Publications by authors named "Corinna Brandsch"

62 Publications

Differential effects of vitamin D vs vitamin D on cellular uptake, tissue distribution and activation of vitamin D in mice and cells.

J Steroid Biochem Mol Biol 2020 11 6;204:105768. Epub 2020 Oct 6.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von-Danckelmann-Platz 2, 06120 Halle (Saale), Germany; Competence Cluster for Nutrition and Cardiovascular Health (nutriCARD) Halle-Jena-Leipzig, Germany. Electronic address:

To combat vitamin D deficiency, vitamin D and vitamin D are commonly used as a supplement or to fortify food sources. Human data show that the response of 25-hydroxyvitamin D (25(OH)D) to supplementation with vitamin D is higher than to vitamin D. To elucidate the metabolic route of both vitamers, we conducted a study with vitamin D-depleted mice, which were allotted into three groups (n = 12) and received equal doses of either deuterated vitamin D, deuterated vitamin D or both for 4 weeks. To further investigate the hepatic uptake and hydroxylation of both D-vitamers to 25(OH)D, we conducted cell culture experiments with murine and human hepatoma cells (Hepa1-6 and HepG2). The vitamin D metabolite concentrations in serum, tissues and cells were analyzed by LC-MS/MS or ELISA. In mice, vitamin D resulted in lower serum and tissue concentrations of vitamin D (P < 0.001) than vitamin D, while the group which received both D-vitamers showed values in between. Interestingly, vitamin D fed mice had 1.9-times and 2.9-times higher serum concentrations of total and free 25(OH)D (P < 0.001) than mice fed vitamin D, while the concentration of 1,25-dihydroxyvitamin D (1,25(OH)D) was 1.8-times lower (P < 0.001). The gene and protein expression of enzymes, involved in the hydroxylation and renal uptake of vitamin D remained largely unaffected by the D-vitamer. In contrast to the mice data, hepatoma cells preferred vitamin D for 25-hydroxylation over vitamin D (P < 0.001). In general, the formation of 25(OH)D was much more pronounced in human than in murine hepatoma cells (P < 0.001). To conclude, in contrast to humans, vitamin D was more efficient in increasing 25(OH)D than vitamin D in mice, although this difference was not caused by a preferential hydroxylation of vitamin D in the liver. The metabolic routes of D and D in mice differ, showing lower circulating 1,25(OH)D and tissue vitamin D concentrations in D- than in D-fed mice.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jsbmb.2020.105768DOI Listing
November 2020

Postprandial Metabolic Response to Rapeseed Protein in Healthy Subjects.

Nutrients 2020 Jul 29;12(8). Epub 2020 Jul 29.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, 06120 Halle, Germany.

Plant proteins have become increasingly important for ecological reasons. Rapeseed is a novel source of plant proteins with high biological value, but its metabolic impact in humans is largely unknown. A randomized, controlled intervention study including 20 healthy subjects was conducted in a crossover design. All participants received a test meal without additional protein or with 28 g of rapeseed protein isolate or soy protein isolate (control). Venous blood samples were collected over a 360-min period to analyze metabolites; satiety was assessed using a visual analog scale. Postprandial levels of lipids, urea, and amino acids increased following the intake of both protein isolates. The postprandial insulin response was lower after consumption of the rapeseed protein than after intake of the soy protein ( < 0.05), whereas the postmeal responses of glucose, lipids, interleukin-6, minerals, and urea were comparable between the two protein isolates. Interestingly, the rapeseed protein exerted stronger effects on postprandial satiety than the soy protein ( < 0.05). The postmeal metabolism following rapeseed protein intake is comparable with that of soy protein. The favorable effect of rapeseed protein on postprandial insulin and satiety makes it a valuable plant protein for human nutrition.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/nu12082270DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469072PMC
July 2020

Vitamin D Status of Mice Deficient in Scavenger Receptor Class B Type 1, Cluster Determinant 36 and ATP-Binding Cassette Proteins G5/G8.

Nutrients 2020 Jul 22;12(8). Epub 2020 Jul 22.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von-Danckelmann-Platz 2, 06120 Halle (Saale), Germany.

Classical lipid transporters are suggested to modulate cellular vitamin D uptake. This study investigated the vitamin D levels in serum and tissues of mice deficient in SR-B1 (Srb1), CD36 (Cd36) and ABC-G5/G8 (Abcg5/g8) and compared them with corresponding wild-type (WT) mice. All mice received triple-deuterated vitamin D (vitamin D-d) for six weeks. All knockout mice vs. WT mice showed specific alterations in their vitamin D concentrations. Srb1 mice had higher levels of vitamin D-d in the serum, adipose tissue, kidney and heart, whereas liver levels of vitamin D-d remained unaffected. Additionally, Srb1 mice had lower levels of deuterated 25-hydroxyvitamin D (25(OH)D-d) in the serum, liver and kidney compared to WT mice. In contrast, Cd36 and WT mice did not differ in the serum and tissue levels of vitamin D-d, but Cd36 vs. WT mice were characterized by lower levels of 25(OH)D-d in the serum, liver and kidney. Finally, Abcg5/g8 mice tended to have higher levels of vitamin D-d in the serum and liver. Major alterations in Abcg5/g8 mice were notably higher levels of 25(OH)D-d in the serum and kidney, accompanied by a higher hepatic mRNA abundance of hydroxylase. To conclude, the current data emphasize the significant role of lipid transporters in the uptake, tissue distribution and activation of vitamin D.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/nu12082169DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469065PMC
July 2020

Impact of dietary propionate on fructose-induced changes in lipid metabolism, gut microbiota and short-chain fatty acids in mice.

Int J Food Sci Nutr 2020 Jun 4:1-13. Epub 2020 Jun 4.

Institute of Agricultural and Nutritional Sciences, Martin-Luther-Universität Halle-Wittenberg, Halle, Germany.

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., , , and ). Interestingly, mice fed the F+ diets had higher levels of propionate and butyrate in the circulation than mice fed the F- diets ( < 0.05). Treatment with propionate influenced neither hepatic or plasma lipids nor levels of circulating SCFAs. With the exception of , other bacterial phyla were not affected by propionate.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/09637486.2020.1773415DOI Listing
June 2020

Markers Indicating Body Vitamin D Stores and Responses of Liver and Adipose Tissues to Changes in Vitamin D Intake in Male Mice.

Nutrients 2020 May 13;12(5). Epub 2020 May 13.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von-Danckelmann-Platz 2, 06120 Halle (Saale), Germany.

