Aortic lesions in copper deficiency: Modification by dietary carbohydrates

1986 ◽  
Vol 44 ◽  
pp. 358-359
Author(s):  
U. Bielenberg
Keyword(s):  
Copper Deficiency ◽  
Male Rats ◽  
Dietary Carbohydrates ◽  
Dietary Copper ◽  
Serum Ceruloplasmin ◽  
Hepatic Copper ◽  
Dietary Treatments ◽  
Feeding Diets ◽  
Ceruloplasmin Activity ◽  
Simple Carbohydrate

Copper deficiency can cause cardiovascular lesions in experimental animals. Previous experiments have shown that the biochemical and itDrphologic lesions induced by deprivation of dietary copper can be suppressed by feeding diets containing starch or can be magnified by a high sucrose diet. In a recent study it was found that the more severe signs of copper deficiency in rats fed sucrose as compared to starch were due to the fructose moiety of sucrose. Although fructose as compared to starch markedly enhanced the symptoms of copper deficiency, the possibility that an effect of dietary carbohydrates due to the nature of the simple carbohydrate (fructose vs glucose) cannot be excluded. The present study was designed to determine if the severity of copper deficiency in rats fed sucrose as compared to starch is due to the glucose as well as the fructose moiety of sucrose. This portion of the study assessed the morphologic changes in aortas of seventy weanling male rats who were fed, for 9 weeks, copper deficient or copper supplemented diets containing either 62% starch, fructose or glucose. The starch-fed copper supplemented group served as the most normal controls. Rats were sacrificed after 9 weeks of dietary treatments. Copper deficiency was verified by reduced serum ceruloplasmin activity and serum and hepatic copper concentration.

Variations in ATP7B in cats with primary copper-associated hepatopathy

2019 ◽  
Vol 22 (8) ◽  
pp. 753-759
Author(s):  
Hajime Asada ◽  
James K Chambers ◽  
Mari Kojima ◽  
Yuko Goto-Koshino ◽  
Taisuke Nakagawa ◽  
...  
Keyword(s):  
The Other ◽  
Copper Accumulation ◽  
Limited Information ◽  
Single Nucleotide ◽  
Serum Ceruloplasmin ◽  
Hepatic Copper ◽  
Single Nucleotide Variations ◽  
Tissue Specimens ◽  
Ceruloplasmin Activity ◽  
Low Serum

Objectives Primary copper-associated hepatopathy (PCH) has been reported in young cats. Although our group recently reported a young cat with PCH harbouring single-nucleotide variations in ATP7B, limited information is available regarding its association with the pathogenesis of feline PCH. The objective of this study was to investigate the prevalence of ATP7B variations in cats with PCH. Methods Rhodanine staining was performed to detect hepatic copper accumulation (HCA) in intraoperative liver tissue specimens from 54 cats. In cats with HCA, variations in ATP7B and COMMD1 and serum ceruloplasmin activity were analysed. Results Based on age, liver histopathological findings and hepatic distribution of accumulated copper, PCH was suspected in 4/54 cats. Sequence analysis of ATP7B and COMMD1 revealed single-nucleotide variations in ATP7B in 3/4 cats with PCH. Among the cats with PCH, one showed remarkably low serum ceruloplasmin activity, while the other three did not. Conclusions and relevance The results of this study suggest that some cats with PCH harbour single-nucleotide variations in ATP7B, suggesting that feline PCH is an equivalent disorder to human Wilson’s disease. This study provides basic evidence facilitating further studies of the pathophysiology and treatment of feline PCH.

scholarly journals Characterization of plasma ceruloplasmin activity and expression following dietary copper deficiency

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Joseph Prohaska ◽  
Margaret Broderius ◽  
Elise Mostad ◽  
Krista Wendroth
Keyword(s):  
Copper Deficiency ◽  
Dietary Copper ◽  
Ceruloplasmin Activity

scholarly journals Relationships between copper, zinc and iron in the plasma, soft tissues and skeleton of the rat during Cu deficiency

1973 ◽  
Vol 29 (1) ◽  
pp. 73-85 ◽  
Author(s):  
Begona Alfaro ◽  
F. W. Heaton
Keyword(s):  
Bone Marrow ◽  
Stainless Steel ◽  
Copper Deficiency ◽  
Soft Tissues ◽  
Male Rats ◽  
Dietary Copper ◽  
Cu Deficiency ◽  
Depletion Period ◽  
Copper Zinc ◽  
Hypertrophy Of The Heart

