Search

Carotenoid dietary intake and their endogenous levels have been associated with a decreased risk of several chronic diseases. There are indications that carotenoid bioavailability depends, in addition to the food matrix, on host factors. These include diseases (e.g. colitis), life-style habits (e.g. smoking), gender and age, as well as genetic variations including single nucleotide polymorphisms that govern carotenoid metabolism. These are expected to explain interindividual differences that contribute to carotenoid uptake, distribution, metabolism and excretion, and therefore possibly also their association with disease risk. For instance, digestion enzymes fostering micellization (PNLIP, CES), expression of uptake/efflux transporters (SR-BI, CD36, NPC1L1), cleavage enzymes (BCO1/2), intracellular transporters (FABP2), secretion into chylomicrons (APOB, MTTP), carotenoid metabolism in the blood and liver (LPL, APO C/E, LDLR), and distribution to target tissues such as adipose tissue or macula (GSTP1, StARD3) depend on the activity of these proteins. In addition, human microbiota, e.g. via altering bile-acid concentrations, may play a role in carotenoid bioavailability. In order to comprehend individual, variable responses to these compounds, an improved knowledge on intra-/interindividual factors determining carotenoid bioavailability, including tissue distribution, is required. Here, we highlight the current knowledge on factors that may explain such intra-/interindividual differences., (© 2017 The Authors. Molecular Nutrition & Food Research published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Scope: The aim of this study was to compare if lycopene also possesses pro-vitamin A (VA) activity comparable to known VA derivatives., Materials and Methods: We used a transgenic retinoic acid response element reporter mouse model (n = 8, per group) for this study, and after the initial wash out of VA using a vitamin A deficient diet (VAD) for 18 weeks, the animals were supplemented further with (a) VAD-fed mice, (b) VAD-fed mice plus retinol (20 mg/kg bw), (c) VAD-fed mice plus β-carotene (40 mg/kg bw), and (d) VAD-fed mice plus lycopene (40 mg/kg bw). Using ex vivo scanning and gene expression analysis of retinoid target and VA marker gene analysis in various organs of these supplemented mice (b, c, d), we found increased luciferase activity and normalized marker and target gene analysis compared to group a., Conclusions: Lycopene can restore VA deficiency and compensate VA for retinoic acid receptor (RAR)-mediated signaling as the major function of VA in the mammalian organism. Lycopene administration can initiate upregulation of RAR-mediated signaling in various organs in VAD-fed animals via potential novel bioactive lycopene metabolites. This indicates that lycopene possesses partial pro-VA activity in mice transmitted via RAR-mediated signaling., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Adiponectin is an adipokine mainly secreted by adipocytes that presents antidiabetic, anti-inflammatory, and antiatherogenic functions. Therefore, modulation of adiponectin expression represents a promising target for prevention or treatment of several diseases including insulin resistance and type II diabetes. Pharmacological agents such as the nuclear hormone receptor synthetic agonists like peroxisome proliferator activated receptor γ agonists are of particular interest in therapeutic strategies due to their ability to increase the plasma adiponectin concentration. Nutritional approaches are also of particular interest, especially in primary prevention, since some active compounds of our diet (notably vitamins, carotenoids, or other essential nutrients) are direct or indirect lipid-activators of nuclear hormone receptors and are modifiers of adiponectin expression and secretion. The aim of the present review is to summarize current knowledge about the nutritional regulation of adiponectin by derivatives of active compounds naturally present in the diet acting as indirect or direct activators of nuclear hormone receptors., (© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Dietary consumption of tomato products and especially the red tomato pigment lycopene has been associated with lower risk of cancer. New evidence is emerging toward metabolic pathways mediating the anti-cancer activities of lycopene. In this review, we explore associations between tomatoes and lycopene intake and cancer and relate this to the metabolic activation pathways of lycopene via carotene oxygenases and further carotenoid/retinoid-metabolizing enzymes to apo-lycopenoids. Several of these apo-lycopenoids have already been identified but up to date no direct connection between lycopene metabolism and apo-lycopenoids mediated receptor activation pathways has been established. Retinoic acid receptors/retinoid-X receptors activation pathways in particular, may be mediated via lycopene metabolites that are related to retinoic acids. Various studies have shown an association between lower concentration of insulin-like growth factor-1 upon lycopene treatment, cancer incidences, and retinoid-mediated signaling. In this review, we interrelate tomato/lycopene ingestion and cancer incidence, with metabolic activation of lycopene and retinoid-mediated signaling. The aim is to discuss a potential mechanism to explain lycopene related anti-cancer activities by modulation of insulin-like growth factor-1 concentrations via lycopene metabolite activation of retinoid-mediated signaling., (© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Scope: Lycopene is a lipophilic carotenoid and provides the red colour to tomatoes and tomato product. Various studies indicated that lycopene and tomatoes/tomato products are able to positively influence various diseases associated with a chronic inflammation. The mechanism of action of lycopene to elicit these effects is partly unknown. A possible mechanism is that biological metabolites of lycopene may activate nuclear hormone receptors in mammalian cells. The aim of this study was to investigate the potential of orally administered lycopene and all-trans retinoic acid (ATRA) for the induction of the retinoic acid receptor (RAR) in a transgenic retinoic acid response-element (RARE)-reporter mouse system., Methods and Results: Orally administered lycopene (100 mg/kg bw in beadlets, n = 6) and ATRA as an endogenous RAR ligand (50 mg/kg bw, n = 6) for the induction of the retinoic acid receptor in male mice using a transgenic RARE-reporter mouse system., Conclusion: Lycopene treatments induced RARE-mediated cell signalling indicated by quantified bioimaging, increased luciferase activity and up-regulated the retinoid target genes in selected organs of the mice. We conclude that lycopene can induce RAR-transcriptional activation in mice and lycopene might be a precursor of still non-identified biologically active metabolites., (© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Vitamin A (VA) and its derivatives, the retinoids, are important factors for the development of the immune system. It has been shown in adult animals that proliferation of lymphocyte populations and antibody secretion are retinoid dependent, while little is known about the effects of retinoids during postnatal development. The aim of this study was to investigate the role of VA on allergic sensitisation during lactation and after weaning using an in vivo system for postnatal allergic sensitisation in mice. Different VA diets (basal/VA elimination/VA (as retinyl palmitate) supplemented) were fed to the dams throughout lactation and directly to the pups after weaning. Allergic sensitisation was induced with a single peritoneal ovalbumin (OVA) injection at day 28 after weaning. The phenotype of lymphocytes was analysed by flow cytometry and functional data were obtained by analysis of (IL-4/IFN-gamma) cytokine production and antibody production (OVA-specific IgG1 and IgE) in the offspring. VA/retinyl palmitate supplementation during lactation and after weaning decreased CD3+, CD4+, CD8+ and B220+ populations in splenic lymphocytes but also significantly enhanced IL-4 production and OVA-specific IgE after sensitisation. In contrast, mice fed VA-elimination diet displayed no significant alteration of lymphocyte numbers and a slightly increased IL-4 production. Our results showed that a single allergen injection during postnatal development induces allergic sensitisation whose degree is modified by the VA content of the maternal diet during lactation and the diet of the pups after weaning, indicating an important role of VA on the severity of the allergic sensitisation.