Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Hypoxia-inducible lipid droplet-associated is not a direct physiological regulator of lipolysis in adipose tissue
Dijk, Wieneke ; Mattijssen, Frits ; La Rosa Rodriguez, Montserrat De; Valdes, Angel Loza ; Loft, Anne ; Mandrup, Susanne ; Kalkhoven, Eric ; Qi, Ling ; Borst, Janwillem ; Kersten, Sander - \ 2017
Endocrinology 158 (2017)5. - ISSN 0013-7227 - p. 1231 - 1251.
Triglycerides are stored in specialized organelles called lipid droplets. Numerous proteins have been shown to be physically associated with lipid droplets and govern their function. Previously, the protein hypoxia-inducible lipid droplet-associated (HILPDA) was localized to lipid droplets and was suggested to inhibit triglyceride lipolysis in hepatocytes. We confirm the partial localization of HILPDA to lipid droplets and show that HILPDA is highly abundant in adipose tissue, where its expression is controlled by the peroxisome proliferator-activated receptor γ and by β-adrenergic stimulation. Levels of HILPDA markedly increased during 3T3-L1 adipocyte differentiation. Nevertheless, silencing of Hilpda using small interfering RNA or overexpression of Hilpda using adenovirus did not show a clear impact on 3T3-L1 adipogenesis. Following β-adrenergic stimulation, the silencing of Hilpda in adipocytes did not significantly alter the release of nonesterified fatty acids (NEFA) and glycerol. By contrast, adenoviral-mediated overexpression of Hilpda modestly attenuated the release of NEFA from adipocytes following β-adrenergic stimulation. In mice, adipocyte-specific inactivation of Hilpda had no effect on plasma levels of NEFA and glycerol after fasting, cold exposure, or pharmacological b-adrenergic stimulation. In addition, other relevant metabolic parameters were unchanged by adipocyte-specific inactivation of Hilpda. Taken together, we find that HILPDA is highly abundant in adipose tissue, where its levels are induced by peroxisome proliferator-activated receptor γ and β-adrenergic stimulation. In contrast to the reported inhibition of lipolysis by HILPDA in hepatocytes, our data do not support an important direct role of HILPDA in the regulation of lipolysis in adipocytes in vivo and in vitro.
Muscle-specific inflammation induced by MCP-1 overexpression does not affect whole-body insulin sensitivity in mice
Evers-van Gogh, Inkie J.A. ; Oteng, Antwi Boasiako ; Alex, Sheril ; Hamers, Nicole ; Catoire, Milene ; Stienstra, Rinke ; Kalkhoven, Eric ; Kersten, Sander - \ 2016
Diabetologia 59 (2016)3. - ISSN 0012-186X - p. 624 - 633.
Inflammation - Insulin resistance - MCP-1 - Muscle-specific - Myokine - Obesity - Type 2 diabetes

Aims/hypothesis: Obesity is associated with a state of chronic low-grade inflammation that is believed to contribute to the development of skeletal muscle insulin resistance. However, the extent to which local and systemic elevation of cytokines, such as monocyte chemoattractant protein 1 (MCP-1), interferes with the action of insulin and promotes insulin resistance and glucose intolerance in muscle remains unclear. Here, we aim to investigate the effect of muscle-specific overexpression of MCP-1 on insulin sensitivity and glucose tolerance in lean and obese mice. Methods: We used Mck–Mcp-1 transgenic (Tg) mice characterised by muscle-specific overexpression of Mcp-1 (also known as Ccl2) and elevated plasma MCP-1 levels. Mice were fed either chow or high-fat diet for 10 weeks. Numerous metabolic variables were measured, including glucose and insulin tolerance tests, muscle insulin signalling and plasma NEFA, triacylglycerol, cholesterol, glucose and insulin. Results: Despite clearly promoting skeletal muscle inflammation, muscle-specific overexpression of Mcp-1 did not influence glucose tolerance or insulin sensitivity in either lean chow-fed or diet-induced obese mice. In addition, plasma NEFA, triacylglycerol, cholesterol, glucose and insulin were not affected by MCP-1 overexpression. Finally, in vivo insulin-induced Akt phosphorylation in skeletal muscle did not differ between Mcp-1-Tg and wild-type mice. Conclusions/interpretation: We show that increased MCP-1 production in skeletal muscle and concomitant elevated MCP-1 levels in plasma promote inflammation in skeletal muscle but do not influence insulin signalling and have no effect on insulin resistance and glucose tolerance in lean and obese mice. Overall, our data argue against MCP-1 promoting insulin resistance in skeletal muscle and raise questions about the impact of inflammation on insulin sensitivity in muscle.

