scholarly journals The concept of sphingolipid rheostat in skin: a driving force for new active ingredients in cosmetic applications

OCL ◽  
2018 ◽  
Vol 25 (5) ◽  
pp. D507 ◽  
Author(s):  
Iuliana Popa
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Stratum Corneum ◽  
Driving Force ◽  
Mammalian Cells ◽  
De Novo ◽  
Oral Treatment ◽  
Sphingolipid Metabolism ◽  
Intercellular Signaling ◽  
Sphingosine 1 Phosphate

Skin is a representative model of the complex metabolism that lipids may trigger. It is known that the biosynthesis of these lipids in mammalian cells generally ensures the cell membranes stability and participates to the signaling function. In the inner layers of the skin, the “de-novo” synthesis is the driving force ensuring proliferation, development and intercellular signaling. To promote stratum corneum formation, lipid catabolism leads to the renewal of ceramides, fatty acids and cholesterol that are responsible for the cohesion of the stratum corneum, its permeability, hydration, moisturization and signalling with the outer skin layers, appendages and inner layers secretion (cytokines, neuropeptides). Some actives applied in local treatments (i.e., peptides, n-3 polyunsaturated fatty acids (PUFA), ceramides, urea or an aqueous extract of Gromwell) and in oral treatment (i.e., sphingomyelin, n-3 polyunsaturated fatty acids (PUFA)) promote sphingosine 1-phosphate (S1P) production by the sphingolipid rheostat via triggering the salvage process along with autophagy and detoxification in aged skin. This review gives some basis for using the concept of sphingolipid metabolism rheostat in skin as the driving force for the development of new cosmetic actives ingredients or for repositioning the benefits of other actives for the skin.

scholarly journals Natural variation in yolk fatty acids, but not androgens, predicts offspring fitness in a wild bird

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Lucia Mentesana ◽  
Martin N. Andersson ◽  
Stefania Casagrande ◽  
Wolfgang Goymann ◽  
Caroline Isaksson ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Maternal Effects ◽  
Natural Variation ◽  
De Novo ◽  
Natural Populations ◽  
Egg Laying ◽  
Interactive Effects ◽  
Free Living ◽  
Offspring Fitness

Abstract Background In egg-laying animals, mothers can influence the developmental environment and thus the phenotype of their offspring by secreting various substances into the egg yolk. In birds, recent studies have demonstrated that different yolk substances can interactively affect offspring phenotype, but the implications of such effects for offspring fitness and phenotype in natural populations have remained unclear. We measured natural variation in the content of 31 yolk components known to shape offspring phenotypes including steroid hormones, antioxidants and fatty acids in eggs of free-living great tits (Parus major) during two breeding seasons. We tested for relationships between yolk component groupings and offspring fitness and phenotypes. Results Variation in hatchling and fledgling numbers was primarily explained by yolk fatty acids (including saturated, mono- and polyunsaturated fatty acids) - but not by androgen hormones and carotenoids, components previously considered to be major determinants of offspring phenotype. Fatty acids were also better predictors of variation in nestling oxidative status and size than androgens and carotenoids. Conclusions Our results suggest that fatty acids are important yolk substances that contribute to shaping offspring fitness and phenotype in free-living populations. Since polyunsaturated fatty acids cannot be produced de novo by the mother, but have to be obtained from the diet, these findings highlight potential mechanisms (e.g., weather, habitat quality, foraging ability) through which environmental variation may shape maternal effects and consequences for offspring. Our study represents an important first step towards unraveling interactive effects of multiple yolk substances on offspring fitness and phenotypes in free-living populations. It provides the basis for future experiments that will establish the pathways by which yolk components, singly and/or interactively, mediate maternal effects in natural populations.

scholarly journals Dietary fatty acids promote lipid droplet diversity through seipin enrichment in an ER subdomain