1. The effect of dietary copper deficiency on the distribution of Cu, zinc and iron between plasma, various soft tissues and bone was investigated in weanling male rats.2. The concentration of Cu decreased in plasma, liver, kidney and femur, and the concentration in plasma correlated with that in all three organs. The total amount of Cu in the liver was reduced over the whole depletion period and a net loss from kidney also occurred over a shorter period, indicating that liver and, to a lesser extent, kidney both provide a mobilizable reserve of Cu.3. Animals in galvanized cages developed Cu deficiency more rapidly than similar rats in stainless-steel cages owing to Zn aggravating the depletion. Zn accumulated in the liver and femur of Cu deficient rats, particularly when they were housed in galvanized cages.4. Cu-deficient animals accumulated Fe in the liver, but had reduced concentrations in plasma, kidney and spleen. The hypertrophy of the heart and bone-marrow observed in Cu-deficient rats appeared to be secondary to the anaemia resulting from this impaired mobilization of hepatic Fe.

scholarly journals Analysis of sex differences in dietary copper-fructose interaction-induced alterations of gut microbial activity in relation to hepatic steatosis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ming Song ◽  
Fang Yuan ◽  
Xiaohong Li ◽  
Xipeng Ma ◽  
Xinmin Yin ◽  
...  
Keyword(s):  
Sex Differences ◽  
Microbial Activity ◽  
Hepatic Steatosis ◽  
Female Rats ◽  
Male Rats ◽  
Calorie Intake ◽  
Dietary Copper ◽  
Male And Female ◽  
Male And Female Rats ◽  
Rrna Sequencing

Abstract Background Inadequate copper intake and increased fructose consumption represent two important nutritional problems in the USA. Dietary copper-fructose interactions alter gut microbial activity and contribute to the development of nonalcoholic fatty liver disease (NAFLD). The aim of this study is to determine whether dietary copper-fructose interactions alter gut microbial activity in a sex-differential manner and whether sex differences in gut microbial activity are associated with sex differences in hepatic steatosis. Methods Male and female weanling Sprague-Dawley (SD) rats were fed ad libitum with an AIN-93G purified rodent diet with defined copper content for 8 weeks. The copper content is 6 mg/kg and 1.5 mg/kg in adequate copper diet (CuA) and marginal copper diet (CuM), respectively. Animals had free access to either deionized water or deionized water containing 10% fructose (F) (w/v) as the only drink during the experiment. Body weight, calorie intake, plasma alanine aminotransferase, aspartate aminotransferase, and liver histology as well as liver triglyceride were evaluated. Fecal microbial contents were analyzed by 16S ribosomal RNA (16S rRNA) sequencing. Fecal and cecal short-chain fatty acids (SCFAs) were determined by gas chromatography-mass spectrometry (GC-MS). Results Male and female rats exhibit similar trends of changes in the body weight gain and calorie intake in response to dietary copper and fructose, with a generally higher level in male rats. Several female rats in the CuAF group developed mild steatosis, while no obvious steatosis was observed in male rats fed with CuAF or CuMF diets. Fecal 16S rRNA sequencing analysis revealed distinct alterations of the gut microbiome in male and female rats. Linear discriminant analysis (LDA) effect size (LEfSe) identified sex-specific abundant taxa in different groups. Further, total SCFAs, as well as, butyrate were decreased in a more pronounced manner in female CuMF rats than in male rats. Of note, the decreased SCFAs are concomitant with the reduced SCFA producers, but not correlated to hepatic steatosis. Conclusions Our data demonstrated sex differences in the alterations of gut microbial abundance, activities, and hepatic steatosis in response to dietary copper-fructose interaction in rats. The correlation between sex differences in metabolic phenotypes and alterations of gut microbial activities remains elusive.

