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Introduction: The reduction of nitrogen (N) and phosphorus (P) in ruminant feed is desirable due to costs and negative environmental impact. Ruminants are able to utilize N and P through endogenous recycling, particularly in times of scarcity. When N and/or P were reduced, changes in mineral homeostasis associated with modulation of renal calcitriol metabolism occurred. The aim of this study was to investigate the potential effects of dietary N- and/or P-reduction on the regulatory mechanisms of mineral transport in the kidney and its hormonal regulation in young goats. Results: During N-reduction, calcium (Ca) and magnesium (Mg) concentrations in blood decreased, accompanied by a lower protein expression of cytochrome P450 family 27 subfamily B member 1 (CYP27B1) (p = 0.016). The P-reduced fed goats had low blood phosphate concentrations with simultaneously high Ca and Mg levels. The insulin-like growth factor 1 concentrations decreased significantly with P-reduction. Furthermore, gene expression of CYP27B1 (p < 0.001) and both gene (p = 0.025) and protein (p = 0.016) expression of the fibroblast growth factor receptor 1c isoform in the kidney were also significantly reduced during a P-reduced diet. ERK1/2 activation exhibited a trend toward reduction in P-reduced animals. Interestingly, calcitriol concentrations remained unaffected by either restriction individually, but interacted significantly with N and P (p = 0.014). Additionally, fibroblast growth factor 23 mRNA expression in bone decreased significantly with P-restriction (p < 0.001). Discussion: These results shed light on the complex metabolic and regulatory responses of mineral transport of young goats to dietary N and P restriction. [ABSTRACT FROM AUTHOR]

Oxidized fats affect animal metabolism in several ways. To gain a comprehensive understanding of the molecular mechanisms underlying the effects of dietary oxidized rats in rats at varying dietary vitamin E concentrations, the gene expression profile of the liver was monitored with an array containing 1176 binding sites for cDNAs. Rats were fed diets with a fresh fat and vitamin E concentrations of 25 or 250 mg [alpha]-tocopherol/kg (FF25, FF250 rats) or a fat heated at 50[degrees]C for 38 d, with vitamin E concentrations of 25 or 250 mg [alpha]-tocopherol/kg (OF25, OF250 rats) for 63 d. Differences in gene expression were considered to be significant at a ratio of at least 1.4. In the OF25 rats, the expression of 47 genes was altered; in the OF250 rats, the expression of 37 genes was altered, and in the FF250 rats, the expression of 21 genes was altered compared with FF25 rats. In both OF25 and OF250 rats, a series of target genes of the peroxisome proliferator-activated receptor [alpha] (PPAR[alpha]) was upregulated. Determination of gene expression of acyl CoA oxidase and activity of catalase confirmed that oxidized fats caused peroxisome proliferation in the liver. In OF25 and OF250 rats, there was also upregulation of 12 and 5 genes involved in xenobiotic metabolism and stress response, of 7 and 7 genes involved in protein metabolism, of 5 and 2 genes encoding intracellular effectors or modulators and of 5 and 6 genes, respectively, encoding activators or repressors of transcription or translation. In conclusion, this study provides indirect evidence that dietary oxidized fats cause an activation of the PPAR[alpha], irrespective of the dietary vitamin E concentration. Identification of several other differentially regulated genes may be helpful to understand the effects of oxidized rats on animal metabolism. KEY WORDS: * rats * oxidized rats * vitamin E * cDNA array * gene expression

The aim of this study was to investigate the effect of dietary oxidized fats on the lipoprotein profile and the atherogenicity of LDL. Two experiments with male Sprague-Dawley rats were conducted. In Experiment 1, diets with either fresh fat or oxidized fat, prepared by heating at temperatures of 50, 105 or 190[degrees]C, containing either 25 or 250 mg [alpha]-tocopherol equivalents/kg were used. In Experiment 2, diets with fresh or oxidized fat, heated at a temperature of 55[degrees]C, containing 25 mg [alpha]-tocopherol equivalents/kg, were used. In Experiment 1, rats fed all types of oxidized fats had higher concentrations of HDL cholesterol and lower ratios between plasma and HDL cholesterol than rats fed the diet containing the fresh fat. As determined from the lag time, the susceptibility of LDL to copper-induced lipid peroxidation was higher in rats fed oxidized fats heated at 105 or 190[degrees]C than in rats fed the diets containing the fresh fat or the oxidized fat treated at 50[degrees]C, irrespective of the dietary vitamin E concentration. However, in Experiment 2, the composition of LDL apolipoproteins and uptake of LDL by macrophages were not different between rats fed the fresh fat diet and those fed the oxidized fat diet. We conclude that ingestion of oxidized fats does not adversely affect the lipoprotein profile in the rat model used, and does not cause modifications of apolipoproteins that would lead to enhanced uptake of LDL via macrophage scavenger receptors. KEY WORDS: * antioxidant status * LDL * oxidized fat * rats

