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A great number of studies have investigated the potential of L-carnitine as feed additive to improve performance of different monogastric and ruminant livestock species, with, however, discrepant outcomes. In order to understand the reasons for these discrepant outcomes, it is important to consider the determinants of L-carnitine status and how L-carnitine status is regulated in the animal's body. While it is a long-known fact that L-carnitine is endogenously biosynthesized in certain tissues, it was only recently recognized that critical determinants of L-carnitine status, such as intestinal L-carnitine absorption, tissue L-carnitine uptake, endogenous L-carnitine synthesis and renal L-carnitine reabsorption, are regulated by specific nutrient sensing nuclear receptors. This review aims to give a more in-depth understanding of the basic mechanisms of the regulation of L-carnitine status in monogastrics taking into account the most recent evidence on nutrient sensing nuclear receptors and evaluates the efficacy of L-carnitine as feed additive in monogastric livestock by providing an up-to-date overview about studies with L-carnitine supplementation in pigs and poultry.

SCOPE Sustainable protein sources are needed to meet the increasing protein demands of a continuously growing world population. This study is focused on the biotechnological production of a protein rich oyster mushroom (Pleurotus sajor-caju; PSC) by valorization of an agricultural side stream and the evaluation of the physiological effects of PSC in a rat model of metabolic syndrome. METHODS AND RESULTS PSC is produced via submerged cultivation in a 150 L bioreactor that utilizes isomaltulose molasses as its sole carbon source, and is further analyzed for its nutritional composition. A feeding trial is performed using Zucker rats which are fed a 5% PSC supplemented diet, for 4 weeks. Biochemical analyses reveal a significant reduction of the liver lipid concentrations and liver inflammation in the PSC fed obese rats in comparison to the obese rats from the control group. Hepatic qPCR analyses, differential transcript profiling, and enzyme activity measurements reveal a number of altered pathways that may be responsible for these anti-steatotic and anti-inflammatory effects of the mushroom. CONCLUSION Bioconversion of a low quality agricultural side stream to an improved protein source is performed by submerged cultured PSC, and the obtained mycelium shows strong anti-steatotic and anti-inflammatory effects.

Scope The hypothesis is tested that insect meal, which has a low methionine content, reduces the hepatic phosphatidylcholine (PC):phosphatidylethanolamine (PE) ratio, which is a critical determinant of hepatic lipid synthesis, by decreasing availability of the methionine metabolite S-adenosylmethionine (SAM). Methods and results Obese rats (n = 24) are randomly divided into two groups (Obese Casein and Obese Insect) of 12 rats each. In addition, lean rats (n = 12) are used as control group (LC). Groups LC and OC receive a control diet with casein as protein source, whereas in the OI group, casein is replaced isonitrogenously by insect meal, which is found to be less digestible (-12% units). Plasma and liver concentrations of lipids and hepatic expression of lipid synthesizing genes are reduced in the OI group compared to the OC group. Plasma and liver concentration of PC and the PC:PE ratio are decreased in the OI group compared to the OC group, while hepatic concentration of SAM and the hepatic SAM:S-adenosylhomocysteine (SAH) ratio is lower in the OI group than in the OC group. Conclusion The decrease of the hepatic PC:PE ratio is probably a key mechanism explaining the pronounced antisteatotic and hypolipidemic action of insect meal in obese rats.

Summary In pigs and other monogastric animal, the weaning phase is commonly accompanied by an increased susceptibility to gut disorders such as diarrhoea owing to the induction of an inflammatory process in the intestine during weaning. Given the unfavourable effects of intestinal inflammation on feed consumption, digestive capacity of the intestine and growth of animals, controlling intestinal inflammation is a reasonable approach for the maintenance of performance characteristics of livestock animals. Therefore, this study aimed to study the anti-inflammatory potential of a commercial polyphenol-rich grape seed (GS) and grape marc (GM) meal-based feed additive in a well-established in vitro intestinal epithelium model (polarized Caco-2 cells). The anti-inflammatory potential was evaluated by studying the effect of an ethanolic extract obtained from the GS and GM meal-based feed additive (GSGME) on the pro-inflammatory transcription factor NF-κB, which is considered to play a key role in the induction of weaning-associated intestinal inflammation. The highest non-cytotoxic concentrations of the ethanolic GSGME dose dependently reduced TNFα-induced NF-κB transactivation and decreased TNFα-induced mRNA levels of the NF-κB target genes IL-1β, IL-8, MCP-1 and CXCL1 in Caco-2 intestinal cells (p

