Dietary Interaction of High Fat and Marginal Copper Deficiency on Cardiac Contractile Function

Relling, David P.; Esberg, Lucy B.; Johnson, W. Thomas; Murphy, Eric J.; Carlson, Edward C.; Lukaski, Henry C.; Saari, Jack T.; Ren, Jun

doi:10.1038/oby.2007.146

Cited by 21 publications

(28 citation statements)

References 71 publications

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“…Our proteomic data of contractile proteins were comparable with the results reported by Gelfi et al [15], who demonstrated that four rat contractile proteins were more abundant in soleus muscle, whereas five were more dominantly expressed in gastrocnemius muscle under normal dietary conditions. Altogether, down regulation of these myofibrillar regulatory proteins may favor decreased contractile capacities when exposed to HFD in both genders [35,36]. Our data clearly demonstrated the existence of gender differences in several proteins involved in muscle contraction, which supports the fact that higher forces of motor units in male muscles can be generated due to higher expressions of contractile proteins.…”

Section: Proteins Involved In Muscle Contractionsupporting

confidence: 68%

Gender Dimorphism in Skeletal Muscle Proteome Between Lean and Diet-induced Obese Rats

Choi

et al. 2011

Cell Physiol Biochem

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Background: Although it has been believed for a long time that gender differences in physiology and metabolism were not relevant beyond the reproductive system, new research has indicated that sexual dimorphism may be more prevalent than previously believed. Therefore, the goal of this study was to develop a global view of the changes in gender-dependent protein abundance in two different types of skeletal muscles (soleus and gastrocnemius) of lean and high fat diet (HFD)-induced obese rats. Methods: To examine differential expression of proteins between gender and diet, we performed differential proteome analysis of skeletal muscle from lean and obese rats of both genders fed a HFD using 2-DE combined with MALDI-TOF-MS. Results: Our gender-specific proteome comparison showed that male and female rats displayed different patterns of proteome regulation including proteins involved in muscle contraction, carbohydrate and lipid metabolism, oxidative phosphorylation, as well as detoxification and antioxidant defenses. Conclusions: most of the candidate proteins identified herein by differential proteomics were previously unrecognized in gender dimorphism of skeletal muscle. Our data can serve as the basis for specific evidence-based interventions allowing for the prevention and treatment of obesity by matching the different needs of women and men such as the development of gender-based medicine.

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Section: Proteins Involved In Muscle Contractionsupporting

confidence: 68%

Gender Dimorphism in Skeletal Muscle Proteome Between Lean and Diet-induced Obese Rats

Choi

et al. 2011

Cell Physiol Biochem

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“…35 Mitochondria were isolated from left ventricles (5 to 6 mice per group) for analysis of mitochondrial respiration. CCO activity was detected by monitoring the change in absorbance at 550 nm (∆A 550 ) resulting from the oxidation of reduced cytochrome c. The CCO activity was monitored until ∆A 550 was ≈0.6 U, at which point potassium cyanide (0.17 mmol/L) was added to terminate the CCO reaction.…”

Section: Methodsmentioning

confidence: 99%

Macrophage Migration Inhibitory Factor Deficiency Augments Doxorubicin‐Induced Cardiomyopathy

Bucala

Ren

2013

JAHA

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BackgroundRecent evidence has depicted a role of macrophage migration inhibitory factor (MIF) in cardiac homeostasis under pathological conditions. This study was designed to evaluate the role of MIF in doxorubicin‐induced cardiomyopathy and the underlying mechanism involved with a focus on autophagy.Methods and ResultsWild‐type (WT) and MIF knockout (MIF−/−) mice were given saline or doxorubicin (20 mg/kg cumulative, i.p.). A cohort of WT and MIF−/− mice was given rapamycin (6 mg/kg, i.p.) with or without bafilomycin A1 (BafA1, 3 μmol/kg per day, i.p.) for 1 week prior to doxorubicin challenge. To consolidate a role for MIF in the maintenance of cardiac homeostasis following doxorubicin challenge, recombinant mouse MIF (rmMIF) was given to MIF−/− mice challenged with or without doxorubicin. Echocardiographic, cardiomyocyte function, and intracellular Ca2+ handling were evaluated. Autophagy and apoptosis were examined. Mitochondrial morphology and function were examined using transmission electron microscopy, JC‐1 staining, MitoSOX Red fluorescence, and mitochondrial respiration complex assay. DHE staining was used to evaluate reactive oxygen species (ROS) generation. MIF knockout exacerbated doxorubicin‐induced mortality and cardiomyopathy (compromised fractional shortening, cardiomyocyte and mitochondrial function, apoptosis, and ROS generation). These detrimental effects of doxorubicin were accompanied by defective autophagolysosome formation, the effect of which was exacerbated by MIF knockout. Rapamycin pretreatment rescued doxorubicin‐induced cardiomyopathy in WT and MIF−/− mice. Blocking autophagolysosome formation using BafA1 negated the cardioprotective effect of rapamycin and rmMIF.ConclusionsOur data suggest that MIF serves as an indispensable cardioprotective factor against doxorubicin‐induced cardiomyopathy with an underlying mechanism through facilitating autophagolysosome formation.

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“…Mild dietary deficiencies of both metals represent an underestimated problem for human health, [1,2] and references therein, because they are not associated to clear signs and clinical symptoms, even though they may cause long-term deleterious effects in cardiovascular system and alterations in lipid metabolism [3]. Since the first direct experimental evidence about the treatment of chlorosis in young woman, many studies have shown that iron and copper metabolism, absorption and systemic distribution are intimately connected.…”

Section: Introductionmentioning

confidence: 99%

Molecular bases of copper and iron deficiency-associated dyslipidemia: a microarray analysis of the rat intestinal transcriptome

et al. 2009

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As essential cofactor in many proteins and redox enzymes, copper and iron are involved in a wide range of biological processes. Mild dietary deficiency of metals represents an underestimated problem for human health, because it does not cause clear signs and clinical symptoms, but it is associated to long-term deleterious effects in cardiovascular system and alterations in lipid metabolism. The aim of this work was to study the biological processes significantly affected by mild dietary deficiency of both metals in rat intestine, in order to better understand the molecular bases of the systemic metabolic alterations, as hypercholesterolemia and hypertriglyceridemia observed in copper-deficient rats. A gene-microarray differential analysis was carried out on the intestinal transcriptome of copper-and iron-deficient rats, thus highlighting the biological processes significantly modulated by the dietary restrictions. The gene array analysis showed a down-regulation of genes involved in mitochondrial and peroxisomal fatty acids beta-oxidation and an up-regulation of genes involved in plasmatic cholesterol transport (apoprotein E and lecithin:cholesterol acyltransferase) in copper deficiency. Furthermore, a severe down-regulation of ApoH was pointed out in iron-deficient animals.

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Dietary Interaction of High Fat and Marginal Copper Deficiency on Cardiac Contractile Function

Cited by 21 publications

References 71 publications

Gender Dimorphism in Skeletal Muscle Proteome Between Lean and Diet-induced Obese Rats

Gender Dimorphism in Skeletal Muscle Proteome Between Lean and Diet-induced Obese Rats

Macrophage Migration Inhibitory Factor Deficiency Augments Doxorubicin‐Induced Cardiomyopathy

Molecular bases of copper and iron deficiency-associated dyslipidemia: a microarray analysis of the rat intestinal transcriptome

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