Circulating 25-hydroxyvitamin D (25(OH)D) is regarded as the most reliable biomarker of vitamin D status. However, limited data exist concerning the suitability of 25(OH)D as an indicator of body vitamin D stores and the ability of adipose tissue to mobilize vitamin D. In the first study, in which male mice received different vitamin D doses for three weeks, we found strong linear response relationships between vitamin D intake and levels of vitamin D in the plasma ( < 0.001), liver ( < 0.001) and adipose tissues ( < 0.001), and strong positive correlations between plasma and tissue stores of vitamin D ( < 0.001). Plasma levels of 25(OH)D and 24,25-dihydroxyvitamin D (24,25(OH)D) showed weak or no correlations with tissue vitamin D stores. Data from a second study demonstrate a strong and rapid response of plasma 25(OH)D in vitamin D-treated mice with a low vitamin D status. Additionally, mice fed a vitamin D-free diet showed a strong and rapid decline in vitamin D in the liver, whereas the decline in different adipose tissues was distinctly lower than that in the liver. To conclude, tissue stores of vitamin D were best reflected by plasma vitamin D. In contrast to the liver, adipose tissues responded less sensitively to an absence of vitamin D intake.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/nu12051391DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284563PMC
May 2020

Intake of ergosterol increases the vitamin D concentrations in serum and liver of mice.

J Steroid Biochem Mol Biol 2019 11 25;194:105435. Epub 2019 Jul 25.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von-Danckelmann-Platz 2, 06120, Halle (Saale), Germany; Competence Cluster for Nutrition and Cardiovascular Health (nutriCARD) Halle-Jena-Leipzig, Germany. Electronic address:

Factors that can modify the bioavailability of orally administered vitamin D are not yet widely known. Ergosterol is a common fungal sterol found in food which has a chemical structure comparable to that of vitamin D. This study aimed to investigate the effect of ergosterol on vitamin D metabolism. Therefore, 36 male wild type-mice were randomly subdivided into three groups (n = 12) and received a diet containing 25 μg vitamin D and either 0 mg (control), 2 mg or 7 mg ergosterol per kg diet for 6 weeks. To elucidate the impact of ergosterol on hepatic hydroxylation of vitamin D, human hepatoma cells (HepG2) were treated with different concentrations of ergosterol. Concentrations of vitamin D and 25-hydroxyvitamin D (25(OH)D) in cells, livers and kidneys of mice and additionally 24,25-dihydroxyvitamin D (24,25(OH)D) in serum were quantified by LC-MS/MS. The concentration of 1,25-dihydroxyvitamin D (1,25(OH)D) in serum was analyzed by commercially-available enzyme immuno assay. The concentrations of cholesterol and triglycerides were analyzed in livers of mice by photometric assays. Analyses revealed that mice receiving 7 mg/kg ergosterol with their diet had 1.3-, 1.7- and 1.5-times higher concentrations of vitamin D in serum, liver and kidney, respectively, than control mice (P < 0.05), whereas no significant effects were observed in mice fed 2 mg/kg ergosterol. The hydroxylation of vitamin D remained unaffected by dietary ergosterol, since the concentration of 25-hydroxyvitamin D in serum and tissues and the concentrations of 1,25(OH)D and 24,25(OH)D in serum were not different between the three groups of mice. The lipid concentrations in liver were also not affected by dietary ergosterol. Data from the cell culture studies showed that ergosterol did not influence the conversion of vitamin D to 25(OH)D. To conclude, ergosterol appears to be a modulator of vitamin D concentrations in the body of mice, without modulating the hydroxylation of vitamin D in liver.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jsbmb.2019.105435DOI Listing
November 2019

Agrimonia procera exerts antimicrobial effects, modulates the expression of defensins and cytokines in colonocytes and increases the immune response in lipopolysaccharide-challenged piglets.

BMC Vet Res 2018 Nov 15;14(1):346. Epub 2018 Nov 15.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von-Danckelmann-Platz 2, 06120, Halle (Saale), Germany.

Background: Because antibiotic use in livestock is assumed to contribute to the emerging public health crisis of antibiotic resistance, alternatives are required. Phytogenic additives are extensively studied due to their antibiotic properties. Components of Agrimonia species have been reported as candidate antimicrobials that possess antioxidative and anti-inflammatory properties. We studied the impact of Agrimonia procera (AP) on the growth of selected strains of gut bacteria, the effect of AP on the mRNA abundance of genes involved in inflammation and bacterial defense in a colon carcinoma cell line, the effect of AP in piglets challenged with lipopolysaccharides, and the effect of AP on the growth performance of healthy piglets.

Results: The in vitro growth rate of different bacteria strains was negatively affected by AP, especially in Pediococcus pentosaceus and all tested E. coli strains. Stimulation of Caco-2 cells with TNFα resulted in elevated mRNA expression of CXCL1, IL-8 and GPX2. After pretreatment of cells with AP, stimulation of Caco-2 cells with TNFα still resulted in elevated mRNA expression of CXCL1 and IL-8 at all measured points in time. However, mRNA expression in AP-pretreated cells was lower after 6 h and 24 h. In addition, expression of DEFB1 and GPX2 was significantly elevated after TNFα stimulation. In vivo, application of lipopolysaccharides induced significantly increased animal body temperatures. Piglets pretreated with AP prior to lipopolysaccharide application showed a faster and larger increase in body temperature than controls. In addition, piglets pretreated with AP appeared to release more TNFα than controls. In healthy piglets, AP treatment had no impact on growth performance parameters. Fecal dry matter and total plasma antioxidant capacity tended to be higher in piglets treated with AP than in control piglets (P = 0.055 and P = 0.087, respectively).

Conclusions: AP has antimicrobial effects in vitro and stimulated the expression of proinflammatory cytokines in Caco-2 cells. The additive had no effect on growth in healthy piglets but increased the immune response in LPS-treated animals. In addition, AP appeared to have antioxidative effects in vivo. Therefore, AP merits testing as a future alternative to antibiotics in animal husbandry.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12917-018-1680-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6238359PMC
November 2018

Vitamin D Does Not Play a Functional Role in Adipose Tissue Development in Rodent Models.

Mol Nutr Food Res 2018 02 12;62(4). Epub 2018 Jan 12.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.

Scope: Several studies have proposed a role of vitamin D in adipogenesis. Here, we sought to study the impact of the vitamin D receptor (Vdr) on adipocyte size in young and old mice and the effect of maternal vitamin D deficiency on fetal adipogenesis.

Methods And Results: Histological analysis of adipose tissues shows that Vdr knockout (KO) mice have smaller adipocytes than wild-type (WT) mice. Next, we compare young and old Vdr-KO and WT mice and find no differences in adipocyte sizes between weaned Vdr-KO and WT mice. However, 1-year-old Vdr-KO mice, suffering from alopecia, have smaller-sized adipocytes than WT mice, although they consume more food. To elucidate whether vitamin D can directly impact adipocyte development at a critical stage of adipogenesis, we feed rat dams a vitamin D deficient (0 IU kg ) or vitamin D adequate (1000 IU kg ) diet. Neither DNA microarray analysis of the adipose tissues of the newborn rats nor the adipocyte sizes of 21-day-old offspring show significant differences between the two groups.

