Adipose triglyceride lipase regulates lipid metabolism in dairy goat mammary epithelial cells

Adipose triglyceride lipase (ATGL) catalyzes the initial step in the lipid lipolysis process, hydrolyzing triglyceride (TG) to produce diacylglycerol (DG) and free fatty acids (FFA). In addition, ATGL regulates lipid storage and release in adipocyte cells. However, its role in mammary gland tissue remains unclear. To assess the role of the ATGL gene in the goat mammary gland, this study analyzed the tissue distribution and expression of key genes together with lipid accumulation after knockdown of the ATGL gene. The mRNA of ATGL was highly expressed in subcutaneous adipose tissue, the lung and the mammary gland with a significant increase in expression during the lactation period compared with the dry period of the mammary gland. Knockdown of the ATGL gene in goat mammary epithelial cells (GMECs) using siRNA resulted in a significant decrease in both ATGL mRNA and protein levels. Silencing of the ATGL gene markedly increased lipid droplet accumulation and intracellular TG concentration (P < 0.05), while it reduced FFA levels in GMECs (P < 0.05). Additionally, the expression of HSL for lipolysis, FABP3 for fatty acid transport, PPARα for fatty acid oxidation, ADFP, BTN1A1, and XDH for milk fat formation and secretion was down-regulated (P < 0.05) after knockdown of the ATGL gene, with increased expression of CD36 for fatty acid uptake (P < 0.05). In conclusion, these data suggest that the ATGL gene plays an important role in triglyceride lipolysis in GMECs and provides the first experimental evidence that ATGL may be involved in lipid metabolism during lactation.     

Meishan neonatal piglets tend to have higher intestinal barrier function than crossbred neonatal piglets

Meishan pigs tend to have higher disease resistance than commercial breeds, although more studies are needed to confirm this difference. This study compared intestinal barrier function between Meishan and crossbred neonatal piglets to provide guidance for both the breeding and nutritional regulation of pigs. Six Meishan piglets and 6 Duroc × (Landrace × Yorkshire) crossbred neonatal piglets (all with normal birth weights) were obtained and allocated into the MEIS and CROSS groups, respectively. Intestinal morphology, goblet cell numbers, antioxidant enzyme activity, and cytokine gene and tight junction protein expression were assessed. The results showed that BW was lower in the MEIS group than in the CROSS group (P < 0.01). The relative lengths of the duodenum (P < 0.05), jejunum (P < 0.01) and ileum (P < 0.01) in the MEIS group were higher than those in the CROSS group. Compared with the CROSS group, the MEIS group exhibited shorter villus lengths in the duodenum and jejunum (P < 0.01), a shallower crypt depth in the ileum (P < 0.001) and denser and longer microvilli in the intestine. The numbers of GCs in the duodenum (P < 0.01) and jejunum (P < 0.001) and the activity levels of glutathione peroxidase (P < 0.05) in the jejunum and of catalase (P < 0.01) and superoxide dismutase (P < 0.01) in the ileum were higher in the MEIS group than in the CROSS group. Compared with the CROSS group, the MEIS group exhibited higher gene expression levels of interleukin (IL) 4 and interferon γ (IFNγ) in the jejunum (P < 0.05); IL2 (P < 0.05), IL4 (P < 0.01) and IFNγ (P < 0.001) in the ileum; and mucin 2 (P < 0.01) and occludin (P < 0.05) in the duodenum. In conclusion, Meishan neonatal piglets showed lower birth weights but higher intestinal barrier function than crossbred piglets.     

Ectopic overexpression of swine PPARγ2 upregulated adipocyte genes expression and triacylglycerol in skeletal muscle of mice

Peroxisome proliferator-activated receptor ??2 (PPAR??2) is a key regulator of adipocyte differentiation, fatty acid uptake and storage in mammals. The primary goal of the present study was to investigate the consequences of PPAR??2 overexpression in the muscle. A swine muscle creatine kinase promoter was used to drive swine PPAR??2 (sPPAR??2) overexpression in the muscle of a transgenic mice model. The results showed that the mRNA of multiple adipocyte genes was increased in the skeletal muscle, as evidenced by the up-regulation of fatty acid synthase (2.11-fold, P?<?0.05), lipoprotein lipase (2.08-fold, P?<?0.01), fatty acid-binding protein 4 (14.30-fold, P?<?0.01), and CD36 antigen (5.50-fold, P?<?0.01). Meanwhile, skeletal muscle triacylglycerol was increased (P?<?0.01) and the fatty acid profile of muscle fat was changed in that more polyunsaturated fats acid were augmented. The present study may further serve to develop transgenic pigs with higher intramuscular fat content and improved pork quality.     