Electric pulse stimulation of myotubes as an in vitro exercise model : Cell-mediated and non-cell-mediated effects
Evers-Van Gogh, Inkie J.A. ; Alex, Sheril ; Stienstra, Rinke ; Brenkman, Arjan B. ; Kersten, Sander ; Kalkhoven, Eric - \ 2015
Scientific Reports 5 (2015). - ISSN 2045-2322 - 11 p.

Regular exercise has emerged as one of the best therapeutic strategies to prevent and treat type-2-diabetes. Exercise-induced changes in the muscle secretome, consisting of myokines and metabolites, may underlie the inter-organ communication between muscle and other organs. To investigate this crosstalk, we developed an in vitro system in which mouse C2C12 myotubes underwent electric pulse stimulation (EPS) to induce contraction. Subsequently the effects of EPS-conditioned media (EPS-CM) on hepatocytes were investigated. Here, we demonstrate that EPS-CM induces Metallothionein 1/2 and Slc30a2 gene expression and reduces Cyp2a3 gene expression in rat hepatocytes. When testing EPS-CM that was generated in the absence of C2C12 myotubes (non-cell EPS-CM) no decrease in Cyp2a3 expression was detected. However, similar inductions in hepatic Mt1/2 and Slc30a2 expression were observed. Non-cell EPS-CM were also applied to C2C12 myotubes and compared to C2C12 myotubes that underwent EPS: here changes in AMPK phosphorylation and myokine secretion largely depended on EPS-induced contraction. Taken together, these findings indicate that EPS can alter C2C12 myotube function and thereby affect gene expression in cells subjected to EPS-CM (Cyp2a3). However, EPS can also generate non-cell-mediated changes in cell culture media, which can affect gene expression in cells subjected to EPS-CM too. While EPS clearly represents a valuable tool in exercise research, care should be taken in experimental design to control for non-cell-mediated effects.

Identification of the human exercise-induced myokines using secretome analysis
Catoire, M. ; Mensink, M.R. ; Kalkhoven, E. ; Schrauwen, P. ; Kersten, A.H. - \ 2014
Physiological genomics 46 (2014)2014. - ISSN 1094-8341 - p. 256 - 267.
human skeletal-muscle - kappa-b activity - plasma interleukin-6 - insulin-resistance - endocrine organ - macrophages - expression - release - cells - mice
Endurance exercise is associated with significant improvements in cardio-metabolic risk parameters. A role for myokines has been hypothesized, yet limited information is available about myokines induced by acute endurance exercise in humans. Therefore, the aim of the study was to identify novel exercise-induced myokines in humans. To this end, we carried out a 1 h one-legged acute endurance exercise intervention in 12 male subjects and a 12 wk exercise training intervention in 18 male subjects. Muscle biopsies were taken before and after acute exercise or exercise training and were subjected to microarray-based analysis of secreted proteins (secretome). For acute exercise, secretome analysis resulted in a list of 86 putative myokines, which was reduced to 29 by applying a fold-change cut-off of 1.5. Based on that shortlist, a selection of putative myokines was measured in the plasma by ELISA or multiplex assay. From that selection, CX3CL1 (fractalkine) and CCL2 (MCP-1) increased at both mRNA and plasma levels. From the known myokines, only IL-6 and FGF 21 changed at the mRNA level, whereas none of the known myokines changed at the plasma level. Secretome analysis of exercise training intervention resulted in a list of 69 putative myokines. Comparing putative myokines altered by acute exercise and exercise training revealed a limited overlap of only 13 genes. In conclusion, this study identified CX3CL1 and CCL2 as myokines that were induced by acute exercise at the gene expression and plasma level and that may be involved in communication between skeletal muscle and other organs.
