleration of atherosclerotic cardiovascular disease risk as plasma cholesterol rises.

Aging↗
PubMed1994

Overfeeding increases very low density lipoprotein diameter and causes the appearance of a unique lipoprotein particle in association with failed yolk deposition.

Structurally specific very low density lipoprotein (VLDL) particles are presumed to redirect VLDL uptake during yolk deposition. Egg production is an energy intensive process, but energy excess negatively affects egg production. This study sought to determine whether overfeeding changed hen lipoprotein profiles, and if so, whether changes were related to egg production. Overfeeding caused 33% of hens to stop yolk deposition and reabsorb unovulated follicles (involute). VLDL of control hens possessed characteristic small particle size (30 nm) and composition indicative of limited intravascular metabolism. Overfeeding generally increased VLDL diameter, the effect being slight (+6.6 nm) in overfed laying hens when compared to overfed-involuted hens (+51.2 nm). Changes in composition indicated that increased intravascular metabolism of VLDL parallelled increases in particle diameter. Overfed-involuted hens showed significant elevations of plasma low density lipoprotein, VLDL cholesteryl ester, and high density lipoprotein (HDL) triacylglycerol content. Overfeeding increased plasma HDL, and in association with involution, caused redistribution of HDL particle sizes, including the appearance of novel HDL approximately 20 nm in diameter, termed HDLR, and a 97 kDa protein within the HDL fraction. The overfed hen model may provide new insight into the role of lipoprotein physical properties in determining the metabolism of triacylglycerol-rich lipoprotein, and the process of reverse lipid transport. Overfeeding generally increases VLDL size and plasma HDL levels suggesting that increased peripheral metabolism, and perhaps mechanical exclusion of enlarged VLDL by the granulosa basal lamina, contribute to the obesity and impaired yolk deposition observed in hens with excessive energy intakes. Temporal definition of massive VLDL enlargement relative to follicular collapse remains to be established.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1993

Fatty liver hemorrhagic syndrome in hens overfed a purified diet. Selected enzyme activities and liver histology in relation to liver hemorrhage and reproductive performance.

A nutritionally adequate, purified diet was developed and used in studies to characterize selected aspects of laying hens in which fatty liver hemorrhagic syndrome (FLHS) was induced by overfeeding. Hens consuming the diet ad libitum or intubated with the diet in quantities equivalent to usual daily energy intake maintained normal rates of lay, did not become obese, and did not develop liver hemorrhage. Overfed hens had a 33% incidence of FLHS, as indicated by the presence of severe liver hemorrhage score, and displayed the full range of symptoms associated with spontaneous outbreaks of FLHS, including definitive lesions of hepatic reticulin. Among four groups of hens clinically classified according to rates of liver hemorrhage and egg production, there were no differences noted in total liver fat, liver fat concentration, or final body weight. Liver hemorrhage was associated with the degree of induction of liver lipogenic accessory enzymes. Serum enzyme activities indicate that overfed hens, unlike the overfed goose, retain hepatocellular membrane integrity. Overfeeding caused altered reproductive performance in 72% of hens. Alterations included erratic laying, increased incidence of double ovulations, shell defects, follicular collapse, and oviduct involution. Pattern of lay preceding necropsy seemed to influence follicle weight at necropsy. The data presented re-emphasize the interdependence among liver, ovary, and oviduct function in the etiology of FLHS.

Animal Feed↗
PubMed1993

Avian fatty liver hemorrhagic syndrome: a comparative review.

Metabolic fatty liver syndromes occur in a variety of species including chickens, humans, cows, and cats. Both energy excess and deficit appear to initiate the accumulation of liver fat. Although the conditions preceding the onset of liver steatosis vary, all syndromes share a common basis in altered lipid utilization, lipoprotein assembly, and secretion. Laying hens and humans appear to develop fatty livers under similar metabolic conditions of energy excess. This similarity and the additional structural requirements inherent in yolk deposition make the laying hen an exciting model in which to study lipoprotein synthesis, assembly, and secretion. The overfed hen provides additional insights into the effects of nutrition and hormones on these same processes. Within this model it may be possible to distinguish the effects of altered gene expression versus altered physical properties (lipids) and postranslational processing (proteins) in mediating the observed responses.

Animals↗
PubMed1991

Relationship between growth and selected liver enzyme activities of individual rainbow trout.

