Composition en lipides et acides gras de deux esèces de Taphrina parasites de Prunus domestica

Four strains of both Taphrina pruni and T. institiae were cultivated under identical conditions and and lipids and fatty acids were quantitatively analysed at two stages of their development. Tri- and diglycerides are the major neutral lipids in both species. Phosphatidylcholine and phosphatidylethanolamine are the most abundant polar lipids. Qualitatively, the two species show identical fatty acid contents, except for margaric acid (17:0) which was only found in Taphrine pruni. Quantitatively there are several differences: palmitoleic acid (16:1) occurs in reasonable amounts regularly and only in Taphrina pruni. The ratios 16:0/18:0 and 18:1/18:2 are generally higher for T. insititiae whereas the degree of unsaturation of fatty acids is higher in the former. The results are discussed with regard to data on other fungal species.     

Histone acetyltransferase general control non‐repressed protein 5 (GCN5) affects the fatty acid composition of Arabidopsis thaliana seeds by acetylating fatty acid desaturase3 (FAD3)

Seed oils are important natural resources used in the processing and preparation of food. Histone modifications represent key epigenetic mechanisms that regulate gene expression, plant growth and development. However, histone modification events during fatty acid (FA) biosynthesis are not well understood. Here, we demonstrate that a mutation of the histone acetyltransferase GCN5 can decrease the ratio of α‐linolenic acid (ALA) to linoleic acid (LA) in seed oil. Using RNA‐Seq and ChIP assays, we identified FAD3, LACS2, LPP3 and PLAIIIβ as the targets of GCN5. Notably, the GCN5‐dependent H3K9/14 acetylation of FAD3 determined the expression levels of FAD3 in Arabidopsis thaliana seeds, and the ratio of ALA/LA in the gcn5 mutant was rescued to the wild‐type levels through the overexpression of FAD3. The results of this study indicated that GCN5 modulated FA biosynthesis by affecting the acetylation levels of FAD3. We provide evidence that histone acetylation is involved in FA biosynthesis in Arabidopsis seeds and might contribute to the optimization of the nutritional structure of edible oils through epigenetic engineering.     

Metabolic effects of intravenous LCT or MCT/LCT lipid emulsions in preterm infants

Most lipid emulsions for parenteral feeding of premature infants are based on long-chain triacylglycerols (LCTs), but inclusion of medium-chain triacylglycerols (MCTs) might provide a more readily oxidizable energy source. The influence of these emulsions on fatty acid composition and metabolism was studied in 12 premature neonates, who were randomly assigned to an LCT emulsion (control) or an emulsion with a mixture of MCT and LCT (1:1). On study day 7, all infants received [13C]linoleic (LA) and [13C]alpha-linolenic acid (ALA) tracers orally. Plasma phospholipid (PL) and triacylglycerol (TG) fatty acid composition and 13C enrichments of plasma PL fatty acids were determined on day 8. After 8 days of lipid infusion, plasma TGs in the MCT/LCT group had higher contents of C8:0 (0.50 +/- 0.60% vs. 0.10 +/- 0.12%; means +/- SD) and C10:0 (0.66 +/- 0.51% vs. 0.15 +/- 0.17%) than controls. LA content of plasma PLs was slightly lower in the MCT/LCT group (16.47 +/- 1.16% vs. 18.57 +/- 2.09%), whereas long-chain polyunsaturated derivatives (LC-PUFAs) of LA and ALA tended to be higher. The tracer distributions between precursors and products (LC-PUFAs) were not significantly different between groups. Both lipid emulsions achieve similar plasma essential fatty acid (EFA) contents and similar proportional conversion of EFAs to LC-PUFAs. The MCT/LCT emulsion seems to protect EFAs and LC-PUFAs from beta-oxidation.     

Lipidomics reveals membrane lipid remodelling and release of potential lipid mediators during early stress responses in a murine melanoma cell line

Membranes are known to respond rapidly to various environmental perturbations by changing their composition and microdomain organization. In previous work we showed that a membrane fluidizer benzyl alcohol (BA) could mimic the effects of heat stress and enhance heat shock protein synthesis in different mammalian cells. Here we explore heat- and BA-induced stress further by characterizing stress-induced membrane lipid changes in mouse melanoma B16 cells. Lipidomic fingerprints revealed that membrane stress achieved either by heat or BA resulted in pronounced and highly specific alterations in lipid metabolism. The loss in polyenes with the concomitant increase in saturated lipid species was shown to be a consequence of the activation of phopholipases (mainly phopholipase A₂ and C). A phospholipase C–diacylglycerol lipase–monoacylglycerol lipase pathway was identified in B16 cells and contributed significantly to the production of several lipid mediators upon stress including the potent heat shock modulator, arachidonic acid. The accumulation of cholesterol, ceramide and saturated phosphoglyceride species with raft-forming properties observed upon both heat and BA treatments of B16 cells may explain the condensation of ordered plasma membrane domains previously detected by fluorescence microscopy and may serve as a signalling platform in stress responses or as a primary defence mechanism against the noxious effects of stresses.     