Conclusion: Data indicate that vitamin D does not play a fundamental role in adipogenesis because vitamin D does not affect fetal adipogenesis. Moreover, the smaller adipocytes observed in adult Vdr-KO mice are presumably caused by an increased energy expenditure due to alopecia.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/mnfr.201700726DOI Listing
February 2018

Impact of chocolate liquor on vascular lesions in apoE-knockout mice.

Clin Sci (Lond) 2017 10 12;131(20):2549-2560. Epub 2017 Oct 12.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Germany

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 D, the chocolate liquor-fed mice did not have measurable 25-hydroxyvitamin D in the serum. These mice even showed a 25% reduction in the level of 25-hydroxyvitamin D compared with the control mice. Overall, present data may contribute to our understanding how chocolate constituents can impact vascular lesion development.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1042/CS20170279DOI Listing
October 2017

The High Calcium, High Phosphorus Rescue Diet Is Not Suitable to Prevent Secondary Hyperparathyroidism in Vitamin D Receptor Deficient Mice.

Front Physiol 2017 10;8:212. Epub 2017 Apr 10.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-WittenbergHalle, Germany.

The vitamin D receptor (VDR) knockout (KO) mouse is a common model to unravel novel metabolic functions of vitamin D. It is recommended to feed these mice a high calcium (2%), high phosphorus (1.25%) diet, termed rescue diet (RD) to prevent hypocalcaemia and secondary hyperparathyroidism. First, we characterized the individual response of VDR KO mice to feeding a RD and found that the RD was not capable of normalizing the parathyroid hormone (PTH) concentrations in each VDR KO mouse. In a second study, we aimed to study whether RD with additional 1 and 2% calcium (in total 3 and 4% of the diet) is able to prevent secondary hyperparathyroidism in the VDR KO mice. Wild type (WT) mice and VDR KO mice that received a normal calcium and phosphorus diet (ND) served as controls. Data demonstrated that the RD was no more efficient than the ND in normalizing PTH levels. An excessive dietary calcium concentration of 4% was required to reduce serum PTH concentrations in the VDR KO mice to PTH levels measured in WT mice. This diet, however, resulted in higher concentrations of circulating intact fibroblast growth factor 23 (iFGF23). To conclude, the commonly used RD is not suitable to normalize the serum PTH in VDR KO mice. Extremely high dietary calcium concentrations are necessary to prevent secondary hyperthyroidism in these mice, with the consequence that iFGF23 concentrations are being raised. Considering that PTH and iFGF23 exert numerous VDR independent effects, data obtained from VDR KO mice cannot be attributed solely to vitamin D.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fphys.2017.00212DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5385385PMC
April 2017

Plant Oils as Potential Sources of Vitamin D.

Front Nutr 2016 12;3:29. Epub 2016 Aug 12.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg , Halle (Saale) , Germany.

To combat vitamin D insufficiency in a population, reliable diet sources of vitamin D are required. The recommendations to consume more oily fish and the use of UVB-treated yeast are already applied strategies to address vitamin D insufficiency. This study aimed to elucidate the suitability of plant oils as an alternative vitamin D source. Therefore, plant oils that are commonly used in human nutrition were first analyzed for their content of vitamin D precursors and metabolites. Second, selected oils were exposed to a short-term UVB irradiation to stimulate the synthesis of vitamin D. Finally, to elucidate the efficacy of plant-derived vitamin D to improve the vitamin D status, we fed UVB-exposed wheat germ oil (WGO) for 4 weeks to mice and compared them with mice that received non-exposed or vitamin D3 supplemented WGO. Sterol analysis revealed that the selected plant oils contained high amounts of not only ergosterol but also 7-dehydrocholesterol (7-DHC), with the highest concentrations found in WGO. Exposure to UVB irradiation resulted in a partial conversion of ergosterol and 7-DHC to vitamin D2 and D3 in these oils. Mice fed the UVB-exposed WGO were able to improve their vitamin D status as shown by the rise in the plasma concentration of 25-hydroxyvitamin D [25(OH)D] and the liver content of vitamin D compared with mice fed the non-exposed oil. However, the plasma concentration of 25(OH)D of mice fed the UVB-treated oil did not reach the values observed in the group fed the D3 supplemented oil. It was striking that the intake of the UVB-exposed oil resulted in distinct accumulation of vitamin D2 in the livers of these mice. In conclusion, plant oils, in particular WGO, contain considerable amounts of vitamin D precursors which can be converted to vitamin D via UVB exposure. However, the UVB-exposed WGO was less effective to improve the 25(OH)D plasma concentration than a supplementation with vitamin D3.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fnut.2016.00029DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4981617PMC
August 2016

Vitamin D supplementation does not modify cardiovascular risk profile of adults with inadequate vitamin D status.

Eur J Nutr 2017 Mar 30;56(2):621-634. Epub 2015 Nov 30.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von-Danckelmann-Platz 2, 06120, Halle/Saale, Germany.

Purpose: The Nutrition Societies in Germany, Austria, and Switzerland recommend a daily intake of 20 µg vitamin D for adults when endogenous synthesis is absent. The current study aimed to elucidate whether this vitamin D dose impacts cardiovascular risk markers of adults during the winter months.

Methods: The study was conducted in Halle (Saale), Germany (51 northern latitude) as a placebo-controlled, double-blinded, randomised trial (from January to April). A total of 105 apparently healthy subjects (male and female, 20-71 years old) were included. Subjects were randomly allocated to two groups. One group received a daily 20-µg vitamin D dose (n = 54), and the other group received a placebo (n = 51) for 12 weeks. Outcome measures included blood pressure, heart rate, concentrations of renin, aldosterone, serum lipids and vascular calcification markers, and haematologic variables such as pro-inflammatory monocytes.

Results: Blood pressure and systemic cardiovascular risk markers remained unchanged by vitamin D supplementation, although serum 25-hydroxyvitamin D increased from 38 ± 14 to 73 ± 16 nmol/L at week 12. The placebo and vitamin D groups did not differ in their final cardiovascular risk profile.

Conclusion: Daily supplementation of 20 µg vitamin D during winter is unlikely to change cardiovascular risk profile.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00394-015-1106-8DOI Listing
March 2017

Vitamin D receptor knockout mice exhibit elongated intestinal microvilli and increased ezrin expression.

