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181	Effects of Essential Fatty Acids and Conjugated Linoleic Acid Supplementation on Fatty Acid Pattern in Blood Plasma and Milk and on the Inflammatory Response in Dairy Cows from Late Gestation to Early Lactation Gnott, Martina 13 November 2023 (has links) This study investigated the effects of abomasal infusion of essential fatty acids, especially alpha-linolenic acid, and conjugated linoleic acid on their distribution in milk fat and blood plasma and on the plasma inflammatory response in dairy cows from late to early lactation. The most important essential fatty acids for ruminants are alpha-linolenic acid and linoleic acid. They are abundant in pasture which is nowadays reduced in the ration of dairy cows due to the replacement of fresh feeds by preserved diets. Conjugated linoleic acid is formed as a by-product during ruminal biohydrogenation of essential fatty acids and has been associated with positive effects on the energy metabolism and immune system. Forty rumen-cannulated Holstein Friesian cows were assigned to four treatment groups in their late second lactation. Prior to supplementation, cows were fed a total mixed rations with a low-fat content. In late gestation cows were abomasally treated with coconut oil, linseed and safflower oil, conjugated linoleic acid, or both. Performance data, milk composition and fatty acid pattern in milk and plasma as well as inflammatory response parameters in plasma were measured regularly. Furthermore, liver tissue was tested for the abundance of genes related to the inflammatory response.:TABLE OF CONTENTS ABBREVIATIONS 1. INTRODUCTION 2. LITERATURE OVERVIEW 2.1 Essential Fatty Acids and Conjugated Linoleic Acid 2.1.1 Essential Fatty Acids (EFA) 2.1.2 Conjugated Linoleic Acid (CLA) 2.1.3 EFA in Dairy Cow Nutrition 2.2 Fatty Acid Distribution in Blood, Erythrocyte Membranes, and Milk Fat 2.2.1 Plasma Lipids 2.2.2 EFA and CLA in Plasma Lipids 2.2.3 EFA and CLA in Erythrocyte Membranes 2.2.4 EFA and CLA in Milk Fat 2.3 Effects of EFA and CLA on Inflammatory Processes during the Transition Period 2.3.1 Metabolic and Immunological Challenges during the Transition Period 2.3.2 Effects of EFA on the Metabolism, Inflammatory- and Immune Response 2.3.3 Effects of CLA on the Metabolism, Inflammatory- and Immune Response 2.4 Scope of the Thesis 3. PUBLICATION 4. GENERAL DISCUSSION 4.1 Abomasal Infusion 4.2 Animal Performance 4.3 Distribution of EFA and CLA in Blood and Milk Fat 4.4 Effects of EFA and CLA on Plasma and Hepatic Acute Phase and Inflammatory Response 4.5 Conclusion and Practical Considerations 4.5.1 Summary of EFA effects 4.5.2 Summary of CLA effects 4.5.3 Summary of synergistic effects of EFA and CLA 4.5.4 Summary of Observations apart from Treatments and Practical Considerations 5. SUMMARY 6. ZUSAMMENFASSUNG 7. REFERENCES APPENDIX info:eu-repo/classification/ddc/636.089 ddc:636.089 info:eu-repo/classification/ddc/630 ddc:630
182	Intestinal Gene Expression Profiling and Fatty Acid Responses to a High-fat Diet Cedernaes, Jonathan January 2013 (has links) The gastrointestinal tract (GIT) regulates nutrient uptake, secretes hormones and has a crucial gut flora and enteric nervous system. Of relevance for these functions are the G protein-coupled receptors (GPCRs) and the solute carriers (SLCs). The Adhesion GPCR subfamily is known to mediate neural development and immune system functioning, whereas SLCs transport e.g. amino acids, fatty acids (FAs) and drugs over membranes. We aimed to comprehensively characterize Adhesion GPCR and SLC gene expression along the rat GIT. Using qPCR we measured expression of 78 SLCs as well as all 30 Adhesion GPCRs in a twelve-segment GIT model. 