Short-chain fatty acids stimulate angiopoietin-like 4 synthesis in human colonocytes by selective PPARγ modulation
Alex, Sheril ; Lange, Katja ; Amolo, Tom ; Grinstead, Jeffrey S. ; Szalowska, Ewa ; Koppen, Arjen ; Mudde, Karin ; Haenen, Danielle ; Al-Lahham, S. ; Roelofsen, Han ; Houtman, René ; Burg, Bart van den; Bonvin, Alexandre M. ; Kalkhoven, Eric ; Muller, Michael ; Hooiveld, Guido ; Kersten, Sander - \ 2013
Homo sapiens - GSE40706 - PRJNA174693
Angiopoietin-like protein 4 (ANGPTL4, also referred to as Fiaf) has been proposed as a circulating mediator between the gut microbiota and fat storage in adipose tissue. Very little is known about the mechanisms of regulation of ANGPTL4 in the colon. Here we show that transcription and subsequent secretion of ANGPTL4 in human T84 and HT-29 colonocytes is highly induced by physiological concentrations of products of bacterial fermentation, the short-chain fatty acids. Short-chain fatty acids induce ANGPTL4 by activating the nuclear receptor PPARγ, as shown by microarray, transactivation assays, coactivator peptide recruitment assay, and use of PPARγ antagonist. At concentrations required for PPARγ activation and ANGPTL4 induction in colonocytes, SCFA do not stimulate PPARγ in mouse 3T3-L1 and human SGBS adipocytes, suggesting that SCFA act as selective PPARγ modulators (SPPARM), which is supported by coactivator peptide recruitment assay and structural modelling. It can be concluded that 1) SCFA potently stimulate ANGPTL4 synthesis in human colonocytes, and 2) SCFA transactivate and bind to PPARγ by serving as selective PPAR modulators. Our data point to activation of PPARγ as a novel mechanism of gene regulation by SCFA in the colon.
Short chain fatty acids stimulate Angiopoietin-like 4 synthesis in human colon adenocarcinoma cells by activating PPARy
Alex, S. ; Lange, K. ; Amolo, T. ; Grinstead, J.S. ; Haakonsson, A.K. ; Szalowska, E. ; Koppen, A. ; Mudde, C.M. ; Haenen, D. ; Al-Lahham, S. ; Roelofsen, H. ; Houtman, R. ; Burg, B. van der; Mandrup, S. ; Bonvin, A.M.J.J. ; Kalkhoven, E. ; Muller, M.R. ; Hooiveld, G.J.E.J. ; Kersten, A.H. - \ 2013
Molecular and Cellular Biology 33 (2013)7. - ISSN 0270-7306 - p. 1303 - 1316.
inflammatory-bowel-disease - ppar-gamma - transcriptional activity - lipoprotein-lipase - skeletal-muscle - gut microbiota - target gene - expression - protein-4 - butyrate
Angiopoietin-like protein 4 (ANGPTL4/FIAF) has been proposed as a circulating mediator between the gut microbiota and fat storage. Here, we show that transcription and secretion of ANGPTL4 in human T84 and HT29 colon adenocarcinoma cells is highly induced by physiological concentrations of short-chain fatty acids (SCFA). SCFA induce ANGPTL4 by activating the nuclear receptor peroxisome proliferator activated receptor ¿ (PPAR¿), as demonstrated using PPAR¿ antagonist, PPAR¿ knockdown, and transactivation assays, which show activation of PPAR¿ but not PPARa and PPARd by SCFA. At concentrations required for PPAR¿ activation and ANGPTL4 induction in colon adenocarcinoma cells, SCFA do not stimulate PPAR¿ in mouse 3T3-L1 and human SGBS adipocytes, suggesting that SCFA act as selective PPAR¿ modulators (SPPARM), which is supported by coactivator peptide recruitment assay and structural modeling. Consistent with the notion that fermentation leads to PPAR activation in vivo, feeding mice a diet rich in inulin induced PPAR target genes and pathways in the colon. We conclude that (i) SCFA potently stimulate ANGPTL4 synthesis in human colon adenocarcinoma cells and (ii) SCFA transactivate and bind to PPAR¿. Our data point to activation of PPARs as a novel mechanism of gene regulation by SCFA in the colon, in addition to other mechanisms of action of SCFA.