Nutr Res 2016 Feb 23;36(2):184-92. Epub 2015 Oct 23.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany. Electronic address:

In addition to its principle function as a calcium regulator, vitamin D can affect cell and tissue morphology. The intestine is an important target tissue of vitamin D, as it must ensure the efficient transport of nutrients across the epithelium while excluding the passage of harmful molecules and bacteria into the organism. These functions require a highly organized morphology, which may be modified by vitamin D deficiency. To elucidate the role of vitamin D in gut morphology and barrier function, we compared the enterocyte microstructures, gut permeability, and cytoskeletal and cell junction protein expression in vitamin D receptor (VDR) knockout (KO) and wild-type (WT) mice. We found that the duodenal epithelial cells in the VDR-KO mice had longer microvilli (+19%) than those of the WT mice (P < .05). Interestingly, microvilli elongation in the VDR-KO mice was associated with higher messenger RNA and protein expression of ezrin, which is involved in the regulation of microvillus morphogenesis. Intestinal tight junction width and permeability were assessed by measuring the fluorescein isothiocyanate dextran concentrations in plasma; the concentrations were comparable between the 2 groups of mice. We further observed a decrease in the messenger RNA and protein expression of the calcium-transporting tight junction protein claudin-2 in the VDR-KO mice compared with the WT mice (P < .05). In conclusion, the mice lacking VDR had longer enterocyte microvilli, likely as a result of increased ezrin expression. However, the morphology of the tight junctions and the intestinal permeability for large molecules were not affected.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.nutres.2015.10.005DOI Listing
February 2016

Fish protein increases circulating levels of trimethylamine-N-oxide and accelerates aortic lesion formation in apoE null mice.

Mol Nutr Food Res 2016 Feb 26;60(2):358-68. Epub 2015 Oct 26.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle/Saale, Germany.

Scope: The protective effect of fish consumption on the cardiovascular system has primarily been ascribed to n-3 fatty acids, but data investigating the vascular effects of fish protein consumption are scarce. This study aimed to investigate the vascular impact of fish protein in a mouse model of atherosclerosis.

Methods And Results: Male apoE null mice were fed a Western diet containing 20% fish (turbot) protein, casein, or soy protein, for 16 wk. Morphometric analysis of the aorta revealed that the atherosclerotic plaque area of fish protein fed mice was twofold larger than that in casein- or soy protein-fed mice. The percentage area of calcification deposits in plaques of fish protein fed mice was higher (7.57%) than that in casein-fed (2.86%) or soy protein-fed (3.46%) mice, and fish protein fed mice exhibited higher plaque expression of CD68, CD36, and IL-6 than the other two groups. Fish protein intake was accompanied by increased serum concentrations of trimethylamine-N-oxide (7.03 ± 2.83 μmol/L), as compared with casein (0.92 ± 0.46 μmol/L) and soy protein (1.32 ± 0.54 μmol/L) intake.

Conclusion: The present data indicate adverse effects of fish protein on the vascular system, which could be attributable to the high serum trimethylamine-N-oxide concentrations in these mice.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/mnfr.201500537DOI Listing
February 2016

Decreased NK cell functions in obesity can be reactivated by fat mass reduction.

Obesity (Silver Spring) 2015 Nov 22;23(11):2233-41. Epub 2015 Sep 22.

Department of Anatomy and Cell Biology, Martin Luther University Halle-Wittenberg, Faculty of Medicine, Halle (Saale), Germany.

Objective: Natural killer (NK) cells are the first defense against malignant cells, and their functions are severely impaired in individuals with obesity. However, it is not known whether functions can be re-activated after weight loss. The alterations of NK cell functions after fat mass reduction were investigated.

Methods: Thirty-two healthy adults with obesity were divided into control and experimental groups. Participants of the experimental group performed a 3-month program of exercise training and nutrition. Anthropometric, physiological, and metabolic parameters and plasma adipocytokines were determined. Peripheral blood mononuclear cells were analyzed by means of flow cytometry and Western blot assay for various NK cell-specific functional parameters and leptin signaling components. NK cell-mediated cytotoxicity assay with leptin stimulation was performed.

Results: Male participants significantly decreased their body fat mass (P < 0.05) and increased physical fitness (P < 0.05). Plasma leptin levels were significantly reduced (P < 0.05) and intracellular interferon gamma (IFN-γ) expression in CD56(dim) NK cells was significantly increased (P < 0.001) 3 months after study end. Stimulation of NK-92 cells with different leptin dosages revealed a significant dose-dependent decrease of specific tumor cell lysis.

Conclusions: The present study demonstrates a reactivation of NK cell functionality after body fat mass reduction in persons with obesity.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/oby.21229DOI Listing
November 2015

Vitamin D3 supplementation: Response and predictors of vitamin D3 metabolites - A randomized controlled trial.

Clin Nutr 2016 Apr 19;35(2):351-358. Epub 2015 May 19.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Germany. Electronic address:

Background & Aims: Large parts of the population are insufficiently supplied with vitamin D, in particular when endogenous synthesis is absent. Therefore many health care providers recommend the use of vitamin D supplements. The current study aimed to investigate the efficacy of an once-daily oral dose of 20 μg vitamin D3 to improve the vitamin D status and to evaluate predictors of response.

Methods: The study was conducted as a double-blind, randomized, placebo-controlled parallel trial from January till April 2013. In total, 105 subjects (20-71 years) were allocated to receive either a vitamin D3 supplement (20 μg/d) or a placebo for 12 weeks. Circulating levels of vitamin D3 metabolites such as the 25(OH)D3 and the 24,25(OH)2D3, and biomarkers of calcium and phosphate metabolism were quantified.

Results: The 25(OH)D3 serum concentrations in the placebo group decreased from 38 ± 15 nmol/L at baseline to 32 ± 14 nmol/L and 32 ± 13 nmol/L at weeks 8 and 12 of the study, respectively (p < 0.01). In the vitamin D3 group, the serum 25(OH)D3 concentration increased from 38 ± 14 nmol/L at baseline to 70 ± 15 nmol/L and 73 ± 16 nmol/L at weeks 8 and 12 of vitamin D3 supplementation (p < 0.001), respectively. As a result, 94% of the vitamin D3-supplemented participants reached 25(OH)D3 concentrations of ≥50 nmol/L and thereof 46% attained 25(OH)D3 levels of ≥75 nmol/L until the end of the study. The extent of the 25(OH)D3 increase upon vitamin D3 supplementation depended on 25(OH)D3 baseline levels, age, body weight and circulating levels of triglycerides. In contrast to 25(OH)D3, the response of 24,25(OH)2D3 to the vitamin D3 treatment was affected only by baseline levels of 24,25(OH)2D3 and age.