Dietary Copper Deficiency Increases the Mast Cell Population of the Rat

1994 ◽  
Vol 207 (3) ◽  
pp. 274-277 ◽  
Author(s):  
D. A. Schuschke ◽  
J. T. Saari ◽  
C. A. West ◽  
F. N. Miller
Keyword(s):  
Mast Cell ◽  
Cell Population ◽  
Copper Deficiency ◽  
Dietary Copper ◽  
Mast Cell Population

Wilson Disease

1996 ◽  
Vol 17 (12) ◽  
pp. 448-448
Author(s):  
Philip O. Ozuah
Keyword(s):  
Biliary Excretion ◽  
Wilson Disease ◽  
Autosomal Recessive ◽  
Copper Metabolism ◽  
The Body ◽  
Hepatolenticular Degeneration ◽  
Dietary Copper ◽  
Hepatic Copper ◽  
Excess Copper ◽  
Excessive Accumulation

Wilson disease (hepatolenticular degeneration) is an autosomal recessive, inherited disorder of copper metabolism resulting in excessive accumulation of copper in the liver, brain, and other organs of the body. The manifestations of the disease are related directly to this accumulation of copper. Copper homeostasis normally is a product of the balance between intestinal absorption of dietary copper and hepatic biliary excretion of excess copper. In Wilson disease, incorporation of hepatic copper into ceruloplasmin is defective and excretion of copper in the bile is reduced. A low level of ceruloplasmin, which until a few years ago was erroneously considered to be the basis for the disease, is a consequence of the underlying metabolic defect.

A comparison of copper-loading disease in Bedlington terriers and Wilson's disease in humans

1982 ◽  
Vol 243 (3) ◽  
pp. G226-G230 ◽  
Author(s):  
L. C. Su ◽  
S. Ravanshad ◽  
C. A. Owen ◽  
J. T. McCall ◽  
P. E. Zollman ◽  
...  
Keyword(s):  
Copper Concentration ◽  
Wilson’S Disease ◽  
Wilson's Disease ◽  
Normal Brain ◽  
Glutamic Pyruvic Transaminase ◽  
Serum Glutamic Pyruvic Transaminase ◽  
Hepatic Copper ◽  
Erythrocyte Survival ◽  
Ceruloplasmin Activity

Eleven Bedlington terriers were found to have a mean hepatic copper concentration of 6,321 micrograms/g dry wt (normal, 200 micrograms/g dry wt) and renal copper concentration that was three or four times normal. Brain copper levels were normal in younger dogs, were elevated in two older dogs, and were 100 times normal in one dog that died of the disease. Increased concentrations of copper in the liver, kidney, and brain also characterize Wilson's disease. Erythrocyte survival was normal in three affected dogs, but serum glutamic-pyruvic transaminase levels were usually elevated. Unlike the hypoceruloplasminemia of patients with Wilson's disease, plasma ceruloplasmin activity was not only normal but was also slightly elevated in the terriers. Despite their normal or excessive ceruloplasmin, the Bedlington terriers could convert ionic 64Cu to radioceruloplasmin but did so only very slowly. These dogs accumulated significantly more 64Cu in their livers than normal, much like patients with Wilson's disease do before symptoms develop.

Copper deficiency increases hepatic apolipoprotein B secretion and mRNA editing in rats

1996 ◽  
Vol 271 (2) ◽  
pp. C595-C604 ◽  
Author(s):  
S. K. Reaves ◽  
R. C. Hoogeveen ◽  
Y. R. Wang ◽  
J. Y. Wu ◽  
K. Y. Lei
Keyword(s):  
Apolipoprotein B ◽  
Copper Deficiency ◽  
Sprague Dawley ◽  
Mrna Editing ◽  
Apob Mrna ◽  
Sprague Dawley Rats ◽  
Differential Increase ◽  
Dietary Treatments ◽  
Parenchymal Cells ◽  
Hepatic Apolipoprotein

Male weanling Sprague-Dawley rats were assigned to copper-deficient (9.0 mumol Cu/kg diet) or copper-adequate (102 mumol Cu/kg diet) dietary treatments for 6 wk. Pulse-chase studies using freshly isolated rat liver parenchymal cells demonstrated that apolipoprotein B (apoB)-48 and apoB-100 syntheses were not altered, but secretion was increased twofold in hepatocytes derived from copper-deficient rats. Both plasma apoB-48 and apoB-100 levels were increased by copper deficiency, but only the apoB-48 increase was significant. Hepatic apoB mRNA editing, expressed as a ratio of apoB-48 mRNA to apoB-48 plus apoB-100 mRNA, was significantly increased from 60.8% in copper-adequate to 70.2% in copper-deficient rats. Moreover, hepatic apoB mRNA abundance was not significantly altered by copper deficiency. Thus the increased amount of nascent apoB-48 secreted into the medium as well as the enhanced apoB mRNA editing may have contributed to the differential increase in plasma apoB-48 over apoB-100 level in copper-deficient rats.

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