Scope: Metabolic stress induced by chronic high-fat (HF) diet feeding or genetically induced diabetes impairs carnitine status. Herein, we tested the hypothesis that regular endurance exercise (EE) improves the HF diet-induced impairment of carnitine status through stimulating the expression of hepatic genes involved in carnitine synthesis and uptake. Methods and results: Eighteen male C57BL/6 mice were assigned to three groups: group S received a standard diet, group HF received a HF diet, and group HF1EE received an HF diet and was regularly exercised on a treadmill. After 10wk, mice of the HF and the HF1EE groups were highly obese and insulin resistant compared with mice of the S group (po0.05), but mice of the HF1EE group were less insulin resistant than those of the HF group (po0.05). The HF group had lower carnitine concentrations and mRNA and protein levels of genes involved in carnitine synthesis and uptake in the liver than the S group (po0.05), whereas these parameters did not differ between the S group and the HF1EE group. Conclusion: These findings indicate that regular EE reverses an HF diet-induced impairment of hepatic carnitine content by stimulating hepatic carnitine synthesis and uptake.

Summary This study was performed to assess the effects of rumen-protected conjugated linoleic acid (CLA) on hepatic lipid metabolism in heifers. In particular, it was of interest whether feeding CLA causes development of fatty liver as observed recently in mice. Thirty-six growing heifers with an initial body weight of 185 kg were allotted to three treatment groups and fed daily 250 g of different rumen-protected fats for 16 weeks: The control group received 250 g of a CLA-free control fat, the CLA100 group received 100 g of a CLA fat containing 2.4% of cis-9, trans-11 CLA and 2.1% of trans-10, cis-12 CLA and 150 g control fat and the CLA250 group received 250 g of the CLA fat. CLA supplementation had no effect on animal performance parameters, liver weight and hepatic triglyceride concentration. Moreover, mRNA expression of hepatic genes involved in lipogenesis, β-oxidation and fatty acid transport was not influenced by dietary CLA. The fatty acid composition of hepatic total lipids, with particular consideration of ratios of fatty acids indicative of Δ9-, Δ6- and Δ5-desaturation, was also less influenced by dietary CLA. In conclusion, the study shows that dietary rumen-protected CLA has less effect on hepatic lipid metabolism in young heifers and does not induce the development of a fatty liver such as in mice.

Although oxidized fats are widely considered to have detrimental effects on human health, a large number of feeding studies with experimental animals have consistently demonstrated that oxidized fats, compared with fresh fats, cause a reduction in the concentrations of triacylglycerols and cholesterol in liver and plasma. The reason for these effects became clear when recently it was shown that thermo-oxidized fats contain characteristic substances such as hydroxylated fatty acids and cyclic fatty acid monomers which are potent ligands and activators of peroxisome proliferator-activated receptor α - a transcription factor controlling genes involved in fatty acid and lipoprotein metabolism. In addition, oxidized fats have also been reported to inhibit expression of genes involved in fatty acid synthesis and cholesterol homeostasis. These effects are mediated by inhibiting the maturation of sterol regulatory-element binding proteins, which are transcription factors regulating genes involved in fatty acid synthesis and cholesterol homeostasis. This review summarizes the phenotypical alterations of lipid metabolism observed in feeding studies dealing with oxidized fats and addresses the molecular mechanisms underlying these lipid metabolism alterations, in particular the lipid lowering effects of dietary oxidized fats.

