China
Africa
Explore chapters and articles related to this topic
Omega-3 Fatty Acids in the Prevention of Maternal and Offspring Metabolic Disorders
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Olatunji Anthony Akerele, Sukhinder Kaur Cheema
An understanding of genetic variations has posed a big question on the appropriateness of the one-size-fits-all recommended dietary allowance. Recent studies on SNPs revealed that the differences from one person to another may be greater than previously thought. SNPs in the genes encoding the fatty acid desaturase and elongase enzymes affect longer chain PUFA production. As such, what is adequate for some may be deficient for others; it is therefore pertinent to consider individual genetic variations and move towards personalized nutrition, especially during pregnancy. Nutritional intervention has been suggested as a tool for improving virtually any condition. Information about person’s SNPs status would proffer a platform for designing a nutritional intervention strategy that can improve the maternal health status. For instance, DHA intake during pregnancy may prevent inflammation-inclined adverse pregnancy outcomes in mothers with low ALA to DHA conversion efficiency.
Genetic Determinants of Nutrient Processing
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
Polyunsaturated fatty acid composition of phospholipids is associated with several common diseases, including the metabolic syndrome [50], CVD [51], psychiatric disorders [52,53], and immune-related disease [54]. Polyunsaturated fatty acid levels in phospholipids are determined by both nutrition and metabolism, with desaturases and elongases catalyzing their conversion. Human desaturases were first cloned and characterized in 1999, owing to their critical role in the availability of polyunsaturated fatty acids, which are important for a number of biological functions including brain development, inflammation, and hemostasis [55,56]. The fatty acid desaturase 1 gene (FADS1) encodes the Δ-5 desaturase, while the fatty acid desaturase 2 gene (FADS2) gene encodes the Δ-6 desaturase. Both the FADS1 and FADS2 genes are located on chromosome 11q12.2 in a head-to-head configuration. The Δ-5 desaturase is expressed at highest levels in the liver, with lower but comparable expression levels in the heart, brain, and lung, and low but detectable levels of expression in placenta, skeletal muscle, kidney, and pancreas. In comparison, the Δ-6 desaturase had a similar expression profile but with a greater overall abundance [55]. As depicted in Figure 2.2, these enzymes catalyze rate-limiting steps in the production of long chain fatty acids, including arachidonic acid (20:4(n-6)) and eicosapentaenoic acid (20:5(n-3)), which are precursors of eicosanoids, which mediate inflammatory processes [57,58].
The Zone Diet
Published in Caroline Apovian, Elizabeth Brouillard, Lorraine Young, Clinical Guide to Popular Diets, 2018
Sears helped to pioneer research proposing that the enzymes required for the synthesis of the eicosanoid precursors (DGLA, AA, and EPA) are common to both the ω-6 and ω-3 fatty acid metabolic pathways, which suggested the potential for manipulation of their enzymatic activity through dietary means. As both DGLA and EPA are substrates for the delta-5 desaturase enzyme, Sears posited that supplementation with EPA would act as a feedback inhibition, suppressing the delta-5 desaturase pathway, thereby reducing the production of AA from DGLA.9,16,17 Alterations in plasma AA:EPA ratio have been cited as causative of dysfunction in the metabolism of obese individuals, cautiously affirming the observation that fatty acid desaturase activity serves as a biomarker for the development of obesity and its related disorders.16,17
Changes in Serum, Red Blood Cell, and Colonic Fatty Acids in a Personalized Omega-3 Fatty Acid Supplementation Trial
Published in Nutrition and Cancer, 2022
Yifan Shen, Ananda Sen, D. Kim Turgeon, Jianwei Ren, Gillian Graifman, Mack T. Ruffin, William L. Smith, Dean E. Brenner, Zora Djuric
Fatty acids in serum, red blood cells, and colon were expressed as a mole percent of total fatty acids, and the ratio of EPA to AA was calculated using the mole percent values. This trial utilized doses of ω-3 fatty acid supplementation that were higher than in many other studies. We therefore calculated several published indices of ω-3 fatty acid status (Table 1). The Omega-3 index was calculated as the relative content of the sum of EPA and DHA in RBC membranes, expressed as a percent of total fatty acids by weight using the calculation method of Harris et al. (32). The ω-3 highly unsaturated fatty acids (HUFA) and ω-6 HUFA represent percentages of total HUFAs present as either ω-3 or ω-6, respectively; HUFAs are fatty acids with 20–22 carbons and more than three double bonds as described by Lands et al. (33). The HUFA quantified were 20:3 ω-6, 20:4 ω-6, 22-4 ω-6, 20:5 ω-3, 22:5 ω-3, and 22:6 ω-3. EPA percent was percentage of EPA in RBC total fatty acids, which has been suggested to serve as a biomarker of colon tumor EPA content by Watson et al. (34). Finally, we calculated fatty acid ratios that represent desaturase activities. These were the ratios of 18:1 to 18:0 and 16:1 to 16:0 to assess stearoyl CoA desaturase (SCD-1, δ-9 desaturase), and ratio of 20:4, ω-6 to 18:2, ω-6 to assess fatty acid desaturase activity (FADS, δ-5 desaturase).
