Biochimica et biophysica acta. Molecular and cell biology of lipids最新文献

{"title":"Blood and tissue docosahexaenoic acid (DHA, 22:6n-3) turnover rates from Ahiflower® oil are not different than from DHA ethyl ester oil in a diet switch mouse model","authors":"Adam H. Metherel ,&nbsp;Brinley J. Klievik ,&nbsp;Giulia Cisbani ,&nbsp;Mackenzie E. Smith ,&nbsp;Greg Cumberford ,&nbsp;Richard P. Bazinet","doi":"10.1016/j.bbalip.2023.159422","DOIUrl":"10.1016/j.bbalip.2023.159422","url":null,"abstract":"<div><p><span>Ahiflower® oil is high in α-linolenic and stearidonic acids, however, tissue/blood docosahexaenoic acid (DHA, 22:6n-3) turnover from dietary Ahiflower oil has not been investigated. In this study, we use compound-specific isotope analysis to determine tissue DHA synthesis/turnover from Ahiflower, flaxseed and DHA oils. Pregnant BALB/c mice (13–17 days) were placed on a 2 % algal DHA oil diet of high carbon-13 content (δ</span>¹³C) and pups (<em>n</em> = 132) were maintained on the diet until 9 weeks old. Mice were then randomly allocated to a low δ¹³C-n-3 PUFA diet of either: 1) 4 % Ahiflower oil, 2) 4.35 % flaxseed oil or 3) 1 % fish DHA ethyl ester oil for 1, 3, 7, 14, 30, 60 or 120 days (<em>n</em> = 6). Serum, liver, adipose and brains were collected and DHA levels and δ¹³C were determined. DHA concentrations were highest (<em>p</em> &lt; 0.05) in the liver and adipose of DHA-fed animals with no diet differences in serum or brain (<em>p</em> &gt; 0.05). Based on the presence or absence of overlapping 95 % C.I.'s, DHA half-lives and synthesis/turnover rates were not different between Ahiflower and DHA diets in the liver, adipose or brain. DHA half-lives and synthesis/turnover rates from flaxseed oil were significantly slower than from the DHA diet in all serum/tissues. These findings suggest that the distinct Ahiflower oil n-3 PUFA composition could support tissue DHA needs at a similar rate to dietary DHA, making it a unique plant-based dietary option for maintaining DHA turnover comparably to dietary DHA.</p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136396015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanism of calcitriol enhances membrane water permeability","authors":"Zanxia Cao,&nbsp;Liling Zhao,&nbsp;Mingcui Chen,&nbsp;Zhihong Shi,&nbsp;Lei Liu","doi":"10.1016/j.bbalip.2023.159430","DOIUrl":"10.1016/j.bbalip.2023.159430","url":null,"abstract":"<div><p><span><em>Helicobacter pylori</em></span> (<em>H. pylori</em><span>) exhibits a unique membrane lipid<span> composition, including dimyristoyl phosphatidylethanolamine<span><span> (DMPE) and cholesterol, unlike other Gram-negative bacteria. Calcitriol has </span>antimicrobial activity against </span></span></span><em>H. pylori</em><span>, but cholesterol enhances antibiotics resistance in </span><em>H. pylori</em><span><span>. This study explored the changes in membrane structure and the molecular mechanisms of cholesterol/calcitriol translocation using well-tempered </span>metadynamics<span><span><span> (WT-MetaD) simulations and microsecond conventional molecular dynamics (CMD) simulations. Calcitriol facilitated water transport across the membrane, while cholesterol had the opposite effect. The differing effects might result from the tail 25-hydroxyl group and a wider range of orientations of calcitriol in the DMPE/dimyristoyl phosphatidylglycerol (DMPG) (3:1) membrane. Calcitriol moves across the </span>bilayer<span> center without changing its orientation along the membrane Z-axis, becomes parallel to the membrane surface at the membrane-water interface, and then rotates approximately 90° in this interface. The translocation mechanism of calcitriol is quite different from the flip-flop of cholesterol. Moreover, calcitriol crossed from one layer to another more easily than cholesterol, causing successive perturbations to the hydrophobic core and increasing water permeation. These results improve our understanding of the relationship between cholesterol/calcitriol concentrations and the lipid bilayer structure and the role of </span></span>lipid composition in water permeation.