21 of the Adhesion GPCRs had a widespread (≥5 segments) or ubiquitous (≥11 segments) expression. Restricted expression patterns were characteristic for most group VII members. Of the SLCs, we found the majority (56 %) of these transcripts to be expressed in all GIT segments. SLCs were predominantly found in the absorption-responsible gut regions. Both Adhesion GPCRs and SLCs were widely expressed in the rat GIT, suggesting important roles. The distribution of Adhesion GPCRs defines them as a potential pharmacological target. FAs constitute an important energy source and have been implicated in the worldwide obesity increase. FAs and their ratios – indices for activities of e.g. the desaturase enzymes SCD-1 (SCD-16, 16:1n-7/16:0), D6D (18:3n-6/18:2n-6) and D5D (20:4n-6/20:3n-6) – have been associated with e.g. overall mortality and BMI. We examined whether differences in FAs and their indices in five lipid fractions contributed to obesity susceptibility in rats fed a high fat diet (HFD), and the associations of desaturase indices between lipid fractions in animals on different diets. We found that on a HFD, obesity-prone (OP) rats had a higher SCD-16 index and a lower linoleic acid (LA) proportions in subcutaneous adipose tissue (SAT) than obesity-resistant rats. Desaturase indices were significantly correlated between many of the lipid fractions. The higher SCD-16 may indicate higher SCD-1 activity in SAT in OP rats, and combined with lower LA proportions may provide novel insights into HFD-induced obesity. The associations between desaturase indices show that plasma measurements can serve as proxies for some lipid fractions, but the correlations seem to be affected by diet and weight gain. Adhesion GPCR delta-5 desaturase delta-6 desaturase desaturase index Diet-induced obesity estimated desaturase activity fatty acid composition gas chromatography gastrointestinal tract G-protein coupled receptor high-fat diet intestine linoleic acid liver mRNA expression palmitoleic acid plasma phospholipids proximodistal RT-qPCR solute carrier SCD-1 SCD-16 SCD-18 stearoyl-CoA desaturase subcutaneous adipose tissue subsection triacylglycerols.
183	Dietary Fatty Acids and Inflammation : Observational and Interventional Studies Bjermo, Helena January 2011 (has links) Dietary fat quality influences the risk of type 2 diabetes and cardiovascular disease. A low-grade inflammation is suggested to contribute to the disease development, often accompanied by obesity. Whereas n-3 polyunsaturated fatty acids (PUFA) have been considered anti-inflammatory, n-6 PUFA have been proposed to act pro-inflammatory. Saturated fatty acids (SFA) act pro-inflammatory in vitro. This thesis aimed to investigate effects of different fatty acids on low-grade inflammation in observational and interventional studies. In Paper I and II, fatty acid composition in serum cholesterol esters was used as objective marker of dietary fat quality and related to serum C-reactive protein (CRP) and other circulating inflammatory markers in two population-based cohorts, conducted in middle-aged men and elderly men and women, respectively. In Paper III and IV, the impact of diets differing in fat quality on inflammation and oxidative stress was investigated in randomised controlled studies, in subjects with metabolic syndrome and abdominal obesity. In Paper I and II, a low proportion of linoleic acid (18:2 n-6) in serum was associated with higher CRP concentrations, indicating that a low intake of vegetable fats may be related to low-grade inflammation. High CRP concentrations were also associated with high proportions of palmitoleic (16:1) and oleic (18:1) acids and high stearoyl coenzymeA desaturase index, possibly reflecting altered fat metabolism and/or high SFA intake in this population. When comparing two high-fat diets rich in either saturated or monounsaturated fat, and two low-fat diets with or without long-chain n-3 PUFA supplementation during 12 weeks (Paper III), no differences in inflammation or oxidative stress markers were observed. Moreover, a 10-week intervention (Paper IV) with high linoleic acid intake showed no adverse effects on inflammation or oxidative stress. Instead, interleukin-1 receptor antagonist and tumor necrosis factor receptor-2 decreased after linoleic acid intake compared with a diet high in SFA. The results in this thesis indicate that dietary n-6 PUFA found in vegetable fats is associated with lower inflammation marker levels, and to some extent reduces systemic inflammation when compared with SFA. Supplementation of n-3 PUFA did not exert any systemic anti-inflammatory effects, maybe due to a relatively low dose. Dietary fat Fatty acids Serum fatty acid composition Linoleic acid Stearoyl coenzymeA desaturase SCD-1 Inflammation C-reactive protein Oxidative stress Lipid peroxidation Isoprostanes Prostaglandins Obesity Epidemiology Dietary intervention Metabolic syndrome Nutrition Näringslära Epidemiology Epidemiologi Public health science Folkhälsovetenskap Immunology Immunologi Diabetology Diabetologi Cardiology Kardiologi