Conclusions: The average improvement of 25(OH)D3 levels in individuals who received 20 μg vitamin D3 per day during the winter months was 41 nmol/L compared to individuals without supplementation. As a result almost all participants with the vitamin D3 supplementation attained 25(OH)D3 concentrations of 50 nmol/L and higher. The suitability of 24,25(OH)2D3 as a marker of vitamin D status needs further investigation. Clinical trial registration number at clinicaltrials.gov: NCT01711905.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.clnu.2015.04.021DOI Listing
April 2016

The Antiatherogenic Effect of Fish Oil in Male Mice Is Associated with a Diminished Release of Endothelial ADAM17 and ADAM10 Substrates.

J Nutr 2015 Jun 29;145(6):1218-26. Epub 2015 Apr 29.

Department of Dermatology,

Background: Growing evidence suggests that disintegrin and metalloprotease (ADAM) 17 (ADAM17) and ADAM10 contribute to the pathogenesis of vascular diseases. ADAM17 promotes inflammatory processes by liberating tumor necrosis factor α, interleukin 6 receptor (IL-6R), and tumor necrosis factor receptor 1 (TNFR1). ADAM17 and ADAM10 modulate vascular permeability by cleaving endothelial adhesion molecules such as junctional adhesion molecule A (JAM-A) and vascular endothelial cadherin (VE-cadherin), respectively.

Objective: This study was designed to investigate whether a link might exist between the protective effects of fish oil (FO) supplementation against atherosclerosis and ADAM function.

Methods: Male LDL receptor knockout (LDLR(-/-)) mice and male wild-type (WT) mice were fed a Western diet (200 g/kg fat, 1.5 g/kg cholesterol) containing either 20% lard (LDLR(-/-)-lard and WT-lard groups) or 10% lard combined with 10% FO (LDLR(-/-)-FO and WT-FO groups) for 12 wk. Atherosclerotic lesion development and fatty acid composition of liver microsomes were evaluated. ADAM10 and ADAM17 expression was determined by quantitative real-time polymerase chain reaction and immunoblot analyses. Concentrations of soluble ADAM substrates in plasma and liver extracts were measured by ELISA.

Results: Diets supplemented with FO markedly reduced development of early atherosclerotic lesions in LDLR(-/-) mice (LDLR(-/-)-lard group vs. LDLR(-/-)-FO group mean ± SD: 29.6 ± 6.1% vs. 22.5 ± 4.2%, P < 0.05). This was not accompanied by changes in expression of ADAM17 or ADAM10 in the aorta or liver. No dietary effects on circulating TNFR1 (LDLR(-/-)-lard group vs. LDLR(-/-)-FO group mean ± SD: 1.22 ± 0.23 vs. 1.39 ± 0.28, P > 0.2) or IL-6R (1.06 ± 0.12 vs. 0.98 ± 0.09 fold of WT-lard group, P > 0.1), classical substrates of ADAM17 on macrophages, and neutrophil granulocytes were observed. However, a reduction in atherosclerotic lesions in the LDLR(-/-)-FO group was accompanied by a significant reduction in the circulating endothelial cell adhesion molecules JAM-A (LDLR(-/-)-lard group vs. LDLR(-/-)-FO group mean ± SD: 1.42 ± 0.20 vs. 0.95 ± 0.56 fold of WT-lard group, P < 0.05), intercellular adhesion molecule 1 (1.15 ± 0.14 vs. 0.88 ± 0.17 fold of WT-lard group, P < 0.05), and VE-cadherin (0.88 ± 0.12 vs. 0.72 ± 0.15 fold of WT-lard group, P < 0.05), reflecting reduced ADAM activity in endothelial cells.

Conclusion: FO exerted an antiatherogenic effect on male LDLR(-/-) mice that was accompanied by a reduced release of ADAM17 and ADAM10 substrates from endothelial cells. It is suggested that FO-decreased ADAM activity contributes to improved endothelial barrier function and thus counteracts intimal lipoprotein insudation and macrophage accumulation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3945/jn.115.211375DOI Listing
June 2015

Isolated Conglutin γ from Lupin, but not Phytate, Lowers Serum Cholesterol Without Influencing Vascular Lesion Development in the ApoE-deficient Mouse Model.

Plant Foods Hum Nutr 2015 Jun;70(2):113-8

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von Danckelmann Platz 2, 06120, Halle (Saale), Germany.

Conglutin γ and phytate are considered as potential biofunctional compounds of lupin protein isolate, but their impact on vascular health is unknown. This study aimed to investigate the effect of conglutin γ and phytate, respectively, on circulating levels of sterols, markers of cholesterol biosynthesis and minerals, and on the development and progression of aortic lesions in apoE-deficient mice. To this end, mice were fed a western diet with either casein (200 g/kg; served as a control), conglutin γ from L. angustifolius (200 g/kg) or casein (200 g/kg) supplemented with phytate (5 g/kg) for 16 weeks. Here we found that conglutin γ but not phytate was capable of reducing the circulating concentration of cholesterol. Plasma levels of desmosterol and lathosterol as markers of the cholesterol synthesis were not affected, and 7-dehydrocholesterol was even higher in mice fed conglutin γ than in mice fed casein or casein + phytate. All mice developed pronounced aortic lesions, but histological characterization of plaque area and composition showed no differences between the three groups of mice. Conclusively, conglutin γ exerts cholesterol-lowering effects but appears to have no anti-atherosclerotic properties in the apoE-deficient mice. Phytate neither affected plasma cholesterol nor aortic lesion development.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11130-015-0481-xDOI Listing
June 2015

Studies on the health impact of Agrimonia procera in piglets.

BMC Vet Res 2014 Sep 9;10:210. Epub 2014 Sep 9.

Background: The weaning period is critical for stress-related diseases and infections. Currently, large amounts of therapeutic antimicrobials are used to treat infections in the livestock production, especially in piglets. Phytogenic feed additives could provide a useful alternative. We hypothesize, that components in agrimonia species which have been used successfully in humans to treat gastrointestinal infections could also improve the health of piglets. We investigated the effects of Agrimonia procera (AP) on the growth performance of piglets and cytokine expression in isolated porcine peripheral blood mononuclear cells (PBMC).

Results: Here we show that piglets that received a diet with 0.56 g/kg AP for 6 weeks tended to ingest more food (+5.1%; P < 0.10), and were characterized by a higher nitrogen retention (+9.6%, P < 0.05) than the control group without AP treatment. Data from a second experiment reveal that piglets fed a diet with 0.87 g/kg AP for 6 weeks had an improved food conversion ratio (1.46 ± 0.04) compared to those that received none (1.54 ± 0.08) or 8.7 g/kg AP (1.60 ± 0.08) with their diets (P < 0.001). However, the food intake, daily weight gain and dry matter of feces were not affected by the AP treatment. Treatment of PBMC for 1 and 6 h with AP extract (APE) reduced the mRNA abundance of tumor necrosis factor (TNF)? in cells challenged with lipopolysaccharides (LPS) but not in cells without LPS stimulation (P < 0.05). The lower mRNA expression of TNF? was accompanied by a trend towards a lower release of TNF? from these cells (P?=?0.067). After the treatment of PBMC with APE for 6 h, the relative mRNA concentration of interleukin (IL)-1? declined (P < 0.05), whereas that of IL-10 remained unchanged. Treatment of LPS-challenged PBMC for 20 h with varying concentrations of APE did not reveal any effect on cytokine expression and TNF? release.