</span></span></p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138046126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lauric acid epigenetically regulates lncRNA HOTAIR by remodeling chromatin H3K4 tri-methylation and modulates glucose transport in SH-SY5Y human neuroblastoma cells: Lipid switch in macrophage activation","authors":"Venkatesan Ramya ,&nbsp;Karuppiah Prakash Shyam ,&nbsp;Arulanandu Angelmary ,&nbsp;Balamuthu Kadalmani","doi":"10.1016/j.bbalip.2023.159429","DOIUrl":"10.1016/j.bbalip.2023.159429","url":null,"abstract":"<div><p><span><span><span>Lauric acid (LA) induces apoptosis in cancer and promotes the proliferation of normal cells by maintaining cellular redox </span>homeostasis<span>. Earlier, we postulated LA-mediated regulation of the NF-κB pathway by an epigenetic mechanism<span><span>. However, the molecular mechanism and possible epigenetic events remained enigmatic. Herein, taking the lead from the alteration in cellular energetics in cancer cells upon LA exposure, we investigated whether LA exposure can epigenetically influence </span>lncRNA </span></span></span>HOTAIR<span>, regulate glucose metabolism<span>, and shift the cellular energetic state. Our results demonstrate LA induced modulation of lncRNA HOTAIR in a dose and time dependent manner. In addition, HOTAIR induces the expression of glucose transporter isoform 1 (GLUT1) and is regulated </span></span></span><em>via</em> NF-κB activation. Silencing HOTAIR by siRNA-mediated knockdown suppressed GLUT1 expression suggesting the key role of HOTAIR in LA-mediated metabolic reprogramming. Further, from our ChIP experiments, we observed that silencing HOTAIR subdues the recruitment of NF-κB on the GLUT1 (<em>SLC2A1</em><span><span><span>) promoter region. In addition, by performing western blot and </span>immunocytochemistry<span><span> studies, we found a dose dependent increase in Histone 3 Lysine 4 tri-methylation (H3K4me3) in the chromatin landscape. Taken together, our study demonstrates the epigenetic regulation in LA-treated SH-SY5Y cancer cells orchestrated by </span>remodeling chromatin H3K4me3 and modulation of lncRNA HOTAIR that apparently governs the GLUT1 expression and regulates </span></span>glucose uptake by exerting transcriptional control on NF-κB activation. Our work provides insights into the epigenetic regulation and metabolic reprogramming of LA through modulation of lncRNA HOTAIR, remodeling chromatin H3K4 tri-methylation, and shifting the energy metabolism in SH-SY5Y neuroblastoma cells.</span></p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134648310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRISPR/Cas9-meditated gene knockout in pigs proves that LGALS12 deficiency suppresses the proliferation and differentiation of porcine adipocytes","authors":"Wenjing Wu ,&nbsp;Yajun Yin ,&nbsp;Jing Huang ,&nbsp;Ruifei Yang ,&nbsp;Qiuyan Li ,&nbsp;Jianzhi Pan ,&nbsp;Jin Zhang","doi":"10.1016/j.bbalip.2023.159424","DOIUrl":"10.1016/j.bbalip.2023.159424","url":null,"abstract":"<div><p>LGALS12, also known as galectin12, belongs to the galectin family with β-galactoside-binding activity. We previously reported that LGALS12 is an important regulator of adipogenesis in porcine adipocytes in vitro, but its value in pig breeding needed to be explored in vivo. In this study, we used CRISPR/Cas9 to construct porcine fetal fibroblasts (PFFs) with a 43 bp deletion in LGALS12 exon 2. Using these PFFs as donor cells, a LGALS12 knockout pig model was generated via somatic cell nuclear transfer. Primary cultures of porcine intramuscular (IM) and subcutaneous (SC) adipocytes were established using cells from LGALS12 knockout pigs and wild-type pigs. A comparison of these cells proved that LGALS12 deficiency suppresses cell proliferation via the RAS-p38MAPK pathway and promotes lipolysis via the PKA pathway in both IM and SC adipocytes. In addition, we observed AKT activation only in IM adipocytes and suppression of the Wnt/β-catenin only in SC adipocytes. Our findings suggest that LGALS12 deficiency affects the adipogenesis of IM and SC adipocytes through different mechanisms.