In vitro studies suggest that high vitamin E supplementation has prooxidative activity, but very few studies have investigated this effect in vivo. We investigated the effect of excess vitamin E on the antioxidative status of rat erythrocytes and indicators of hemolysis. Six groups of growing male Sprague-Dawley rats were fed purified diets with three different vitamin E doses [100, 1000 and 10,000 mg all-rac-[alpha]-tocopheryl acetate (TA)/kg diet] and two different dietary fats (salmon oil and lard) for 8 wk. The rats whose diet contained salmon oil and 10,000 mg TA/kg had lower activities of superoxide dismutase (P < 0.05), glutathione peroxidase (P < 0.05), catalase (P < 0.05) and glucose-6-phosphate dehydrogenase (P < 0.05) and a lower concentration of glutathione (P < 0.05) in the erythrocyte cytosol than rats whose diet contained 100 mg TA/kg. The concentration of free hemoglobin and the binding capacity of haptoglobin in plasma, both indicators of in vivo hemolysis, did not differ between rats fed the salmon oil diet with 100 or 10,000 mg TA/kg. In the rats whose diet contained lard, the activities of antioxidant enzymes in erythrocytes and indicators of in vivo hemolysis were independent of the dietary vitamin E concentration. The results of the study suggest that an excessive vitamin E intake, when combined with salmon oil in the diet, lowers the activities of antioxidant enzymes in erythrocytes without affecting in vivo hemolysis. KEY WORDS: * rats * erythrocytes * vitamin E * hemolysis * antioxidative enzymes

Abstract Background In rodents and pigs, it has shown that carnitine synthesis and uptake of carnitine into cells are regulated by peroxisome proliferator-activated receptor α (PPARA), a transcription factor which is physiologically activated during fasting or energy deprivation. Dairy cows are typically in a negative energy balance during early lactation. We investigated the hypothesis that genes of carnitine synthesis and uptake in dairy cows are enhanced during early lactation. Results mRNA abundances of PPARA and some of its classical target genes and genes involved in carnitine biosynthesis [trimethyllysine dioxygenase (TMLHE), 4-N-trimethylaminobutyraldehyde dehydrogenase (ALDH9A1), γ-butyrobetaine dioxygenase (BBOX1)] and uptake of carnitine [novel organic cation transporter 2 (SLC22A5)] as well as carnitine concentrations in liver biopsy samples of 20 dairy cows in late pregnancy (3 wk prepartum) and early lactation (1 wk, 5 wk, 14 wk postpartum) were determined. From 3 wk prepartum to 1 wk postpartum, mRNA abundances of PPARΑ and several PPARΑ target genes involved in fatty acid uptake, fatty acid oxidation and ketogenesis in the liver were strongly increased. Simultaneously, mRNA abundances of enzymes of carnitine synthesis (TMLHE: 10-fold; ALDH9A1: 6-fold; BBOX1: 1.8-fold) and carnitine uptake (SLC22A5: 13-fold) and the concentration of carnitine in the liver were increased from 3 wk prepartum to 1 wk postpartum (P < 0.05). From 1 wk to 5 and 14 wk postpartum, mRNA abundances of these genes and hepatic carnitine concentrations were declining (P < 0.05). There were moreover positive correlations between plasma concentrations of non-esterified fatty acids (NEFA) and hepatic carnitine concentrations at 1 wk, 5 wk and 14 wk postpartum (P < 0.05). Conclusions The results of this study show for the first time that the expression of hepatic genes of carnitine synthesis and cellular uptake of carnitine is enhanced in dairy cows during early lactation. These changes might provide an explanation for increased hepatic carnitine concentrations observed in 1 wk postpartum and might be regarded as a physiologic means to provide liver cells with sufficient carnitine required for transport of excessive amounts of NEFA during a negative energy balance.

