Two experiments were conducted to evaluate the influence of dietary selenium (Se) on tissue levels of selenoprotein W (Se-W) in rats. Se dependent glutathione peroxidase (GPX) activity and Se levels were also determined for comparative measurements. In the first experiment, rats were fed a basal diet deficient in Se or supplemented with either 0.1 or 4.0 mg Se (as selenite) per kg diet for 6 wk. Se-W levels were significantly higher in muscle, spleen and testes of rats fed 0.1 mg Se per kg diet compared to those fed the deficient diet (controls), and those fed 4.0 mg Se per kg diet had significantly higher levels in muscle, brain and spleen (P < 0. 05) than those fed 0.1 mg Se per kg diet. No further increases, however, occurred in the tests. There was a significant increase (P < 0.05) of mRNA encoding Se-W in muscle with each increase of dietary Se. In the second experiment rats were fed the basal diet or this diet plus 0.01, 0.03, 0.06, 0.1, 1.0, 2.0 or 4.0 mg Se per kg diet. The levels of Se-W in muscle did not increase (P < 0.05) until 0.06 mg Se per kg diet were fed to rats. A very marked increase (P < 0.05) occurred when 1.0 mg Se per kg diet was fed with no further increases with higher levels. There was a linear increase of Se-W in brain (r = 0.89) and spleen (r = 0.98) with the Se concentration in the diet up to 0.1 mg Se per kg where a plateau was reached. The testes showed a different pattern in that a very marked increase (P < 0.01) occurred when only 0.01 mg Se per kg diet was fed where an inflection was reached. Except for muscle, GPX activities reached a plateau in all tissues when diets containing 0.06 to 0.1 mg supplemental Se per kg were fed. The Se concentration in these tissues increased at a linear rate with the Se concentration in the diets up to 0.1 mg Se per kg where it continued to rise at a different rate. The results indicate that in rats, the regulation of Se-W by Se is different for various tissues and differs from that for GPX.
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http://dx.doi.org/10.1093/jn/127.11.2165 | DOI Listing |
Metab Brain Dis
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Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Federal do Rio Grande do Sul, Avenida Ipiranga, 2752, Porto Alegre, CEP 90610-000, RS, Brazil.
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Facultad de Industrias Alimentarias, Universidad Nacional Agraria La Molina, Lima, Peru.
This review aimed to explore the impact of extrusion on Andean grains, such as quinoa, kañiwa, and kiwicha, highlighting their macromolecular transformations, technological innovations, and contributions to food security. These grains, which are rich in starch, high-quality proteins, and antioxidant compounds, are versatile raw materials for extrusion, a continuous and efficient process that combines high temperatures and pressures to transform structural and chemical components. Extrusion improves the digestibility of proteins and starches, encourages the formation of amylose-lipid complexes, and increases the solubility of dietary fiber.
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January 2025
Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Unitat de Farmacologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
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View Article and Find Full Text PDFDiabetologia
January 2025
Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
The incidence of type 2 diabetes has risen globally, in parallel with the obesity epidemic and environments promoting a sedentary lifestyle and low-quality diet. There has been scrutiny of ultra-processed foods (UPFs) as a driver of type 2 diabetes, underscored by their increasing availability and intake worldwide, across countries of all incomes. This narrative review addresses the accumulated evidence from investigations of the trends in UPF consumption and the relationship with type 2 diabetes incidence.
View Article and Find Full Text PDFExposure to toxins causes lasting damaging effects on the body. Numerous studies in humans and animals suggest that diet has the potential to modify the epigenome and these modifications can be inherited transgenerationally, but few studies investigate how diet can protect against negative effects of toxins. Potential evidence in the primary literature supports that caloric restriction, high-fat diets, high protein-to-carbohydrate ratios, and dietary supplementation protect against environmental toxins and strengthen these effects on their offspring's epigenome.
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