</p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92152586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of angiogenic switch in reprogramming browning and lipid metabolism in white adipocytes","authors":"Sreelekshmi Sreekumar ,&nbsp;Karyath Palliyath Gangaraj ,&nbsp;Manikantan Syamala Kiran","doi":"10.1016/j.bbalip.2023.159423","DOIUrl":"10.1016/j.bbalip.2023.159423","url":null,"abstract":"<div><p>Thermogenic activation <em>via</em> trans-and <em>de novo</em><span> browning of white adipocytes is a promising strategy to accelerate lipid metabolism for regulating obesity-related disorders. In this study, we investigated the intricate interplay between angiogenic regulation and browning in white adipocytes using the bioactive compound, resveratrol (Rsv). Rsv has previously been documented for its regulatory influence on the trans and </span><em>de novo</em><span> browning of white adipocytes. Our findings revealed that concurrent activation of angiogenesis is prerequisite for inducing browning within the microenvironment of white adipocytes when exposed to browning activators. Additionally, we observed a significant browning effect on white adipocytes when the local adipose tissue environment was prompted to undergo angiogenesis, notably facilitated by a proangiogenic molecule known as Vascular endothelial growth factor (VEGF). Intriguingly, this effect was reversed when angiogenesis was inhibited by treatment with the antiangiogenic agent thalidomide. Furthermore, the study revealed the role of VEGF in paracrine activation of white adipocytes resulting in the induction of browning in both 3T3-L1 cell lines and primary mouse white adipocytes. The cross-talk between angiogenesis and browning was found to be initiated </span><em>via</em><span><span> the transcriptional activation<span> of Estrogen receptor α (ERα) triggering the VEGF/VEGFR2 </span></span>signaling pathway leading to browning and a reconfiguration of lipid metabolism within adipocytes. In conclusion, this study sheds light on the intricate cross-talk between angiogenesis and browning of white adipocytes. Notably, the findings underscore the reciprocal relationship between these processes, wherein inhibition of one process exerts discernible effects on the other.</span></p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92152587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Docosahexaenoic acid (DHA) inhibits abdominal fat accumulation by promoting adipocyte apoptosis through PPARγ-LC3-BNIP3 pathway-mediated mitophagy","authors":"Chenchen Bian ,&nbsp;Xiangtong Yuan ,&nbsp;Caihong Zeng ,&nbsp;Jian Sun ,&nbsp;Gen Kaneko ,&nbsp;Hong Ji","doi":"10.1016/j.bbalip.2023.159425","DOIUrl":"10.1016/j.bbalip.2023.159425","url":null,"abstract":"<div><p><span>Obesity has always been an overwhelming health concern worldwide. Docosahexaenoic acid<span><span> (DHA) reduces abdominal fat accumulation<span> by inducing adipocyte apoptosis, but the underlying mechanism remains unclear. Mitophagy, the process of maintaining mitochondrial </span></span>homeostasis<span>, has a double-edged sword effect that positively or negatively regulates apoptosis. In this study, grass carp (</span></span></span><em>Ctenopharyngodon idellus</em><span><span>) was used as an animal model to investigate the role of mitophagy in regulating apoptosis and the potential molecular mechanisms for DHA-induced mitophagy in vivo and in vitro. Firstly, we found that DHA induced the </span>intrinsic apoptosis<span> in grass carp adipocytes, accompanying by activating BNIP3/NIX-mediated mitophagy. Then, suppression of mitophagy alleviated apoptosis and eliminated the inhibition of lipid accumulation