Propionate has antimicrobial activity and is suggested to influence lipid metabolism. Here, we investigated the effect of propionate on lipid metabolism and the gut microbiome in fructose-fed mice as a model of diet-induced steatosis and gut dysbiosis. Therefore, 48 male wild-type mice were fed isoenergetic diets with either 0% fructose (F-) or 40% fructose (F+) that contained 0% propionate (P-) or 1% propionate (P+) for 7 weeks. Mice that received the F+ diets developed fatty livers, had fewer small intestinal proteobacteria and colonic actinobacteria and were characterised by changes in bacterial genera (e.g., Allobaculum, Lachnospiraceae, and Escherichia). Interestingly, mice fed the F+ diets had higher levels of propionate and butyrate in the circulation than mice fed the F- diets (p < 0.05). Treatment with propionate influenced neither hepatic or plasma lipids nor levels of circulating SCFAs. With the exception of Verrucomicrobia, other bacterial phyla were not affected by propionate. [ABSTRACT FROM AUTHOR]

For more than 3 decades, extracorporeal shock wave therapy (ESWT) has been clinically implemented in urologic and orthopaedic indications. Here, we present the case of a patient with envenomation from a highly toxic jellyfish-like siphonophore (Physalia physalis) with a toxic contact dermatitis resulting in chronic eruptive skin lesions. The skin lesions on the dorsal right hand lasted more than 16 weeks and were refractive to local cortisone treatment. They finally healed after 8 applications of low-energy planar/defocused ESWT over 4 weeks. In detail, the clinical course, ESWT specifications and the possible mechanisms of ESWT in the light of the current literature are discussed. Our case indicates that ESWT is an underestimated, promising non-invasive, non-immunosuppressive treatment for chronic eruptive skin lesions after jellyfish or related toxin envenomations. [ABSTRACT FROM AUTHOR]

Cocoa polyphenols are thought to reduce the risk of cardiovascular diseases. Thus, cocoa-containing foods may have significant health benefits. Here, we studied the impact of chocolate liquor on vascular lesion development and plaque composition in a mouse model of atherosclerosis. Apolipoprotein E (apoE)-knockout mice were assigned to two groups and fed a Western diet that contained 250 g/kg of either chocolate liquor or a polyphenol-free isoenergetic control paste for 16 weeks. In addition to fat, protein and fibers, the chocolate liquor contained 2 g/kg of polyphenols. Compared with the control group, mice fed the chocolate liquor had larger plaque areas in the descending aorta and aortic root, which were attributed to a higher mass of vascular smooth muscle cells (VSMCs) and collagen. Vascular lipid deposits and calcification areas did not differ between the two groups. The aortic tissue level of interleukin-6 (IL-6) mRNA was 5-fold higher in the mice fed chocolate liquor than in the control mice. Chocolate-fed mice exhibited an increased hepatic saturated to polyunsaturated fatty acid ratio than the controls. Although the chocolate liquor contained 14 μg/kg of vitamin D2, the chocolate liquor-fed mice did not have measurable 25-hydroxyvitamin D2 in the serum. These mice even showed a 25% reduction in the level of 25-hydroxyvitamin D3 compared with the control mice. Overall, present data may contribute to our understanding how chocolate constituents can impact vascular lesion development. [ABSTRACT FROM AUTHOR]

Introduction Due to the high prevalence of vitamin D deficiency, strategies are needed to improve vitamin D status. Food components can affect vitamin D metabolism and have to be considered when estimating the efficacy of vitamin D supplements. 7-dehydrocholesterol (7-DHC) occurs naturally in food, but its impact on vitamin D metabolism has not yet been examined. Methods Three groups of male C57BL/6 mice ( n = 12 per group) were placed on a diet that contained 0, 2.5 or 5 mg 7-DHC per kg diet over a period of 6 weeks. Vitamin D and other sterols in the serum, skin, liver and kidney were quantified by LC–MS/MS. The relative mRNA abundance of hepatic genes encoding vitamin D hydroxylation enzymes and transporters was analyzed by real-time RT-PCR. Results We found a substantial dose-dependent increase of non-hydroxylated vitamin D 3 in the liver and kidney of mice fed a diet containing 7-DHC. The vitamin D 3 content in the liver was 2.80 ± 0.61 pmol/g, 7.34 ± 4.28 pmol/g and 12.9 ± 3.58 pmol/g in groups that received 0, 2.5 and 5 mg/kg 7-DHC, respectively. In the kidney, the vitamin D 3 content of these groups was 1.78 ± 1.17 pmol/g, 3.55 ± 1.06 and 6.36 ± 2.29 pmol/g, respectively. The serum and tissue concentrations of 25-hydroxyvitamin D 3 (25(OH)D 3 ) remained unaffected by 7-DHC. The relative mRNA data provided no plausible mechanism for the observed effects of 7-DHC on vitamin D 3 . All groups of mice had similar concentrations of cholesterol, desmosterol and 7-DHC in their serum and tissues. Conclusion The current findings provide the first evidence that dietary 7-DHC seems to affect vitamin D metabolism. The underlying mechanism remains elusive and needs further investigation. [ABSTRACT FROM AUTHOR]