Consumer attitudes toward consumption of meat products containing offal and offal extracts

The development of food products containing offal and offal extracts could be part of the solution to the upcoming demand for animal protein. This study aimed to determine Spanish consumers’ attitudes toward offal and the development of meat products containing offal extracts. Consumers’ perceptions were evaluated by means of focus group discussions and a survey (N = 400) to validate the focus group results in various Spanish provinces. The theory of planned behavior was used to examine consumer attitudes. Results indicated that nutritional properties, environmental sustainability, and affordability were the main drivers, while sensory attributes, low frequency consumption, and perceived higher content of undesirable compounds were the main barriers. Three segments were identified according to their beliefs: those in favor of these products, those that were health and environmentally conscious, and those who were reluctant about them. The identification of these segments and their profiles demonstrated the necessity to focus efforts on providing reliable information on sensory and health-related issues to improve acceptability. Attitude was the most important predictor of behavioral intention regarding the global model, while the social component (subjective norm) was significant for two of the identified segments, emphasizing the relevance of the social component for acceptability.This work was supported by industrial abattoirs: Patel SAU, Olot Meats S.A., Friselva S.A., Frigoríficos del Nordeste S.A., and Frigoríficos Costa Brava S.A., with financial support of Government of Catalonia (Project Ref. 56.21.031.2016 3A), the National Institute for Agriculture and Food Research and Technology (INIA) (RTA2017-00024-C04-01), and CERCA program from Generalitat de Catalunya. R. Bou was in part supported through the Ramon y Cajal Program (RYC-2013-12745) and M. Llauger was supported by the Ministry of the Economy, Industry and Competitiveness (Grant Number PRE2018-084247).Peer ReviewedPostprint (published version

Assessment of the levels of degradation in fat co- and by-products for feed uses and their relationships with some lipid composition parameters

This paper discusses the levels of degradation of some co- and byproducts of the food chain intended for feed uses. As the first part of a research project, 'Feeding Fats Safety', financed by the sixth Framework Programme-EC, a total of 123 samples were collected from 10 European countries, corresponding to fat co- and byproducts such as animal fats, fish oils, acid oils from refining, recycled cooking oils, and other. Several composition and degradation parameters (moisture, acid value, diacylglycerols and monoacylglycerols, peroxides, secondary oxidation products, polymers of triacylglycerols, fatty acid composition, tocopherols, and tocotrienols) were evaluated. These findings led to the conclusion that some fat by- and coproducts, such as fish oils, lecithins, and acid oils, show poor, nonstandardized quality and that production processes need to be greatly improved. Conclusions are also put forward about the applicability and utility of each analytical parameter for characterization and quality control

Aging Negatively Affects Estrogens-Mediated Effects on Nitric Oxide Bioavailability by Shifting ERα/ERβ Balance in Female Mice

AIMS: Aging is among the major causes for the lack of cardiovascular protection by estrogen (E2) during postmenopause. Our study aims to determine the mechanisms whereby aging changes E2 effects on nitric oxide (NO) production in a mouse model of accelerated senescence (SAM). METHODS AND RESULTS: Although we found no differences on NO production in females SAM prone (SAMP, aged) compared to SAM resistant (SAMR, young), by either DAF-2 fluorescence or plasmatic nitrite/nitrate (NO2/NO3), in both cases, E2 treatment increased NO production in SAMR but had no effect in SAMP. Those results are in agreement with changes of eNOS protein and gene expression. E2 up-regulated eNOS expression in SAMR but not in SAMP. E2 is also known to increase NO by decreasing its catabolism by superoxide anion (O(2)(-)). Interestingly, E2 treatment decreased O(2)(-) production in young females, while increased O(2)(-) in aged ones. Furthermore, we observed that aging changed expression ratio of estrogen receptors (ERβ/ERα) and levels of DNA methylation. Increased ratio ERβ/ERα in aged females is associated to a lack of estrogen modulation of NO production and with a reversal in its antioxidant effect to a pro-oxidant profile. CONCLUSIONS: Together, our data suggest that aging has detrimental effects on E2-mediated benefits on NO bioavailability, partially by affecting the ability of E2 to induce up regulation of eNOS and decrease of O(2)(-). These modifications may be associated to aging-mediated modifications on global DNA methylation status, but not to a specific methylation at 5'flanking region of ERα gene