Mapping and tissue mRNA expression analysis of the pig solute carrier 27A (SLC27A) multigene family

Solute-carrier family 27A molecules are integral transmembrane proteins that play a fundamental role in the uptake of long-chain fatty acids into mammalian cells. Our goal was to characterize this multigene family in pigs. Chromosomal location of the six porcine SLC27A genes was determined by radiation hybrid mapping and indicated that the six genes map to six different chromosomal locations. Moreover, we analyzed SLC27A mRNA expression in six pig tissues by quantitative RT-PCR. While SLC27A1, SLC27A3 and SLC27A4 were expressed in most, if not all, analyzed tissues, SLC27A2, SLC27A5 and SLC27A6 were predominantly expressed in the liver. In general, pig and human SLC27A mRNA expression profiles were remarkably concordant, although important differences were observed for SLC27A1 and SLC27A6 mRNAs. Discrepancies between mRNA expression profiles have been observed even in closely related primate species, and they might reflect the acquisition of regulatory changes promoting evolutionary adaptation.     

Aging and caloric restriction impact adipose tissue,adiponectin, and circulating lipids

Adipose tissue expansion has been associated with system‐wide metabolic dysfunction and increased vulnerability to diabetes, cancer, and cardiovascular disease. A reduction in adiposity is a hallmark of caloric restriction (CR), an intervention that extends longevity and delays the onset of these same age‐related conditions. Despite these parallels, the role of adipose tissue in coordinating the metabolism of aging is poorly defined. Here, we show that adipose tissue metabolism and secretory profiles change with age and are responsive to CR. We conducted a cross‐sectional study of CR in adult, late‐middle‐aged, and advanced‐aged mice. Adiposity and the relationship between adiposity and circulating levels of the adipose‐derived peptide hormone adiponectin were age‐sensitive. CR impacted adiposity but only levels of the high molecular weight isoform of adiponectin responded to CR. Activators of metabolism including PGC‐1a, SIRT1, and NAMPT were differentially expressed with CR in adipose tissues. Although age had a significant impact on NAD metabolism, as detected by biochemical assay and multiphoton imaging, the impact of CR was subtle and related to differences in reliance on oxidative metabolism. The impact of age on circulating lipids was limited to composition of circulating phospholipids. In contrast, the impact of CR was detected in all lipid classes regardless of age, suggesting a profound difference in lipid metabolism. These data demonstrate that aspects of adipose tissue metabolism are life phase specific and that CR is associated with a distinct metabolic state, suggesting that adipose tissue signaling presents a suitable target for interventions to delay aging.     

苜蓿中华根瘤菌desA基因功能的鉴定

为研究苜蓿中华根瘤菌脂肪酸脱饱和酶desA基因在不饱和脂肪酸合成、共生结瘤固氮以及应对逆境胁迫中的功能,为高效利用苜蓿中华根瘤菌提供理论依据,本文通过异体遗传互补和脂肪酸组成薄层层析,分析SmdesA编码蛋白是否具有脱饱和酶的活性并参与不饱和脂肪酸的合成,构建SmdesA的缺失突变株和互补菌株,比较各菌株在不同逆境胁迫条件下的生长速率以及回接宿主植物后与紫花苜蓿共生结瘤的能力.结果表明SmdesA不能互补大肠杆菌CY57中EcfabA的突变,但具有将饱和脂肪酸脱饱和形成不饱和的棕榈油酸和十八碳烯酸的能力.另外,SmdesA缺失突变对苜蓿中华根瘤菌的脂肪酸组成影响不大,但会显著影响低温和高盐条件下菌株的生长速率以及与紫花苜蓿共生结瘤的能力.我们推测,SmdesA参与的脱饱和途径可能是苜蓿中华根瘤菌不饱和脂肪酸合成的补偿途径,其编码的蛋白DesA不是不饱和脂肪酸合成的关键酶,但在应对逆境胁迫和共生结瘤中具有重要的生物学功能.     

Peroxisome-generated succinate induces lipid accumulation and oxidative stress in the kidneys of diabetic mice

Diabetes normally causes lipid accumulation and oxidative stress in the kidneys, which plays a critical role in the onset of diabetic nephropathy; however, the mechanism by which dysregulated fatty acid metabolism increases lipid and reactive oxygen species (ROS) formation in the diabetic kidney is not clear. As succinate is remarkably increased in the diabetic kidney, and accumulation of succinate suppresses mitochondrial fatty acid oxidation and increases ROS formation, we hypothesized that succinate might play a role in inducing lipid and ROS accumulation in the diabetic kidney. Here we demonstrate a novel mechanism by which diabetes induces lipid and ROS accumulation in the kidney of diabetic animals. We show that enhanced oxidation of dicarboxylic acids by peroxisomes leads to lipid and ROS accumulation in the kidney of diabetic mice via the metabolite succinate. Furthermore, specific suppression of peroxisomal β-oxidation improved diabetes-induced nephropathy by reducing succinate generation and attenuating lipid and ROS accumulation in the kidneys of the diabetic mice. We suggest that peroxisome-generated succinate acts as a pathological molecule inducing lipid and ROS accumulation in kidney, and that specifically targeting peroxisomal β-oxidation might be an effective strategy in treating diabetic nephropathy and related metabolic disorders.