2018 ◽  
Author(s):  
Zhe Cao ◽  
Yan Hao ◽  
Yiu Yiu Lee ◽  
Pengfei Wang ◽  
Xuesong Li ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Lipid Droplet ◽  
Mammalian Cells ◽  
Dietary Fatty Acids ◽  
Fat Storage ◽  
Over Expression ◽  
C Elegans ◽  
Cyclopropane Fatty Acids ◽  
Host Metabolism

AbstractExogenous metabolites from microbial and dietary origins have profound effects on host metabolism. Here, we report that a sub-population of lipid droplets (LDs), which are conserved organelles for fat storage, is defined by metabolites-driven targeting of theC. elegansseipin ortholog, SEIP-1. Loss of SEIP-1 function reduced the size of a subset of LDs while over-expression of SEIP-1 had the opposite effect. Ultrastructural analysis revealed SEIP-1 enrichment in an endoplasmic reticulum (ER) subdomain, which co-purified with LDs. Analyses ofC. elegansand bacterial genetic mutants indicated a requirement of polyunsaturated fatty acids (PUFAs) and microbial cyclopropane fatty acids (CFAs) for SEIP-1 enrichment, as confirmed by dietary supplementation experiments. In mammalian cells, heterologous expression of SEIP-1 promoted lipid droplet expansion from ER subdomains in a conserved manner. Our results suggest that microbial and polyunsaturated fatty acids serve unexpected roles in regulating cellular fat storage by enforcing LD diversity.

scholarly journals Feeding Stimulates Sphingosine-1-Phosphate Mobilization in Mouse Hypothalamus

2019 ◽  
Vol 20 (16) ◽  
pp. 4008
Author(s):  
Valentina Vozella ◽  
Natalia Realini ◽  
Alessandra Misto ◽  
Daniele Piomelli
Keyword(s):  
De Novo ◽  
Sphingolipid Metabolism ◽  
Rt Pcr ◽  
Liquid Chromatography Tandem Mass ◽  
Sphingosine 1 Phosphate ◽  
Phosphate Mobilization ◽  
S1p Receptor ◽  
Free Feeding ◽  
G Protein Coupled ◽  
Sphingolipid Biosynthesis

Previous studies have shown that the sphingolipid-derived mediator sphingosine-1-phosphate (S1P) reduces food intake by activating G protein-coupled S1P receptor-1 (S1PR1) in the hypothalamus. Here, we examined whether feeding regulates hypothalamic mobilization of S1P and other sphingolipid-derived messengers. We prepared lipid extracts from the hypothalamus of C57Bl6/J male mice subjected to one of four conditions: free feeding, 12 h fasting, and 1 h or 6 h refeeding. Liquid chromatography/tandem mass spectrometry was used to quantify various sphingolipid species, including sphinganine (SA), sphingosine (SO), and their bioactive derivatives SA-1-phosphate (SA1P) and S1P. In parallel experiments, transcription of S1PR1 (encoded in mice by the S1pr1 gene) and of key genes of sphingolipid metabolism (Sptlc2, Lass1, Sphk1, Sphk2) was measured by RT-PCR. Feeding increased levels of S1P (in pmol-mg−1 of wet tissue) and SA1P. This response was accompanied by parallel changes in SA and dihydroceramide (d18:0/18:0), and was partially (SA1P) or completely (S1P) reversed by fasting. No such effects were observed with other sphingolipid species targeted by our analysis. Feeding also increased transcription of Sptlc2, Lass1, Sphk2, and S1pr1. Feeding stimulates mobilization of endogenous S1PR1 agonists S1P and SA1P in mouse hypothalamus, via a mechanism that involves transcriptional up-regulation of de novo sphingolipid biosynthesis. The results support a role for sphingolipid-mediated signaling in the central control of energy balance.

scholarly journals Resveratrol Targets Sphingolipid Metabolism to Induce Growth Inhibition in FLT3 ITD Acute Myeloid Leukemia