Characterization of Ion Channels Involved in the Proliferative Response of Femoral Artery Smooth Muscle Cells

31 páginas, 6 figuras, adicionales 6 figuras y 3 tablas.[Objective]: Vascular smooth muscle cells (VSMCs) contribute significantly to occlusive vascular diseases by virtue of their ability to switch to a noncontractile, migratory, and proliferating phenotype. Although the participation of ion channels in this phenotypic modulation (PM) has been described previously, changes in their expression are poorly defined because of their large molecular diversity. We obtained a global portrait of ion channel expression in contractile versus proliferating mouse femoral artery VSMCs, and explored the functional contribution to the PM of the most relevant changes that we observed. [Methods and Results]: High-throughput real-time polymerase chain reaction of 87 ion channel genes was performed in 2 experimental paradigms: an in vivo model of endoluminal lesion and an in vitro model of cultured VSMCs obtained from explants. mRNA expression changes showed a good correlation between the 2 proliferative models, with only 2 genes, Kv1.3 and Kvβ2, increasing their expression on proliferation. The functional characterization demonstrates that Kv1.3 currents increased in proliferating VSMC and that their selective blockade inhibits migration and proliferation. [Conclusion]: These findings establish the involvement of Kv1.3 channels in the PM of VSMCs, providing a new therapeutical target for the treatment of intimal hyperplasia.This work was supported by Ministerio de Sanidad, Instituto de Salud Carlos III grants R006/009 (Red Heracles), FS041139-0 (M.R.), and PI041044 (J.R.L.-L.); Ministerio de Educacio´n y Ciencia grants BFU2004-05551 (M.T.P.-G.) and BFU2007-61524 (J.R.L.-L.); and Junta de Castilla y Leon grant GR242. Dr Moreno-Domínguez is a fellow of the Spanish Ministerio de Educacion y Ciencia.Peer reviewe

Factores responsables de la pérdida de los efectos beneficiosos de los estrógenos en el sistema cardiovascular