induced by DHA in vivo and in vitro. Mechanistically, the DHA-induced mitophagy was caused by activating PPARγ<span> and its DNA binding capacity to the LC3 promoter, which promoted the interaction of BNIP3 (rather than NIX) with LC3. However, the inhibition of PPARγ in vitro significantly decreased the expression of autophagy-related genes (</span></span></span><em>P</em><span> &lt; 0.05), reducing the colocalization of mitochondria and lysosomes while preventing BNIP3/NIX-mediated mitophagy-mediated apoptosis and subsequently alleviating the inhibition of lipid accumulation in adipocytes induced by DHA. For the first time, we demonstrated that DHA activates mitophagy by regulating the PPARγ-LC3-BNIP3 pathway, consequently inducing apoptosis, which decreases adipocytes, inhibiting lipid accumulation in grass carp. These findings provide new insight into the mechanism of DHA-induced apoptosis mediated by mitophagy as the potential therapeutic target of inhibiting abdominal fat accumulation in vertebrates.</span></p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89716756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obesity induced disruption on diurnal rhythm of insulin sensitivity via gut microbiome-bile acid metabolism","authors":"Xiaozhen Guo ,&nbsp;Jiawen Wang ,&nbsp;Hualing Xu ,&nbsp;Yangyang Wang ,&nbsp;Yutang Cao ,&nbsp;Yingquan Wen ,&nbsp;Jiaqi Li ,&nbsp;Yameng Liu ,&nbsp;Kanglong Wang ,&nbsp;Jue Wang ,&nbsp;Xianchun Zhong ,&nbsp;Chuying Sun ,&nbsp;Yongxin Zhang ,&nbsp;Jingyi Xu ,&nbsp;Cuina Li ,&nbsp;Pengxiang Mu ,&nbsp;Lingyan Xu ,&nbsp;Cen Xie","doi":"10.1016/j.bbalip.2023.159419","DOIUrl":"10.1016/j.bbalip.2023.159419","url":null,"abstract":"<div><p><span>The disruption of the diurnal rhythm has been recognized as a significant contributing factor to metabolic dysregulation. The important role of gut microbiota<span><span> and bile acid metabolism has attracted extensive attention. However, the function of the gut microbiota-bile acid axis in regulating the diurnal rhythms of metabolic </span>homeostasis remains largely unknown. Herein, we aimed to investigate the interplay between rhythmicity of host metabolism and gut microbiota-bile acid axis, as well as to assess the impact of obesity on them. We found that high fat diet feeding and </span></span><em>Leptin</em> gene deficiency (<em>ob/ob</em><span><span><span>) significantly disturbed the rhythmic patterns of insulin sensitivity and serum </span>total cholesterol levels<span>. The bile acid profiling unveiled a conspicuous diurnal rhythm oscillation of </span></span>ursodeoxycholic acid<span><span> (UDCA) in lean mice, concomitant with fluctuations in insulin sensitivity, whereas it was absent in </span>obese mice<span>. The aforementioned diurnal rhythm oscillations were largely desynchronized by gut microbiota depletion, suggesting the indispensable role of gut microbiota in diurnal regulation of insulin sensitivity and bile acid metabolism. Consistently, 16S rRNA sequencing revealed that UDCA-associated bacteria exhibited diurnal rhythm oscillations that paralleled the fluctuation in insulin sensitivity. Collectively, the current study provides compelling evidence regarding the association between diurnal rhythm of insulin sensitivity and gut microbiota-bile acid axis. Moreover, we have elucidated the deleterious effects of obesity on gut microbiome-bile acid metabolism in both the genetic obesity model and the diet-induced obesity model.