CD1d-restricted NKT cell function prevents insulin resistance in lean mice, and is regulated by adipocytes and is regulated by adipocytes
Schipper, Henk S. ; Rakhshandehroo, Maryam ; Graaf, Stan F. van de; Venken, Koen ; Koppen, Arjen ; Stienstra, Rinke ; Prop, Serge ; Meerding, Jenny ; Hamers, Nicole ; Besra, Gurdyal ; Boon, Louis ; Nieuwenhuis, Edward E. ; Elewaut, Dirk ; Prakken, Berent ; Kersten, Sander ; Boes, Marianne ; Kalkhoven, Eric - \ 2012
Mus musculus - GSE39534 - PRJNA171064
Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell–deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue–resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue–resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance.
Quantitative Profiling of Oxylipins through Comprehensive LC-MS/MS Analysis: Application in cardiac surgery
Strassburg, K. ; Huijbrechts, A.M.L. ; Kortekaas, K. ; Lindeman, J. ; Pedersen, T.L. ; Newman, J.W. ; Dane, A. ; Berger, R. ; Brenkman, A. ; Hankemeier, T. ; Duynhoven, J.P.M. van; Kalkhoven, E. ; Vreeken, R. - \ 2012
Analytical and Bioanalytical Chemistry 404 (2012)5. - ISSN 1618-2642 - p. 1413 - 1426.
tandem mass-spectrometry - soluble epoxide hydrolase - arachidonic-acid - human plasma - lipidomic analysis - fatty-acids - in-vivo - dihydroxyeicosatrienoic acids - hydroxyeicosatetraenoic acids - simultaneous quantification
Oxylipins, including eicosanoids, affect a broad range of biological processes, such as the initiation and resolution of inflammation. These compounds, also referred to as lipid mediators, are (non-) enzymatically generated by oxidation of polyunsaturated fatty acids such as arachidonic acid (AA). A plethora of lipid mediators exist which makes the development of generic analytical methods challenging. Here we developed a robust and sensitive targeted analysis platform for oxylipins and applied it in a biological setting, using high performance liquid chromatography coupled to tandem mass spectrometry (HPLC-MS/MS) operated in dynamic multiple reaction monitoring (dMRM). Besides the well-described AA metabolites, oxylipins derived from linoleic acid, dihomo-¿-linolenic acid, a-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid were included. Our comprehensive platform allows the quantitative evaluation of approximately 100 oxylipins down to low nanomolar levels. Applicability of the analytical platform was demonstrated by analyzing plasma samples of patients undergoing cardiac surgery. Altered levels of some of the oxylipins, especially in certain monohydroxy fatty acids such as 12-HETE and 12-HEPE, were observed in samples collected before and 24 h after cardiac surgery. These findings indicate that this generic oxylipin profiling platform can be applied broadly to study these highly bioactive compounds in relation to human disease.
Natural killer T cells in adipose tissue prevent insulin resistance
Schipper, H.S. ; Rakhshandehroo, M. ; Graaf, S.F.J. van de; Venken, K. ; Koppen, A. ; Stienstra, R. ; Prop, S. ; Meerding, J. ; Hamers, N. ; Besra, G.S. ; Boon, L. den; Nieuwenhuis, E.E.S. ; Elewaut, D. ; Prakken, B. ; Kersten, A.H. ; Boes, M. ; Kalkhoven, E. - \ 2012
The Journal of Clinical Investigation 122 (2012)9. - ISSN 0021-9738 - p. 3343 - 3354.