Antecedentes: Estudios experimentales y observacionales sugieren que los estrógenos y los moduladores selectivos de los ERs (SERMs), como el raloxifeno, juegan un papel clave en la protección vascular femenina. Por otro lado, estudios clínicos importantes sobre el tratamiento con estrógenos y raloxifeno en mujeres posmenopáusicas, incluyendo los ensayos recientes WHI y RUTH han demostrado que el uso de estrógenos para la prevención de las ECV no tiene ningún beneficio aparente y en algunos casos incluso puede suponer un riesgo para el sistema cardiovascular. Para entender estos resultados tan contradictorios es importante conocer los mecanismos que afectan a la función de los estrógenos. Entre las diferentes hipótesis se ha barajado el tipo de estrógeno utilizado (estrógenos conjugados equinos), y que los resultados negativos se obtuvieron en una población de mujeres que tuvo la menopausia, de media, diez años antes de empezar con la terapia, por lo que podrían presentar lesiones vasculares significativas debido al envejecimiento y a la presencia de ECV asintómaticas. Hipótesi y objetivo principal: Investigar los efectos negativos de la edad y del tipo de estrógeno así como la existencia de ECV previa tienen sobre el mecanismo protector de acción de las hormonas. Metodología: Los efectos del envejecimiento se determinan en tejido vascular de ratones hembra SAMP (modelo murino de envejecimiento). Los mecanismos que pueden alterar las respuestas moduladas por estrógenos se valorarán mediante la expresión del receptor de estrógenos (ER), de eNOS, la producción de NO, estrés oxidativo su actividad y su estado de la metilación del DNA genómico. Los efectos de los diferentes tipos de estrógenos, se valorarán mediante expresión de ER, producción de NO, expresión y actividad de eNOS, expresión de ER y estudio computacional de las moléculas. Resultados: El primer estudio demuestra que los estrógenos presentes en la mezcla de estrógenos conjugados equinos (CEE) son menos eficaces que los estrógenos naturales de la mujer (17b-estradiol y estrona) en modular la producción del óxido nítrico (NO) de las células endoteliales. El segundo trabajo describe como el envejecimiento afecta negativamente a la protección de los estrógenos en la función cardiovascular, principalmente mediante alteraciones en la producción de NO y en el estrés oxidativo. Conclusiones: 1. Los estrógenos equinos (CEE) no modulan la producción de NO tan efectivamente como los estrógenos naturales de la mujer, por presentar menor capacidad para activar la transcripción y la actividad de eNOS que los estrógenos naturales de la mujer. 2. La presencia de un grupo hidroxil en el carbono 17 y el grado de saturación del anillo B de la molécula estrogénica aportan más estabilidad al complejo receptor-hormona, además de provocar cambios en la hidrofobicidad y en la acidez del complejo receptor-hormona lo que facilitaría su unión al DNA y/o a los diferentes cofactores necesarios para la transcripción. 3. El envejecimiento contribuye a la pérdida de los efectos beneficiosos de los estrógenos en la pared vascular. Por un lado disminuye el efecto de “up-regulation” de los estrógenos en la producción de NO y en la expresión de eNOS. Por otro lado, modifica el mecanismo de modulación del estrés oxidativo transformando los estrógenos en substancias prooxidantes. 4. El envejecimiento aumenta la ratio ERβ/ERα después del tratamiento con estrógenos. Este aumento está directamente relacionado con un incremento de los efectos prooxidantes en el vaso que podrían justificar la pérdida de los efectos beneficiosos de los estrógenos 5. El envejecimiento aumenta significativamente el porcentaje de metilación global pero no afecta a la metilación específica del gen ERα. Por tanto, no podemos asociar los cambios en la metilación del DNA con la disminución observada en la expresión del gen ERα con el envejecimiento

K+ channels expression in hypertension after arterial injury, and effect of selective Kv1.3 blockade with PAP-1 on intimal hyperplasia formation

et al.[Introduction]: K+ channels are central to vascular pathophysiology. Previous results demonstrated that phenotypic modulation associates with a change in Kv1.3 to Kv1.5 expression, and that Kv1.3 blockade inhibits proliferation of VSMCs cultures. [Purpose]: To explore whether the Kv1.3 to Kv1.5 switch could be a marker of the increased risk of intimal hyperplasia in essential hypertension and whether systemic treatment with Kv1.3 blockers can prevent intimal hyperplasia after endoluminal lesion. [Methods]: Morphometric and immunohistochemical analysis were performed in arterial segments following arterial injury and constant infusion of the Kv1.3 blocker PAP-1 during 28 days. Differential expression of K+ channel genes was studied in VSMC from hypertensive (BPH) and normotensive (BPN) mice, both in control and after endoluminal lesion. Finally, the migration and proliferation rate of BPN and BPH VSMCs was explored in vitro. [Results]: Changes in mRNA expression led to an increased Kv1.3/Kv1.5 ratio in BPH VSMC. Consistent with this, arterial injury in BPH mice induced a higher degree of luminal stenosis, (84 ± 4 % vs. 70 ± 5 % in BPN, p < 0.01), although no differences in migration and proliferation rate were observed in cultured VSMCs. The in vivo proliferative lesions were significantly decreased upon PAP-1 systemic infusion (18 ± 6 % vs. 58 ± 20 % with vehicle, p < 0.05). [Conclusions]: Hypertension leads to a higher degree of luminal stenosis in our arterial injury model, that correlates with a decreased expression of Kv1.5 channels. Kv1.3 blockers decreased in vitro VSMCs proliferation, migration, and in vivo intimal hyperplasia formation, pointing to Kv1.3 channels as promising therapeutical targets against restenosis.This work was funded by the Ministerio de Economia y Competitividad, Instituto de Salud Carlos III, (RIC RD12/0042/0006, Red Heracles) to MR, MH, MTP and JRL; FIS-Instituto Carlos III, PI11/00225 to MR, VALTEC 09-1-0042 to MR, a grant from the Spanish Heart Association to MR., Ministerio de Ciencia e Innovación grant BFU2010-15898 to MTPG and, Junta de Castilla y León grant VA094A11-2 to, JRLLPeer Reviewe