Proceedings ◽  
2019 ◽  
Vol 40 (1) ◽  
pp. 4
Author(s):  
Ersöz ◽  
Adan
Keyword(s):  
Growth Inhibition ◽  
Cell Fate ◽  
De Novo ◽  
Therapeutic Potential ◽  
Annexin V ◽  
Sphingolipid Metabolism ◽  
Ceramide Synthase ◽  
Cytotoxic Effects ◽  
Sphingosine 1 Phosphate ◽  
First Time

Sphingolipids are important signaling lipids which play crucial roles to determine the cell fate. Ceramide, apoptotic central molecule of sphingolipid metabolism, which is produced through de novo pathway by serine palmitoyl transferase (SPT) and can be converted to antiapoptotic sphingosine-1-phosphate (S1P) and glucosyl ceramide (GC) by sphingosine kinase (SK) and glucosyl ceramide synthase (GCS), respectively. It is aimed to investigate therapeutic potential of resveratrol on FLT3-ITD (Internal Tandem Duplication) AML cells and to identify potential mechanism behind resveratrol-mediated growth inhibition by targeting of ceramide metabolism. The cytotoxic effects of resveratrol, SPT inhibitor (myricoin), SK-1 inhibitor (SKI II), GCS inhibitor (PDMP), resveratrol: SPT inhibitor, resveratrol: SK-1 inhibitor and resveratrol: GCS inhibitor combinations on MOLM-13 and MV4-11 FLT3 ITD AML cells were investigated by cell proliferation assay. Apoptosis was evaluated by annexin V/PI double staining. There were synergistic cytotoxic effects of resveratrol with co-administration of SPT inhibitor, SK-1 inhibitor and GCS inhibitor and apoptosis was synergistically induced for resveratrol and its combinations. This preliminary data showed for the first time that resveratrol might inhibit the growth of FLT3 ITD AML cells through targeting ceramide metabolism.

The effect of altered sphingolipid acyl chain length on various disease models

2015 ◽  
Vol 396 (6-7) ◽  
pp. 693-705 ◽  
Author(s):  
Woo-Jae Park ◽  
Joo-Won Park
Keyword(s):  
Chain Length ◽  
De Novo ◽  
Case Reports ◽  
Acyl Chain ◽  
Fatty Acyl ◽  
Sphingolipid Metabolism ◽  
Lipid Mediator ◽  
Disease Models ◽  
Acyl Chain Length ◽  
Sphingosine 1 Phosphate

Abstract Sphingolipids have emerged as an important lipid mediator in intracellular signalling and metabolism. Ceramide, which is central to sphingolipid metabolism, is generated either via a de novo pathway, by attaching fatty acyl CoA to a long-chain base, or via a salvage pathway, by degrading pre-existing sphingolipids. As a ‘sphingolipid rheostat’ has been proposed, the balance between ceramide and sphingosine-1-phosphate has been the object of considerable attention. Ceramide has recently been reported to have a different function depending on its acyl chain length: six ceramide synthases (CerS) determine the specific ceramide acyl chain length in mammals. All CerS-deficient mice generated to date show that sphingolipids with defined acyl chain lengths play distinct pathophysiological roles in disease models. This review describes recent advances in understanding the associations of CerS with various diseases and includes clinical case reports.

scholarly journals Polyunsaturated Fatty Acids Stimulate De novo Lipogenesis and Improve Glucose Homeostasis during Refeeding with High Fat Diet

2017 ◽  
Vol 8 ◽  
Author(s):  
Raffaella Crescenzo ◽  
Arianna Mazzoli ◽  
Rosa Cancelliere ◽  
Francesca Bianco ◽  
Antonia Giacco ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
De Novo ◽  
De Novo Lipogenesis ◽  
High Fat

scholarly journals Sphingosine-1-phosphate receptor subtype 1 activation in the central nervous system contributes to morphine withdrawal in rodents