The gut bacterium Extibacter muris produces secondary bile acids and influences liver physiology in gnotobiotic mice
Published in Gut Microbes, 2021
Theresa Streidl, Isabel Karkossa, Rafael R. Segura Muñoz, Claudia Eberl, Alex Zaufel, Johannes Plagge, Robert Schmaltz, Kristin Schubert, Marijana Basic, Kai Markus Schneider, Mamdouh Afify, Christian Trautwein, René Tolba, Bärbel Stecher, Heidi L. Doden, Jason M. Ridlon, Josef Ecker, Tarek Moustafa, Martin von Bergen, Amanda E. Ramer-Tait, Thomas Clavel
The observed shifts in liver proteomes were not linked to pathological changes in anthropometric measurements, blood parameters, inflammatory cytokines, or hepatic dysfunction as indicated by increased serum aspartate aminotransferase levels,65 or histological changes such as inflammatory infiltration or cell death.66,67 Kuno et al.65 suggested that liver toxicity is dependent on the concentration of secondary bile acids, with physiological levels actually contributing to homeostasis. The levels of DCA and LCA observed in E. muris-colonized mice are in the range of concentrations normally detected in SPF mice and can therefore be considered as physiological.56,68 The effects of colonization on lipid pathways detected by proteomics did not translate into alterations of hepatic fatty acid profiles. In contrast to experiments by others, HF diet feeding did not lead to significantly increased amounts of total fatty acids in the liver, perhaps because diets were only fed for 8 weeks.69 Shifts from MUFA- to PUFA-dominated profiles due to dietary fat (lard in this study) have not been described before. The observed high levels of the fatty acid C22:6 n-3 appear remarkable due to its absence in both diets, maybe due to increased activity of host-derived PUFA-metabolizing enzymes, such as fatty acid desaturases (FADS) 1 and 2, and elongases (ELOVL) 2 and 5.70–72
Plasma fatty acids as markers for desaturase and elongase activities in spinal cord injured males
Published in The Journal of Spinal Cord Medicine, 2019
Lynnette M. Jones, Michael Legge
The results from this study indicate that there are significant differences between serum fatty acids for the SCI and control groups in the four major groups of fatty acids investigated (saturated fatty acids, SFA; monounsaturated fatty acids, MUFA; n-6 polyunsaturated fatty acids, n-6 PUFA, and n-3 PUFA). Taking these results into consideration, we investigated the inter-relationship of the fatty acid desaturases and elongase activities between both groups. High concentrations of palmitic acid (C16:0) and low concentrations of linoleic acid (C18:2 n-6) and proportionately elevated palmitoleic acid (C16:1) have been described as characteristic of individuals with high insulin levels and at risk for metabolic syndrome.11,14 Previously, it has been demonstrated that stearoyl – CoA destaturase (a liver microsomal enzyme) is the rate limiting step in the biosynthesis of palmitoleoyl and oleoyl CoAs from their respective substrates palmitoyl and stearoyl CoAs, via a Δ9 desaturation reaction.24,25 However, direct analysis of this enzyme in human material is difficult and the ratios of the fatty acids oleate (C18:1/stearate (C18:0) and palmitoleate (C16:1)/palmitate (C16:0) are reliable analytes to indicate surrogate enzyme activity.9,12