Assessment of the levels of degradation in fat co- and by-products for feed uses and their relationships with some lipid composition parameters

This paper discusses the levels of degradation of some co- and byproducts of the food chain intended for feed uses. As the first part of a research project, 'Feeding Fats Safety', financed by the sixth Framework Programme-EC, a total of 123 samples were collected from 10 European countries, corresponding to fat co- and byproducts such as animal fats, fish oils, acid oils from refining, recycled cooking oils, and other. Several composition and degradation parameters (moisture, acid value, diacylglycerols and monoacylglycerols, peroxides, secondary oxidation products, polymers of triacylglycerols, fatty acid composition, tocopherols, and tocotrienols) were evaluated. These findings led to the conclusion that some fat by- and coproducts, such as fish oils, lecithins, and acid oils, show poor, nonstandardized quality and that production processes need to be greatly improved. Conclusions are also put forward about the applicability and utility of each analytical parameter for characterization and quality control

Role of KV1.3 channels in intimal hyperlasia

Resumen del póster presentado al American College of Cardiology - 61st Annual Scientific Seesion & Expo celebrado en Chicago (US) del 24 al 27 de marzo de 2012.[Background]: Vascular smooth muscle cells (VSMCs) are able to switch from a contractile to a proliferative phenotype, and this process is central to intimal hyperplasia formation. Phenotypic modulation requires a change in gene expression profile, including a switch in ion transport mechanisms. Potassium (K+) channels have been suggested to have a role in the processes of cell proliferation. Changes in K+ channels expression are associated with functional changes in the electrophysiological properties of VSMCs, which are linked to cell growth. We have previously obtained a global portrait of ion channel expression in contractile versus proliferating VSMCs in different vascular beds, in vitro and in vivo, and have identified a marked increase in Kv1.3 mRNA expression during the switch to a proliferative phenotype. The aim of our study is to investigate the effect of the selective blockade of Kv1.3 channels in VSMC proliferation. For this purpose, we have selected PAP-1 (phenoxyalkoxypsoralen-1), a potent suppressor of T cells proliferation in vitro, which inhibits Kv1.3 with a high selectivity over other K+ channels. [Methods]: Porcine coronary SMCs were isolated and cell proliferation analysis was measured with a BrdU incorporation assay. Using an arterial injury model previously validated by our group, an endothelial denudation injury was induced to murine femoral arteries. A constant infusion of PAP-1 (50 microg/Kg) was administered after injury, through the subcutaneous implant of Alzet osmotic mini-pumps, during 28 days, time-point at which animals were euthanized and arterial segments collected for morphometric and immunohistochemical analysis. [Results]: PAP-1 (10 nM) significantly reduced cell proliferation versus control cells (13,2±1% vs. 18±1%, p<0,05). Intimal proliferation was reduced in PAP-1-treated animals, compared with control, vehicle-treated, mice (Intima-to-media ratios of 0,18±0,11 vs. 1,06±0,40; p=0,01). [Conclusion]: The selective blockade of Kv1.3 channels decreases in vitro VSMCs proliferation and in vivo intimal hyperplasia formation. Our results point to Kv1.3 channels as a new promising therapeutical target to avoid restenosis.Peer reviewe

Primers designed for qPCR experiments.

<p>Primers designed for qPCR experiments.</p