Conclusions: The results indicate that low dosages of AP may improve the growth performance of piglets and seem to exert antiinflammatory effects in porcine immune cells challenged with LPS.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12917-014-0210-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4173061PMC
September 2014

Dietary vitamin D inadequacy accelerates calcification and osteoblast-like cell formation in the vascular system of LDL receptor knockout and wild-type mice.

J Nutr 2014 May 19;144(5):638-46. Epub 2014 Mar 19.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle/Saale, Germany.

Vitamin D insufficiency is highly associated with cardiovascular morbidity and mortality. We have demonstrated enhanced vascular calcification in LDL receptor knockout (LDLR(-/-)) mice fed a diet low in vitamin D. This study aimed to investigate the impact of a diet low in vitamin D on vascular calcification in wild-type (WT) mice lacking atherosclerotic plaques and the effects of a persistent and discontinuous vitamin D insufficiency on atherosclerotic plaque composition in LDLR(-/-) mice. The study was performed with 4-wk-old male WT and LDLR(-/-) mice that were fed a normal calcium/phosphate Western diet (210 g/kg fat, 1.5 g/kg cholesterol) containing either adequate (+D; 1000 IU/kg) or low (-D; 50 IU/kg) amounts of vitamin D-3 for 16 wk. Four groups of LDLR(-/-) mice received 1 of the 2 diets for additional 16 wk (total 32 wk) and were compared with mice fed the diets for only 16 wk. WT and LDLR(-/-) mice that were fed the -D diet for 16 wk tended to develop more calcified spots in the aortic valve than mice fed the +D diet (+50% and +56%, respectively; P < 0.10). In LDLR(-/-) mice, the extent of calcification increased from week 16 to week 32 and was higher in the -D than in the +D group (P < 0.05). The calcification, owing to the -D diet, was accompanied by highly expressed osteoblast differentiation factors, indicating a transdifferentiation of vascular cells to osteoblast-like cells. Feeding the +D diet subsequent to the -D diet reduced the vascular calcification (P < 0.05). LDLR(-/-) mice fed the -D diet for 32 wk had higher plaque lipid depositions (+48%, P < 0.05) and a higher expression of cluster of differentiation 68 (+31%, P < 0.05) and tumor necrosis factor α (+134%, P < 0.001) than the +D group. Collectively, the findings imply low vitamin D status as a causal factor for vascular calcification and atherosclerosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3945/jn.113.189118DOI Listing
May 2014

Lupin protein isolate versus casein modifies cholesterol excretion and mRNA expression of intestinal sterol transporters in a pig model.

Nutr Metab (Lond) 2014 Feb 3;11(1). Epub 2014 Feb 3.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von-Danckelmann-Platz 2, 06120 Halle (Saale), Germany.

Background: Lupin proteins exert hypocholesterolemic effects in man and animals, although the underlying mechanism remains uncertain. Herein we investigated whether lupin proteins compared to casein modulate sterol excretion and mRNA expression of intestinal sterol transporters by use of pigs as an animal model with similar lipid metabolism as humans, and cellular cholesterol-uptake by Caco-2 cells.

Methods: Two groups of pigs were fed cholesterol-containing diets with either 230 g/kg of lupin protein isolate from L. angustifolius or 230 g/kg casein, for 4 weeks. Faeces were collected quantitatively over a 5 d period for analysis of neutral sterols and bile acids by gas chromatographically methods. The mRNA abundances of intestinal lipid transporters were analysed by real-time RT-PCR. Cholesterol-uptake studies were performed with Caco-2 cells that were incubated with lupin conglutin γ, phytate, ezetimibe or albumin in the presence of labelled [4-14C]-cholesterol.

Results: Pigs fed the lupin protein isolate revealed lower cholesterol concentrations in total plasma, LDL and HDL than pigs fed casein (P < 0.05). Analysis of faeces revealed a higher output of cholesterol in pigs that were fed lupin protein isolate compared to pigs that received casein (+57.1%; P < 0.05). Relative mRNA concentrations of intestinal sterol transporters involved in cholesterol absorption (Niemann-Pick C1-like 1, scavenger receptor class B, type 1) were lower in pigs fed lupin protein isolate than in those who received casein (P < 0.05). In vitro data showed that phytate was capable of reducing the uptake of labelled [4-14C]-cholesterol into the Caco-2 cells to the same extend as ezetimibe when compared to control (-20.5% vs. -21.1%; P < 0.05).

Conclusions: Data reveal that the cholesterol-lowering effect of lupin protein isolate is attributable to an increased faecal output of cholesterol and a reduced intestinal uptake of cholesterol. The findings indicate phytate as a possible biofunctional ingredient of lupin protein isolate.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1743-7075-11-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922606PMC
February 2014

Maternal vitamin D deficiency causes smaller muscle fibers and altered transcript levels of genes involved in protein degradation, myogenesis, and cytoskeleton organization in the newborn rat.

Mol Nutr Food Res 2014 Feb 21;58(2):343-52. Epub 2013 Aug 21.

Institute of Agricultural and Nutritional Sciences, Martin-Luther-University Halle-Wittenberg, Halle/Saale, Germany.

Scope: Epidemiologic data reveal associations between low serum concentrations of 25-hydroxyvitamin D (25(OH)D) and higher risk of falls and muscle weakness. Fetal stage is critical for the development of skeletal muscle, but little information is available on the impact of maternal vitamin D deficiency on muscles of offspring.

Methods And Results: To investigate the morphology and transcriptome of gastrocnemius muscle in newborns in response to maternal vitamin D deficiency, 14 female rats were fed either a vitamin D₃ deficient (0 IU/kg) or a vitamin D₃ adequate diet (1000 IU/kg) 8 weeks prior to conception, during pregnancy, and lactation. Analysis of cholecalciferol, 25(OH)D₃ and 1,25-dihydroxyvitamin D₃ show that dams fed the vitamin D deficient diet and their newborns suffered from a relevant vitamin D deficiency. Muscle cells of vitamin D deficient newborns were smaller than those of vitamin D adequate newborns (p < 0.05). Muscle transcriptome of the newborns revealed 426 probe sets as differentially expressed (259 upregulated, 167 downregulated) in response to vitamin D deficiency (fold change ≥1.5, p < 0.05). The effected genes are involved in protein catabolism, cell differentiation and proliferation, muscle cell development, and cytoskeleton organization.