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Timothy M. Doyle ◽  
Mark R. Hutchinson ◽  
Kathryn Braden ◽  
Kali Janes ◽  
Vicky Staikopoulos ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Side Effects ◽  
De Novo ◽  
Morphine Withdrawal ◽  
Sphingolipid Metabolism ◽  
Receptor Subtype ◽  
Precipitated Withdrawal ◽  
Sphingosine 1 Phosphate ◽  
Withdrawal Behaviors ◽  
The Impact

Abstract Opioid therapies for chronic pain are undermined by many adverse side effects that reduce their efficacy and lead to dependence, abuse, reduced quality of life, and even death. We have recently reported that sphingosine-1-phosphate (S1P) 1 receptor (S1PR1) antagonists block the development of morphine-induced hyperalgesia and analgesic tolerance. However, the impact of S1PR1 antagonists on other undesirable side effects of opioids, such as opioid-induced dependence, remains unknown. Here, we demonstrate that naloxone-precipitated morphine withdrawal in mice altered de novo sphingolipid metabolism in the dorsal horn of the spinal cord and increased S1P that accompanied the manifestation of several withdrawal behaviors. Blocking de novo sphingolipid metabolism with intrathecal administration of myriocin, an inhibitor of serine palmitoyltransferase, blocked naloxone-precipitated withdrawal. Noteworthy, we found that competitive (NIBR-15) and functional (FTY720) S1PR1 antagonists attenuated withdrawal behaviors in mice. Mechanistically, at the level of the spinal cord, naloxone-precipitated withdrawal was associated with increased glial activity and formation of the potent inflammatory/neuroexcitatory cytokine interleukin-1β (IL-1β); these events were attenuated by S1PR1 antagonists. These results provide the first molecular insight for the role of the S1P/S1PR1 axis during opioid withdrawal. Our data identify S1PR1 antagonists as potential therapeutics to mitigate opioid-induced dependence and support repurposing the S1PR1 functional antagonist FTY720, which is FDA-approved for multiple sclerosis, as an opioid adjunct.

scholarly journals Toxoplasma gondiisalvages sphingolipids from the host Golgi through the rerouting of selected Rab vesicles to the parasitophorous vacuole

2013 ◽  
Vol 24 (12) ◽  
pp. 1974-1995 ◽  
Author(s):  
Julia D. Romano ◽  
Sabrina Sonda ◽  
Emily Bergbower ◽  
Maria Elisa Smith ◽  
Isabelle Coppens
Keyword(s):  
Toxoplasma Gondii ◽  
Mammalian Cells ◽  
De Novo ◽  
Parasitophorous Vacuole ◽  
Parasite Growth ◽  
Sphingolipid Metabolism ◽  
Obligate Intracellular ◽  
Membrane Bound ◽  
Parasite Replication

The obligate intracellular protozoan Toxoplasma gondii actively invades mammalian cells and, upon entry, forms its own membrane-bound compartment, named the parasitophorous vacuole (PV). Within the PV, the parasite replicates and scavenges nutrients, including lipids, from host organelles. Although T. gondii can synthesize sphingolipids de novo, it also scavenges these lipids from the host Golgi. How the parasite obtains sphingolipids from the Golgi remains unclear, as the PV avoids fusion with host organelles. In this study, we explore the host Golgi–PV interaction and evaluate the importance of host-derived sphingolipids for parasite growth. We demonstrate that the PV preferentially localizes near the host Golgi early during infection and remains closely associated with this organelle throughout infection. The parasite subverts the structure of the host Golgi, resulting in its fragmentation into numerous ministacks, which surround the PV, and hijacks host Golgi–derived vesicles within the PV. These vesicles, marked with Rab14, Rab30, or Rab43, colocalize with host-derived sphingolipids in the vacuolar space. Scavenged sphingolipids contribute to parasite replication since alterations in host sphingolipid metabolism are detrimental for the parasite's growth. Thus our results reveal that T. gondii relies on host-derived sphingolipids for its development and scavenges these lipids via Golgi-derived vesicles.

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