http://www.dietcan.net/docs/Polifenoles%20en%20alimentos%20y%20biodisponibilidad.pdf

Polyphenols: food sources and bioavailability

Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

Fish bioaccumulation and biomarkers in environmental risk assessment: a review

Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

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Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.

Bioavailability and bioefficacy of polyphenols in humans. I. Review of 97 bioavailability studies

The risk of obesity (OB) in adulthood is strongly influenced by maternal body composition. Here we examined the hypothesis that maternal OB influences white adipose tissue (WAT) transcriptome and increases propensity for adipogenesis in the offspring, prior to the development of OB, using an established model of long-term metabolic programming. Employing an overfeeding-based rat model, in which exposure to OB is limited to preconception and gestation alone, we conducted global transcriptomic profiling in WAT, and gene/protein expression analysis of lipogenic and adipogenic pathways and examined adipogenic differentiation of WAT stromal-vascular cells ex vivo. Using reduced representation bisulfite sequencing we also evaluated genome-scale changes in DNA methylation in offspring WAT. Maternal OB led to extensive changes in expression of genes (± 1.8-fold, P ≤ .05), revealing a distinct up-regulation of lipogenic pathways in WAT. mRNA expression of a battery of sterol regulatory element-binding protein-1-regulated genes was increased in OB-dam offspring, which were confirmed by immunoblotting. In conjunction with lipogenic gene expression, OB-dam offspring showed increased glucose transporter-4 mRNA/protein expression and greater AKT phosphorylation following acute insulin challenge, suggesting sensitization of insulin signaling in WAT. Offspring of OB dams also exhibited increased in vivo expression of adipogenic regulators (peroxisome proliferator-activated receptor-γ, CCAAT enhancer binding protein α [C/EBP-α] and C/EBP-β), associated with greater ex vivo differentiation of WAT stromal-vascular cells. These transcriptomic changes were associated with alterations in DNA methylation of CpG sites and CGI shores, proximal to developmentally important genes, including key pro-adipogenic factors (Zfp423 and C/EBP-β). Our findings strongly suggest that the maternal OB in utero alters adipocyte commitment and differentiation via epigenetic mechanisms.

/pdf/maternal-obesity-enhances-white-adipose-tissue-o3z30gy4xu.pdf

Maternal obesity enhances white adipose tissue differentiation and alters genome-scale DNA methylation in male rat offspring.

Intragastric infusion of ethanol to male rats as part of a system of total enteral nutrition allows chronic ethanol treatment without the nutritional and feeding problems associated with traditional liquid diets. Even though ethanol was infused at a constant rate 24 h a day, blood alcohol concentrations were observed to cycle over a 5- to 7-day period from values less than 10 mg/dl to greater than 400 mg/dl. Examination of the hepatic microsomal mono-oxygenase system in animals chronically treated with ethanol using this model revealed variable induction of cytochrome P450 CYP 2E1, the principal component of the microsomal ethanol oxidizing system. Correlations were observed between urine alcohol concentrations (UACs) and 1) the level of expression of CYP 2E1 mRNA in Northern blot analysis, 2) the level of CYP 2E1 apoprotein in Western blot analysis and, 3) microsomal p-nitrophenol (PNP) hydroxylation. The data from ethanol-treated animals were expressed as low UAC group (UACs 300 mg/dl) and compared to total enteral nutrition controls. In the low UAC group, a 6- to 7-fold induction in microsomal PNP hydroxylase (a CYP 2E1-dependent activity) was accompanied by a 4- to 5-fold increase in CYP 2E1 apoprotein, but no increase in CYP 2E1 mRNA levels. In contrast, in the high UAC group, induction of PNP hydroxylase was 15- to 16-fold, induction of CYP 2E1 apoprotein was 12- to 13-fold and CYP 2E1 mRNA was elevated 5- to 6-fold.(ABSTRACT TRUNCATED AT 250 WORDS)

Cytochrome P450 CYP 2E1 induction during chronic alcohol exposure occurs by a two-step mechanism associated with blood alcohol concentrations in rats.

P2-123 Maternal obesity at conception programs obesity in the offspring

To determine the effects of feeding soy or isoflavones on lipid homeostasis in early development, weanling rats were fed AIN-93G diets made with casein, soy protein isolate (SPI+), isoflavone-reduced SPI+ (SPI-), or casein supplemented with genistein or daidzein for 14 d. PPARalpha-regulated genes and proteins involved in fatty acid degradation were upregulated by SPI+ (P < 0.05) accompanied by increased promoter binding and expression of PPARalpha mRNA (P < 0.05). Feeding SPI- or pure isoflavones did not alter PPARalpha-regulated pathways. SPI+ feeding had similar effects on PPARgamma signaling. SPI+, SPI-, and casein plus isoflavones all increased liver X-receptor (LXR)alpha-regulated genes and enzymes involved in cholesterol homeostasis. Feeding SPI+ increased promoter binding of LXRalpha, expression of the transcription factor mRNA, and protein (P < 0.05). In a second experiment, male Sprague-Dawley rats were fed casein diets from postnatal d (PND) 24 to PND64 or were fed high-fat Western diets containing 5 g x kg(-1) cholesterol made with either casein or SPI+. Insulin resistance, steatosis, and hypercholesterolemia in the Western diet-fed rats were partially prevented by SPI+ (P < 0.05). Nuclear sterol receptor element binding protein (SREBP)-1c protein and mRNA and protein expression of enzymes involved in fatty acid synthesis were increased by feeding Western diets containing casein but not SPI+ (P < 0.05). These data suggest that activation of PPAR and LXR signaling and inhibition of SREBP-1c signaling may contribute to insulin sensitization and improved lipid homeostasis in SPI+-fed rats after consumption of diets high in fat and cholesterol.

/pdf/dietary-soy-protein-isolate-attenuates-metabolic-syndrome-in-5094y0joo0.pdf

Dietary Soy Protein Isolate Attenuates Metabolic Syndrome in Rats via Effects on PPAR, LXR, and SREBP Signaling

Epidemiological and clinical studies have linked consumption of soy foods with low incidences of a number of chronic diseases, such as cardiovascular diseases, cancer, and osteoporosis. Over the past decades, enormous research efforts have been made to identify bioactive components in soy. Isoflavones and soy protein have been suggested as the major bioactive components in soy and have received considerable attention. However, there are hundreds of phytochemical components in soybeans and soy-based foods. In recent years, accumulating evidence has suggested that the isoflavones or soy proteins stripped of phytochemicals only reflect certain aspects of health effects associated with soy consumption. Other phytochemicals, either alone or in combination with isoflavones or soy protein, may be involved in the health effects of soy. This review attempts to summarize major non-isoflavone phytochemicals in soy, as well as their bioavailability and health effects. In addition, a brief discussion of components formed during food processing is also included.

Thomas M. Badger

Papers

Maternal obesity enhances white adipose tissue differentiation and alters genome-scale DNA methylation in male rat offspring.

Cytochrome P450 CYP 2E1 induction during chronic alcohol exposure occurs by a two-step mechanism associated with blood alcohol concentrations in rats.

P2-123 Maternal obesity at conception programs obesity in the offspring

Dietary Soy Protein Isolate Attenuates Metabolic Syndrome in Rats via Effects on PPAR, LXR, and SREBP Signaling

Non-isoflavone phytochemicals in soy and their health effects.