invariant nkt cells - alternatively activated macrophages - nonobese diabetic mice - hepatic steatosis - metabolic syndrome - innate immunity - obese mice - inflammation - fat - disease
Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance
Peroxisome Proliferator-activated Receptor gamma Regulates Expression of the Anti-lipolytic G-protein-coupled Receptor 81 (GPR81/Gpr81)
Jeninga, E.H. ; Bugge, A. ; Nielsen, R. ; Kersten, A.H. ; Hamers, N. ; Dani, C. ; Wabitsch, M. ; Berger, R. ; Stunnenberg, H.G. ; Mandrup, S. ; Kalkhoven, E. - \ 2009
Journal of Biological Chemistry 284 (2009)39. - ISSN 0021-9258 - p. 26385 - 26393.
nicotinic-acid receptor - type-2 diabetes-mellitus - mature 3t3-l1 adipocytes - necrosis-factor-alpha - human adipose-tissue - free fatty-acids - ppar-gamma - puma-g - insulin-resistance - molecular-identification
The ligand-inducible nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR gamma) plays a key role in the differentiation, maintenance, and function of adipocytes and is the molecular target for the insulin-sensitizing thiazoledinediones (TZDs). Although a number of PPAR gamma target genes that may contribute to the reduction of circulating free fatty acids after TZD treatment have been identified, the relevant PPAR gamma target genes that may exert the anti-lipolytic effect of TZDs are unknown. Here we identified the anti-lipolytic human G-protein-coupled receptor 81 (GPR81), GPR109A, and the (human-specific) GPR109B genes as well as the mouse Gpr81 and Gpr109A genes as novel TZD-induced genes in mature adipocytes. GPR81/Gpr81 is a direct PPAR gamma target gene, because mRNA expression of GPR81/Gpr81 (and GPR109A/Gpr109A) increased in mature human and murine adipocytes as well as in vivo in epididymal fat pads of mice upon rosiglitazone stimulation, whereas small interfering RNA-mediated knockdown of PPAR gamma in differentiated 3T3-L1 adipocytes showed a significant decrease in Gpr81 protein expression. In addition, chromatin immunoprecipitation sequencing analysis in differentiated 3T3-L1 cells revealed a conserved PPAR: retinoid X receptor-binding site in the proximal promoter of the Gpr81 gene, which was proven to be functional by electromobility shift assay and reporter assays. Importantly, small interfering RNA-mediated knockdown of Gpr81 partly reversed the inhibitory effect of TZDs on lipolysis in 3T3-L1 adipocytes. The coordinated PPAR gamma-mediated regulation of the GPR81/Gpr81 and GPR109A/Gpr109A genes (and GPR109B in humans) presents a novel mechanism by which TZDs may reduce circulating free fatty acid levels and perhaps ameliorate insulin resistance in obese patients.
Peroxisome Proliferator-Activated Receptor ß/ (PPARß/) but Not PPAR Serves as a Plasma Free Fatty Acid Sensor in Liver
Sanderson, L. ; Degerhardt, T. ; Desvergne, B. ; Koppen, A. ; Kalkhoven, E. ; Müller, M.R. ; Kersten, A.H. - \ 2009
Molecular and Cellular Biology 29 (2009)23. - ISSN 0270-7306 - p. 6257 - 6267.
element-binding protein-1 - hepatic lipid-metabolism - gene-expression - target genes - transcription factor - hypolipidemic drugs - coactivator pgc-1 - fasting response - lipogenic genes - gamma
Peroxisome proliferator-activated receptor alpha (PPAR alpha) is an important transcription factor in liver that can be activated physiologically by fasting or pharmacologically by using high-affinity synthetic agonists. Here we initially set out to elucidate the similarities in gene induction between Wy14643 and fasting. Numerous genes were commonly regulated in liver between the two treatments, including many classical PPAR alpha target genes, such as Aldh3a2 and Cpt2. Remarkably, several genes induced by Wy14643 were upregulated by fasting independently of PPAR alpha, including Lpin2 and St3gal5, suggesting involvement of another transcription factor. Using chromatin immunoprecipitation, Lpin2 and St3gal5 were shown to be direct targets of PPAR beta/delta during fasting, whereas Aldh3a2 and Cpt2 were exclusive targets of PPAR alpha. Binding of PPAR beta/delta to the Lpin2 and St3gal5 genes followed the plasma free fatty acid (FFA) concentration, consistent with activation of PPAR beta/delta by plasma FFAs. Subsequent experiments using transgenic and knockout mice for Angptl4, a potent stimulant of adipose tissue lipolysis, confirmed the stimulatory effect of plasma FFAs on Lpin2 and St3gal5 expression levels via PPAR beta/delta. In contrast, the data did not support activation of PPAR alpha by plasma FFAs. The results identify Lpin2 and St3gal5 as novel PPAR beta/delta target genes and show that upregulation of gene expression by PPAR beta/delta is sensitive to plasma FFA levels. In contrast, this is not the case for PPAR alpha, revealing a novel mechanism for functional differentiation between PPARs.