Conclusion: Maternal vitamin D deficiency has a major impact on morphology and gene expression profile of skeletal muscle in newborns.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/mnfr.201300360DOI Listing
February 2014

PPARα modulates the TSH β-subunit mRNA expression in thyrotrope TαT1 cells and in a mouse model.

Mol Nutr Food Res 2013 Mar 18;57(3):376-89. Epub 2012 Dec 18.

Institute of Agricultural and Nutritional Sciences, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.

Scope: Fasting leads to a significant downregulation of the hypothalamus-pituitary-thyroid axis, and peroxisome proliferator-activated receptor (PPAR) α is a key transcription factor in mediating a magnitude of adaptive responses to fasting. In this study, we examined the role of PPARα in regulation of the hypothalamus-pituitary-thyroid axis.

Methods And Results: Thyroid-stimulating hormone β-subunit (TSHβ) mRNA abundance was being reduced in response to treatment of TαT1 cells with PPARα agonists (p < 0.05), indicating an inhibitory transcriptional regulation of TSHβ by PPARα. As expected, fasting significantly downregulated TSHβ mRNA expression in a two-factorial study with fed or fasted wild-type (WT) and PPARα knockout mice (p < 0.05). In contrast to the in vitro data, fasted PPARα knockout mice revealed lower mRNA concentrations of pituitary TSHβ (-64%) and TSH-regulated thyroid genes, and lower plasma concentrations of thyroxine (T4, -25%), triiodothyronine (T3, -25%), free T4 (-60%), and free T3 (-35%) than fasted WT mice (p < 0.05). Those differences were not observed in fed mice.

Conclusions: Data from thyrotrope cells revealed that PPARα could contribute to the fasting-associated downregulation of the TSHβ mRNA expression. In a mouse model, fasting led to a significant reduction in TSHβ mRNA level, but unexpectedly this effect was stronger in mice lacking PPARα than in WT mice.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/mnfr.201200409DOI Listing
March 2013

A comparative study on effects of normal versus elevated temperatures during preimaginal and young adult period on body weight and fat body content of mature Coccinella septempunctata and Harmonia axyridis (Coleoptera: Coccinellidae).

Environ Entomol 2012 Jun;41(3):676-87

Julius Kühn-Institut, Institute for Strategies and Technology Assessment, Kleinmachnow, Germany.

Two climate chamber experiments were performed to simulate the effects of global warming on life table parameters of coccinellids. We investigated the effects of two daily temperature profiles during preimaginal development (larval and pupal) and the young adult period (first 10 d) on body weight and fat body content of adult Coccinella septempunctata L. and Harmonia axyridis (Pallas) fed English grain aphids [Sitobion avenae (F.)] ad libitum: 1) normal, i.e., current daily temperatures in central Europe (T0: mean, 17.8°C; maximum, 21.8°C; minimum, 13.4°C) and 2) increased by 3K (T3: mean, 20.8°C; maximum, 25.5°C; minimum, 15.7°C). The first experiment was performed at the same temperatures (T0 or T3) during both periods to establish the responses of the two species to temperature. The second was conducted to identify the period (preimaginal or adult) in which the responses occurred and to confirm the results of the first experiment. Compared with normal temperatures (T0), elevated temperatures (T3) resulted in significant decreases in preimaginal development time and increases in aphid consumption rates in both species. C. septempunctata (10-d-old adults) had the highest weights when reared at T3, H. axyridis at T0. C. septempunctata was significantly heavier than H. axyridis in most cases, particularly in females. The body fat content of C. septempunctata was higher than that of H. axyridis at T0 and T3 temperatures. At T3 temperatures, fat accumulation in C. septempunctata increased, whereas that in H. axyridis remained relatively low. Body weight and fat body content of 10-d-old adults of both species seemed to be determined by temperature conditions during preimaginal development.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1603/EN11267DOI Listing
June 2012

Vitamin D receptor deficiency and low vitamin D diet stimulate aortic calcification and osteogenic key factor expression in mice.

PLoS One 2012 20;7(4):e35316. Epub 2012 Apr 20.

Institute of Agricultural and Nutritional Sciences, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.

Low levels of 25-hydroxy vitamin D (25(OH)D) are associated with cardiovascular diseases. Herein, we tested the hypothesis that vitamin D deficiency could be a causal factor in atherosclerotic vascular changes and vascular calcification. Aortic root sections of vitamin D receptor knockout (VDR(-/-)) mice that were stained for vascular calcification and immunostained for osteoblastic differentiation factors showed more calcified areas and a higher expression of the osteogenic key factors Msx2, Bmp2, and Runx2 than the wild-type mice (P<0.01). Data from LDL receptor knockout (LDLR(-/-)) mice that were fed western diet with either low (50 IU/kg), recommended (1,000 IU/kg), or high (10,000 IU/kg) amounts of vitamin D(3) over 16 weeks revealed increasing plasma concentrations of 25(OH)D (P<0.001) with increasing intake of vitamin D, whereas levels of calcium and phosphorus in plasma and femur were not influenced by the dietary treatment. Mice treated with the low vitamin D diet had more calcified lesions and a higher expression of Msx2, Bmp2, and Runx2 in aortic roots than mice fed recommended or high amounts of vitamin D (P<0.001). Taken together, these findings indicate vitamin D deficiency as a risk factor for aortic valve and aortic vessel calcification and a stimulator of osteogenic key factor expression in these vascular areas.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0035316PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335028PMC
August 2012

Effect of short-term UVB exposure on vitamin D concentration of eggs and vitamin D status of laying hens.

J Agric Food Chem 2012 Jan 11;60(3):799-804. Epub 2012 Jan 11.

Institute of Agricultural and Nutritional Sciences, Martin-Luther-University Halle-Wittenberg, D-06108 Halle, Germany.

Vitamin D deficiency in humans is widespread, and only a few food items are important natural sources of vitamin D. This study investigated the effect of UVB exposure of laying hens on the vitamin D content in egg yolk. In a two-factorial design, hens fed a vitamin D-deficient (-D) or -adequate (+D) diet were nonexposed or exposed to UVB light over a period of 4 weeks. UVB exposure of the -D group caused nearly normal egg production rate and egg shell quality; exposure of the +D group did not further improve these parameters. UVB exposure tended to improve the concentration of plasma 25-hydroxycholecalciferol (25(OH)D(3)), but had no effect on 1,25-dihydroxycholecalciferol in plasma or on cholecalciferol and 25(OH)D(3) in egg yolk. The present study shows that a short-term exposure of laying hens to UVB light is not an appropriate way to improve the vitamin D content of egg yolk.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/jf204273nDOI Listing
January 2012

Effects of untreated and thermally treated lupin protein on plasma and liver lipids of rats fed a hypercholesterolemic high fat or high carbohydrate diet.