</span></span></span></p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89716757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PNPLA-mediated lipid hydrolysis and transacylation – At the intersection of catabolism and anabolism","authors":"Mariana Colaço-Gaspar ,&nbsp;Peter Hofer ,&nbsp;Monika Oberer ,&nbsp;Rudolf Zechner","doi":"10.1016/j.bbalip.2023.159410","DOIUrl":"10.1016/j.bbalip.2023.159410","url":null,"abstract":"<div><p>Patatin-like phospholipase domain containing proteins (PNPLAs) play diverse roles in lipid metabolism. In this review, we focus on the enzymatic properties and predicted 3D structures of PNPLA1-5. PNPLA2-4 exert both catabolic and anabolic functions. Whereas PNPLA1 is predominantly expressed in the epidermis and involved in sphingolipid biosynthesis, PNPLA2 and 4 are ubiquitously expressed and exhibit several enzymatic activities, including hydrolysis and transacylation of various (glycero-)lipid species. This review summarizes known biological roles for PNPLA-mediated hydrolysis and transacylation reactions and highlights open questions concerning their physiological function.</p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1388198123001348/pdfft?md5=5883a92590a14f2d45e8121e7133de8c&pid=1-s2.0-S1388198123001348-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89716758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abnormal expression of sphingolipid-metabolizing enzymes in the heart of spontaneously hypertensive rat models","authors":"Giuseppe Pepe ,&nbsp;Maria Cotugno ,&nbsp;Federico Marracino ,&nbsp;Luca Capocci ,&nbsp;Ludovica Pizzati ,&nbsp;Maurizio Forte ,&nbsp;Rosita Stanzione ,&nbsp;Pamela Scarselli ,&nbsp;Alba Di Pardo ,&nbsp;Sebastiano Sciarretta ,&nbsp;Massimo Volpe ,&nbsp;Speranza Rubattu ,&nbsp;Vittorio Maglione","doi":"10.1016/j.bbalip.2023.159411","DOIUrl":"10.1016/j.bbalip.2023.159411","url":null,"abstract":"<div><p><span><span>Sphingolipids exert important roles within the cardiovascular system and related diseases. Perturbed </span>sphingolipid metabolism was previously reported in cerebral and renal tissues of </span>spontaneously hypertensive rats (SHR). Specific defects related to the synthesis of sphingolipids and to the metabolism of Sphingosine-1-Phospahte (S1P) were exclusively identified in the stroke-prone (SHRSP) with the respect to the stroke-resistant (SHRSR) strain.</p><p>In this study, we explored any existing perturbation in either protein or gene expression of enzymes involved in the sphingolipid pathways in cardiac tissue from both SHRSP and SHRSR strains, compared to the normotensive Wistar Kyoto (WKY) strain.</p><p><span><span>The two hypertensive rat models showed an overall perturbation of the expression of different enzymes involved in the sphingolipid metabolism in the heart. In particular, whereas the expression of the S1P-metabolizing-enzyme, SPHK2, was significantly reduced in both SHR strains, SGPL1 protein levels were decreased only in SHRSP. The protein levels of </span>S1P receptors 1–3 were reduced only in the cardiac tissue of SHRSP, whereas S1PR2 levels were reduced in both SHR strains. The </span><em>de novo</em> synthesis of sphingolipids was aberrant in the two hypertensive strains. A significant reduction of mRNA expression of the <span><em>Sgms1</em></span> and <span><em>Smpd3</em></span><span> enzymes, implicated in the metabolism of sphingomyelin, was found in both hypertensive strains. Interestingly, </span><em>Smpd2</em>, devoted to sphingomyelin degradation, was reduced only in the heart of SHRSP.</p><p>In conclusion, alterations in the expression of sphingolipid-metabolizing enzymes may be involved in the susceptibility to cardiac damage of hypertensive rat strains. Specific differences detected in the SHRSP, however, deserve further elucidation.</p></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72208230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Dehydroepiandrosterone reduces accumulation of lipid droplets in primary chicken hepatocytes by biotransformation mediated via the cAMP/PKA-ERK1/2 signaling pathway” [BBA Mol. Cell Biol. Lipids 1863 (2018) 625–638]","authors":"Longlong Li,&nbsp;Chongyang Ge,&nbsp;Dian Wang,&nbsp;Lei Yu,&nbsp;Jinlong Zhao,&nbsp;Haitian Ma","doi":"10.1016/j.bbalip.2023.159408","DOIUrl":"https://doi.org/10.1016/j.bbalip.2023.159408","url":null,"abstract":"","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49819144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}