Effect of Synthetic Dietary Triglycerides: A Novel Research Paradigm for Nutrigenomics
Sanderson-Kjellberg, L.M. ; Groot, P.J. de; Hooiveld, G.J.E.J. ; Koppen, A. ; Kalkhoven, E. ; Müller, M.R. ; Kersten, A.H. - \ 2008
PLoS One 3 (2008)2. - ISSN 1932-6203
Background The effect of dietary fats on human health and disease are likely mediated by changes in gene expression. Several transcription factors have been shown to respond to fatty acids, including SREBP-1c, NF-¿B, RXRs, LXRs, FXR, HNF4¿, and PPARs. However, it is unclear to what extent these transcription factors play a role in gene regulation by dietary fatty acids in vivo. Methodology/Principal Findings Here, we take advantage of a unique experimental design using synthetic triglycerides composed of one single fatty acid in combination with gene expression profiling to examine the effects of various individual dietary fatty acids on hepatic gene expression in mice. We observed that the number of significantly changed genes and the fold-induction of genes increased with increasing fatty acid chain length and degree of unsaturation. Importantly, almost every single gene regulated by dietary unsaturated fatty acids remained unaltered in mice lacking PPAR¿. In addition, the majority of genes regulated by unsaturated fatty acids, especially docosahexaenoic acid, were also regulated by the specific PPAR¿ agonist WY14643. Excellent agreement was found between the effects of unsaturated fatty acids on mouse liver versus cultured rat hepatoma cells. Interestingly, using Nuclear Receptor PamChip® Arrays, fatty acid- and WY14643-induced interactions between PPAR¿ and coregulators were found to be highly similar, although several PPAR¿-coactivator interactions specific for WY14643 were identified. Conclusions/Significance We conclude that the effects of dietary unsaturated fatty acids on hepatic gene expression are almost entirely mediated by PPAR¿ and mimic those of synthetic PPAR¿ agonists in terms of regulation of target genes and molecular mechanism. Use of synthetic dietary triglycerides may provide a novel paradigm for nutrigenomics research.
Natuur en identiteit; een rapport over 2002: groenblauwe dooradering is belangrijk voor natuur en identiteit in het agrarisch cultuurlandschap
Geertsema, W. ; Griffioen, A. ; Meeuwsen, H.A.M. ; Kalkhoven, J.T.R. - \ 2003
Wageningen : Alterra (Alterra-rapport 712) - 82
landschap - landschapsecologie - kwaliteit - natuurbescherming - biodiversiteit - nederland - cultuurlandschap - agrobiodiversiteit - netwerken - landscape - landscape ecology - quality - nature conservation - biodiversity - netherlands - cultural landscape - agro-biodiversity - networks
De groen-blauwe dooradering bestaat uit het netwerk van halfnatuurlijke landschapselementen in het agrarisch cultuurlandschap. We gaan in op de bijdrage van groen-blauwe dooradering aan de landschappelijke identiteit en de natuurwaarde. Eerst wordt een landschapstypologie beschreven die aan beide aspecten (natuur en identiteit) aandacht geeft. Het blijkt dat veel typen landschapselementen in alle landschapstypen aanwezig zijn, maar dat de hoeveelheden enorm variëren tussen de verschillende landschapstypen. We ontwikkelen een theoretisch kader voor natuurkwaliteit in groen-blauwe dooradering. Uitgangspunt is dat in een landschapselement (bijv. droge grazige stroken, natte ruigten of bomenrijen) in een landschapstype potentieel een groep soorten voorkomt. Factoren die milieu, ruimtelijke kwaliteit en dynamiek beschrijven bepalen welke van de potentiële soorten daadwerkelijk voor kunnen komen.