Scope: Carnitine improves protein accretion, muscle mass, and protein:fat accretion in piglets. The underlying mechanisms, however, are largely unknown. Methods and results: To gain insight into mechanisms through which carnitine exerts these effects, we fed piglets either a control or a carnitine-supplemented diet, and analyzed the transcriptome in skeletal muscle. Carnitine concentrations in plasma and muscle were about four-fold higher in the carnitine group when compared to the control group. Transcript profiling revealed 211 genes to be differentially expressed in muscle by carnitine supplementation. The identified genes were mainly involved in molecular processes such as cytoskeletal protein binding, insulin-like growth factor (IGF) binding, transcription factor activity, and insulin receptor binding. Identified genes with the molecular function transcription factor activity encoded primarily transcription factors, most of which were down-regulated by carnitine, including pro-apoptotic transcription factors such as proto-oncogene c-fos, proto-oncogene c-jun and activating transcription factor 3. Furthermore, atrophy-related genes such as atrogin-1, MuRF1, and DRE1 were significantly down-regulated by carnitine. IGF signalling and insulin signalling were identified as significantly up-regulated regulatory pathways in the carnitine group. Conclusion: Carnitine may have beneficial effects on skeletal muscle mass through stimulating the anabolic IGF-1 pathway and suppressing pro-apoptotic and atrophy-related genes, which are involved in apoptosis of muscle fibers and proteolysis of muscle proteins, respectively.

Conjugated linoleic acids (CLAs) are biologically highly active lipid compounds that have attracted great scientific interest due to their ability to cause either inhibition of atherosclerotic plaque development or even regression of pre-established atherosclerotic plaques in mice, hamsters and rabbits. The underlying mechanisms of action, however, are only poorly understood. Since cell culture experiments are appropriate to gain insight into the mechanisms of action of a compound, the present review summarizes data from cell culture studies about the metabolism and the actions of CLAs on atherosclerosis-related events in endothelial cells (ECs) and smooth muscle cells (SMCs), which are important cells contributing to atherosclerotic lesion development. Based on these studies, it can be concluded that CLAs exert several beneficial actions including inhibition of inflammatory and vasoactive mediator release from ECs and SMCs, which may help explain the anti-atherogenic effect of CLAs observed in vivo. The observation that significant levels of CLA metabolites, which have been reported to have significant biological activities, are well detectable in ECs and SMCs indicates that the anti-atherogenic effects observed with CLAs are presumably mediated not only by CLAs themselves but also by their metabolites.

Two experiments with rats were carried out to investigate the effect of dietary fish oil and oxidized cholesterol on the concentration of 7β-hydroxycholesterol, an oxysterol of mainly nonenzymatic origin, in liver, plasma, low density lipoproteins and erythrocytes of rats at different vitamin E supply. In Experiment 1, four groups of rats received diets with coconut oil or salmon oil (100 g/kg diet) and vitamin E concentrations of 40 or 240 mg α-tocopherol equivalents/kg. In Experiment 2, eight groups of rats received diets supplemented with pure or oxidized cholesterol (5 g/kg), coconut oil or salmon oil (100 g/kg diet) and vitamin E concentrations of 40 or 240 mg α-tocopherol equivalents/ kg. Rats fed the salmon oil diets had significantly higher concentrations of 7β-hydroxycholesterol in liver, plasma, low density lipoproteins and erythrocytes than rats fed coconut oil diets. Rats fed the diets supplemented with oxidized cholesterol had significantly higher concentrations of 7β-hydroxycholesterol in all the samples analyzed than rats fed pure cholesterol. Increasing the dietary vitamin E concentration from 40 to 240 mg α-tocopherol equivalents/kg diet reduced the concentration of 7β-hydroxycholesterol in plasma; the concentrations of 7β-hydroxycholesterol in liver, low density lipoproteins and erythrocytes were not influenced by the dietary vitamin E concentration. The study suggests that diets with fish oil or oxidized cholesterol are critical with respect to the formation of 7β-hydroxycholesterol.

Summary Fibroblast growth factor 21 (FGF21) has been identified as a novel hormonal factor involved in the regulation of metabolic adaptations during energy deprivation. The present study aimed to investigate the expression of the FGF21 gene in the liver of dairy cows during the transition from pregnancy to lactation. Therefore, the relative mRNA abundance of FGF21 in liver biopsy samples of 20 dairy cows in late pregnancy (3 weeks pre-partum) and early lactation (1, 5, 14 weeks post-partum) was determined. It was observed that hepatic mRNA abundance of FGF21 at 1 week post-partum was dramatically increased (110-fold) compared to 3 weeks pre-partum (p