Interpretation of enzymatic data requires consideration of the food intake of each animal studied. Food intake and body mass gain are closely correlated in rapidly growing animals. Direct measurement of food intake by individual fish within a school is nearly impossible. We examined the relationship between growth and liver enzyme activity as a means of inferring the food intake of individual fish within a school. Trout, identified by passive integrated transponder implants, were fed either 0, 0.3, 1, or 2% body mass/d to produce a wide range of growth rates. The activities of five enzymes, predominantly localized in liver, were measured. Results showed that, although the magnitude of response differed, increases in total liver activities of all five enzymes measured were linearly related to growth. Hexokinase (EC 2.7.1.1) increased at a rate below, and beta-D-glucose:NAD(P)+1-oxidoreductase (EC 1.1.1.47) increased at a rate equivalent to, observed increases in total liver mass. Malic enzyme (EC 1.1.1.40), glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and 6-phosphogluconate dehydrogenase (EC 1.1.1.44) showed preferential increases in activity as food intake increased. Correlation of enzyme activities measured in fish fed restricted rations with either growth or nominal feeding rate showed that growth of individual fish was more closely related to liver enzyme activities than nominal feeding rate.

Animals↗
PubMed1988

Thiamin absorption is not compromised in folate-deficient rats.

Thiamin absorption and excretion were assessed in rats with severe folate deficiency (FD) by determining the fate of oral 3H-labeled and intravenous 14C-labeled thiamin over a 6-h test period. Thiamin status was evaluated in these same rats by measuring transketolase activity levels of blood before (TKA) and after (TPPE) addition of thiamin pyrophosphate to the incubation mixture of the assay procedure. Two additional experiments assessed active transport of thiamin and the effect of dietary succinylsulfathiazole (SST) on TKA and TPPE in rats with moderate FD. Intestinal absorption in general and thiamin absorption in particular and thiamin status were unaltered in rats with severe FD. Inanition associated with severe FD may impair thiamin status. Thiamin absorption by active transport was not compromised in FD, and dietary succinylsulfathiazole did not affect thiamin status.

Animals↗
PubMed1988

Folate deficiency in rats fed diets containing free amino acids or intact proteins.

Development of folate deficiency (FD) was evaluated in weanling rats fed diets containing mixtures of free amino acids or of vitamin-free casein and gelatin as sources of dietary nitrogen. FD could be produced in 21 d with amino acid diets that promoted maximum growth rate, were completely devoid of folate and contained 1% succinylsulfathiazole. Growth retardation and blood dyscrasia associated with FD could not be demonstrated in rats fed diets containing casein and gelatin as nitrogen sources because the vitamin-free casein contained low but measurable levels of folate. The most effective protocol to produce experimental FD in rats is to feed a folate-free diet that otherwise supports maximum growth in young animals. Additional modifications such as use of methotrexate or amino acid-imbalanced or protein-deficient diets are unnecessary.

Animals↗
PubMed1983

Folate deficiency in rats fed amino acid diets.

Growth rate, hematological changes, serum, erythrocyte and liver folate levels, and urinary excretion of formiminoglutamic acid (FIGLU) were measured in rats fed p-aminobenzoic acid (PABA)-free, sulfonamide-supplemented purified amino acid diets with and without folic acid and fiber, individually and in combination. Fiber had no effect on growth but was necessary to prevent mortality in the absence of folic acid. Folic acid did not affect growth during the first 40 days, but after this period rats failed to gain weight in the absence of folic acid. Although blood hematocrit was lower when the diet was devoid of fiber and folic acid and leucocyte counts were lower when the diets were devoid of folic acid, the hematological values remained within normal physiological limits for healthy rats of comparable age. FIGLU excretion was increased and serum, erythrocyte and liver folate levels were depressed when rats were fed folic acid-free diets for 28 days. Neutrophil hypersegmentation was clearly evident after 28 days of feeding the folic acid-free diets. The use of an amino acid diet without PABA but containing 5% fiber and 1% succinylsulfathiazole is a useful system to study chronic folic acid deficiency in the rat.

Amino Acids↗
PubMed1983

Purine synthesis and reutilization in folate-deficient rat hepatocytes.

Although folic acid is known to be involved in the pathways of purine metabolism, the precise changes brought about in purine synthesis, reutilization, pool sizes, and ratios by experimental folate deficiency are not clear. Consequently, these aspects of purine metabolism were measured in hepatocytes from control and folate-deficient rats fed an amino acid diet with and without folic acid, respectively. Purine synthesis and reutilization were measured as the rates of incorporation of [U-14C]glycine and [G-3H]hypoxanthine, respectively, into the adenine and guanine pools of freshly isolated hepatocytes after a 3-hour incubation in folate-free, as well as folate- and/or thymidine-supplemented culture media. Hepatocytes from folate-deficient rats had the same rates of purine synthesis as those from control rats. Purine reutilization, purine pool sizes, and the adenine:guanine ratios were lower in hepatocytes from deficient compared with control rats. Purine synthesis was increased when folic acid or thymidine was added to the culture medium. Although hepatocytes from folate-deficient rats had a lower rate of purine reutilization compared with those from control rats, the reutilization rates did not respond to the addition of folic acid or thymidine to the culture medium. The data suggest that purine synthesis was not impaired but purine reutilization was diminished in folate deficiency. Thymidine was as effective as folic acid in stimulating purine synthesis in both control and folate-deficient hepatocytes.

Animals↗