Fauna
Kalkhoven, J.T.R. - \ 2003
In: Kleine bossen in het landschap; geschiedenis, waarde en beheer. / van Dort, K.W., Grashof-Bokdam, C.J., van Hees, A.F.M., Hommel, P.W.F.M., Kalkhoven, J.T.R., Schelhaas, M.J., Wageningen : Alterra (Alterra-rapport 643) - p. 93 - 112.
fauna - dieren - zoögeografie - habitats - standplaatsfactoren - bossen - nederland - animals - zoogeography - site factors - forests - netherlands
Analyse van voorkomende dieren in het bos, met nadruk op zoogdieren, broedvogels, reptielen, amfibieën, dagvlinders en sprinkhanen
Plaaginsecten op bomen
Moraal, L.G. - \ 2003
In: Natuurcompendium 2003; natuur in cijfers / van Duuren, L., Eggink, G.J., Kalkhoven, J.T.R., Notenboom, J., van Strien, A.J., Wortelboer, R., Bilthoven / Wageningen / Voorburg / Heerlen : MNP / CBS - ISBN 906960101X - p. 230 - 231.
Eikenprocessierups en klimaatverandering
Moraal, L.G. - \ 2003
In: Natuurcompendium 2003; natuur in cijfers / van Duuren, L., Eggink, G.J., Kalkhoven, J.T.R., Notenboom, J., van Strien, A.J., Wortelboer, R., Bilthoven / Wageningen / Voorburg / Heerlen : MNP / CBS - ISBN 906960101X - p. 158 - 158.
Natuurcompendium 2003; natuur in cijfers
Duuren, L. van; Eggink, G.J. ; Kalkhoven, J.T.R. ; Notenboom, J. ; Strien, A.J. van; Wortelboer, R. - \ 2003
Unknown Publisher
biodiversiteit - ecologie - landschap - milieu - natuurbeleid - natuurbescherming - monitoring
Vegetatie
Dort, K.W. van; Hommel, P.W.F.M. - \ 2003
In: Kleine bossen in het landschap; geschiedenis, waarde en beheer. / van Dort, K.W., Grashof-Bokdam, C.J., van Hees, A.F.M., Hommel, P.W.F.M., Kalkhoven, J.T.R., Schelhaas, M.J., Wageningen : Alterra (Alterra-rapport 643) - p. 73 - 92.
habitats - vegetatie - standplaatsfactoren - bossen - vegetation - site factors - forests
Terwijl bossen meestal aangeplant zijn, is de vegetatie eronder meestal spontaan gevestigd (struiken, kruiden, mossen). Er kunnen diverse vegetatietypen onderscheiden worden. Ze zijn afhankelijk van het abiotisch milieu (bodem en water) en het karakter van de boomlaag (loofbos of naaldbos)
Ruimtelijke rangschikking
Grashof-Bokdam, C.J. - \ 2003
In: Kleine bossen in het landschap; geschiedenis, waarde en beheer. / van Dort, K.W., Grashof-Bokdam, C.J., van Hees, A.F.M., Hommel, P.W.F.M., Kalkhoven, J.T.R., Schelhaas, M.J., Wageningen : Alterra (Alterra-rapport 643) - p. 63 - 71.
Regionale variatie
Dort, K.W. van; Hommel, P.W.F.M. - \ 2003
In: Kleine bossen in het landschap; geschiedenis, waarde en beheer. / van Dort, K.W., Grashof-Bokdam, C.J., van Hees, A.F.M., Hommel, P.W.F.M., Kalkhoven, J.T.R., Schelhaas, M.J., Wageningen : Alterra (Alterra-rapport 643) - p. 25 - 61.
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