Plant Foods Hum Nutr 2010 Dec;65(4):410-6

Institute of Agricultural and Nutritional Sciences, Martin-Luther-University Halle-Wittenberg, Von-Danckelmann-Platz 2, 06120 Halle (Saale), Germany.

Lupin protein is capable of reducing plasma lipids in hypercholesterolemic man and animals. Whether lipid-lowering properties of lupin protein will be influenced by thermal treatment or by other nutrients has not been elucidated. In a two-factorial study, rats were fed hypercholesterolemic diets based on high amounts of carbohydrates (HC) or fat (HF), which contained either (20.4% of energy) untreated or thermally treated lupin protein (steam: 120 °C, 30 min) or casein as control protein. Lupin protein lowered plasma lipid concentrations in rats fed the HF diet but not in those fed the HC diet (P<0.05). Among rats fed the HF diet, plasma and VLDL triglyceride concentrations were lower in rats fed thermally treated (-46% and -44%, P<0.05) and untreated lupin protein (-47% and -46%, P<0.05) than in those fed casein; whereas liver triglycerides were reduced only in rats fed untreated lupin protein (P<0.05). Compared to casein, untreated lupin protein had slightly stronger cholesterol-lowering effects in plasma, LDL and HDL (-34%, -37%, -35%; P<0.05) than thermally treated lupin protein (-23%, -29%, -31%, P<0.10). In conclusion, the lipid-lowering effect of lupin protein strongly depends on composition of the basal diet, and thermal treatment is accompanied by a slight reduction of its hypocholesterolemic properties.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11130-010-0201-5DOI Listing
December 2010

Glutathione deficiency down-regulates hepatic lipogenesis in rats.

Lipids Health Dis 2010 May 19;9:50. Epub 2010 May 19.

Institute of Agricultural and Nutritional Sciences, Martin-Luther-University Halle-Wittenberg, Von-Danckelmann-Platz 2, D-06120 Halle (Saale), Germany.

Background: Oxidative stress is supposed to increase lipid accumulation by stimulation of hepatic lipogenesis at transcriptional level. This study was performed to investigate the role of glutathione in the regulation of this process. For that purpose, male rats were treated with buthionine sulfoximine (BSO), a specific inhibitor of gamma-glutamylcysteine synthetase, for 7 days and compared with untreated control rats.

Results: BSO treatment caused a significant reduction of total glutathione in liver (-70%), which was attributable to diminished levels of reduced glutathione (GSH, -71%). Glutathione-deficient rats had lower triglyceride concentrations in their livers than the control rats (-23%), whereas the circulating triglycerides and the cholesterol concentrations in plasma and liver were not different between the two groups of rats. Livers of glutathione-deficient rats had lower mRNA abundance of sterol regulatory element-binding protein (SREBP)-1c (-47%), Spot (S)14 (-29%) and diacylglycerol acyltransferase 2 (DGAT-2, -27%) and a lower enzyme activity of fatty acid synthase (FAS, -26%) than livers of the control rats. Glutathione-deficient rats had also a lower hepatic activity of the redox-sensitive protein-tyrosine phosphatase (PTP)1B, and a higher concentration of irreversible oxidized PTP1B than control rats. No differences were observed in protein expression of total PTP1B and the mature mRNA encoding active XBP1s, a key regulator of unfolded protein and ER stress response.

Conclusion: This study shows that glutathione deficiency lowers hepatic triglyceride concentrations via influencing lipogenesis. The reduced activity of PTP1B and the higher concentration of irreversible oxidized PTP1B could be, at least in part, responsible for this effect.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1476-511X-9-50DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881051PMC
May 2010

Fasting Upregulates PPARalpha Target Genes in Brain and Influences Pituitary Hormone Expression in a PPARalpha Dependent Manner.

PPAR Res 2009 ;2009:801609

Institute of Agricultural and Nutritional Sciences, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.

PPARalpha is a lipid-activable transcription factor that mediates the adaptive response to fasting. Recent data indicate an important role of brain PPARalpha in physiological functions. However, it has not yet been shown whether PPARalpha in brain can be activated in the fasting state. Here we demonstrate that fasting of rats increased mRNA concentrations of typical PPARalpha target genes implicated in beta-oxidation of fatty acids (acyl-CoA oxidase, carnitine palmitoyltransferase-1, medium chain acyl-CoA dehydrogenase) and ketogenesis (mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase) in pituitary gland and partially also in frontal cortex and diencephalon compared to nonfasted animals. These data strongly indicate that fasting activates PPARalpha in brain and pituitary gland. Furthermore, pituitary prolactin and luteinizing hormone-beta mRNA concentrations were increased upon fasting in wild-type mice but not in mice lacking PPARalpha. For proopiomelanocortin and thyrotropin-beta, genotype-specific differences in pituitary mRNA concentrations were observed. Thus, PPARalpha seems to be involved in transcriptional regulation of pituitary hormones.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1155/2009/801609DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2786200PMC
July 2011

Lupin protein isolate and cysteine-supplemented casein reduce calcification of atherosclerotic lesions in apoE-deficient mice.

Br J Nutr 2010 Jan 27;103(2):180-8. Epub 2009 Aug 27.

Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Von Danckelmann Platz 2, D-06120 Halle (Saale), Germany.

Protein from lupin is supposed to have anti-atherogenic effects due to its lipid-lowering properties in laboratory animals. It is further suggested that the amino acid cysteine plays a crucial role in this aspect. The objective of the present study was to compare the effects of lupin protein and cysteine-supplemented casein with those of casein on atherosclerotic lesion development in apoE-deficient mice. For that purpose, thirty mice were fed an egg albumin-based Western-type diet containing test protein (100 g/kg) for 4 months. ApoE-deficient mice fed the lupin protein or the cysteine-supplemented casein had more than 50 % less aortic calcification than mice fed casein (P < 0.05). The quantified lesion area as a percentage of the total surface area, as well as the collagen and fat content of the lesions were not different between the three groups of mice. The concentration of VLDL TAG was higher in mice fed the lupin protein and the cysteine-supplemented casein than in mice fed casein (P < 0.05). The cholesterol concentrations of VLDL, LDL and HDL from mice fed the lupin protein and cysteine-supplemented casein were not different compared with the mice fed casein. Also, the plasma concentrations of homocysteine, Ca, inorganic phosphate, and the activity of glutathione peroxidase in plasma and liver did not differ between the three groups of mice. The present study shows that lupin protein and cysteine-supplemented casein compared with casein reduce the calcification of atherosclerotic lesions in apoE-deficient mice. This effect seems not to be mediated by effects on plasma lipoproteins, homocysteine and circulating minerals.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1017/S0007114509991565DOI Listing
January 2010