184	Elucidating the metabolism of n-3 polyunsaturated fatty acids and formation of bioactive lipid mediators in human skin Kiezel-Tsugunova, Magdalena January 2017 (has links) Human skin has distinct lipid metabolism and production of bioactive lipid mediators that can be modulated by nutritional supplementation with omega-3 polyunsaturated fatty acids (n-3 PUFA), of which eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids exert anti-inflammatory effects. The aims of this project were to gain better understanding of their individual mechanisms in human epidermis and dermis. HaCaT keratinocytes, 46BR.1N fibroblasts, primary human epidermal keratinocytes and dermal fibroblasts were treated with EPA or DHA for 72h and then sham-irradiated or exposed to 15 mJ/cm2 ultraviolet radiation (UVR). Viability was measured by the MTT assay. The expression of cyclooxygenase-2 (COX-2), microsomal prostaglandin synthase-1 (mPGES-1) and 15-hydroxyprostaglandin dehydrogenase (15-PGDH) proteins was explored by western blotting. Human skin explants (n=4 donors) were cultured for 3 or 6 days and supplemented with EPA, DHA or vehicle. Culture media were collected to evaluate tissue damage and PUFA cytotoxicity (lactate dehydrogenase assay). Epidermal and dermal lipid profiles were assessed by gas chromatography and liquid chromatography coupled to tandem mass spectrometry. Primary keratinocytes were treated with fatty acids and various lipid mediators for 48h. Their effect was determined by the scratch assay and transepithelial electrical resistance. UVR upregulated COX-2 in HaCaT and primary epidermal keratinocytes, but did not affect mPGES-1 and 15-PGDH protein expression. UVR upregulated COX-2 and mPGES-1 in 46BR.1N fibroblasts but had no effect on 15-PGDH expression. The same UVR dose did not alter the expression of COX-2, mPGES-1 and 15-PGDH in primary dermal fibroblasts. Only EPA attenuated COX-2 expression in HaCaT and primary keratinocytes and either EPA or DHA had any effect in 46BR.1N and primary fibroblasts. Skin explants showed initial post-biopsy tissue damage. EPA and DHA supplementation augmented cellular levels of the corresponding fatty acids in both epidermis and dermis to a different extent. Increased uptake of DHA in the dermis was accompanied by reduced arachidonic acid levels. EPA treatment stimulated the production of PGE3 and various HEPE in epidermis, while DHA treatment caused high levels of HDHA species in dermis. N-3 PUFA and their derivatives delayed wound healing, cell migration and epidermal barrier permeability, while n-6 PUFA lipids showed the opposite effect. Overall, these findings suggest that EPA and DHA differently affect skin cells and skin, with EPA preference in epidermis and DHA in the dermis. These results highlight the importance of differential skin responses that could be important in skin health and disease. 612.3
185	Einfluss von freien Fettsäuren und Triglyceriden auf die Expression von proinflammatorischen Mediatoren und Adhäsionsmolekülen in Hepatozyten und Kupffer-Zellen (der Ratte) / Effect of free fatty acids and triglycerides on the expression of proinflammatory mediators and adhesion molecules in hepatocytes and Kupffer cells (of the rat) Demuth, Julia Elisabeth 01 December 2009 (has links) No description available. 610 Medizin, Gesundheit Medicine Julia Demuth NASH Fettleber Steatosis Hepatis Leberentzündung Two-Hit-Hypothese Hepatozyten Kupffer-Zellen Hep G2 Linolsäure Palmitinsäure Triglyceride Lipofundin iNOS CINC1 CINC2 MIP IL-6 TNFa ICAM PECAM Julia Demuth Non Alcoholic Fatty Liver Disease NASH fatty liver Steatosis Hepatis hepatitis Two-Hit-Hypothese hepatocytes Kupffer cells Hep G2 linoleic acid palmatic acid triglyceride Lipofundin iNOS CINC1 CINC2 MIP IL-6 TNFa ICAM PECAM 44.87 MED 415: Hepatologie

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