Effects of dietary conjugated linoleic acid on metabolic status,BW and expression of genes related to lipid metabolism in adipose tissue of dairy cows during peripartum

Conjugated linoleic acid (CLA) dietary supplementation reduces milk fat content and yield, but its effects on lipid metabolism and energy status remain controversial. The objective of this study was to investigate the effects of dietary CLA on adipose tissue (AT) mRNA abundance of genes related to lipid metabolism, plasma indicators of metabolic status, body condition score (BCS) and BW changes in dairy cows. Sixteen multiparous Holstein cows (3.2 ± 1.4 lactations, 615 ± 15 kg BW) were randomly assigned to treatments: 1) CLA; rumen-protected CLA (75 g/d) or 2) Control; equivalent amount of rumen inert fatty acid (FA) as the previous diet (78 g/d), from − 20.2 ± 3.2 (mean ± SEM) to 21 d relative to calving (d 0). Subcutaneous AT was biopsied from the tail-head region at d 21 to determine the mRNA abundance of genes related to lipid metabolism. Blood samples were collected at − 20.2 ± 3.2, 0, 7, 14 and 21 d relative to calving to determine plasma non-esterified fatty acids (NEFA), beta-hydroxybutyrate (BHBA), insulin and glucose. Conjugated linoleic acid decreased milk fat yield and milk fat content by 15 and 16%, respectively. Cows fed CLA had lower plasma NEFA and BHBA and greater glucose and insulin concentrations (P < 0.05). Mean BCS at 21 d postpartum was greater (P < 0.01; 2.89 vs 2.25), and BCS loss from the day of enrollment to 21 d postpartum was reduced (P < 0.01; − 0.13 vs − 0.64) in the CLA group. The expression of acylcoenzyme A oxidase, carnitine palmitoyltransferase 1A, hormone-sensitive lipase, β2 adrenergic receptor and acetyl-CoA carboxylase was downregulated by CLA supplementation, whereas the expression of sterol regulatory element binding protein, lipoprotein lipase and peroxisome proliferator-activated receptor gamma was upregulated (P < 0.01). In summary, CLA-supplemented cows showed signs of better metabolic status and less severe fat mobilization. Moreover, CLA increased mRNA abundance of genes related to lipogenesis and decreased mRNA abundance of genes related to FA oxidation and lipolysis in the AT of dairy cows during early lactation.     

Anti-adipogenic activity of compounds isolated from Idesia polycarpa on 3T3-L1 cells

Recently, obesity is a complex multifactorial chronic disease increasing the risk for type 2 diabetes, coronary heart disease and hypertension, and has become a major worldwide health problem. In the course of screening natural products employing 3T3-L1 cells as an in vitro system, the methanol extract of Idesia polycarpa Maxim. Fruits (Flacourtiaceae) significantly inhibited adipocyte differentiation by measuring lipid contents using oil red O staining. One new compound, 6-(oxymethyl)-2-hydroxyphenyl-O-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranoside (8), was isolated along with nine known compounds (1–7 and 9–10) from CHCl₃ and n-BuOH fractions of the methanol extract of I. polycarpa fruits. Among them, idescarpin (1) with 1-hydroxy-6-oxo-2-cyclohexenecarboxylate moiety showed the most potent inhibitory activity on adipocyte differentiation with IC₅₀ values of 23.2 μM. Idescarpin (1) dramatically suppressed the induction of C/EBPα expression, whereas it significantly increased the induction of PPARγ expression, supported by quantitative real time PCR and Western blot analysis. The down-regulation in mRNA levels of SREBP1c, SCD-1, and FAS by idescarpin (1) during adipocyte differentiation revealed that the inhibition of adipocyte differentiation was mediated by the regulation of lipogenesis. Taken together, we suggest that idescarpin (1) shows a great potential against obesity and diabetes though the anti-adipogenic activity and the up-regulation of PPARγ.     

SR-BI deficiency disassociates obesity from hepatic steatosis and glucose intolerance development in high fat diet-fed mice

Scavenger receptor BI (SR-BI) has been suggested to modulate adipocyte function. To uncover the potential relevance of SR-BI for the development of obesity and associated metabolic complications, we compared the metabolic phenotype of wild-type and SR-BI deficient mice fed an obesogenic diet enriched in fat. Both male and female SR-BI knockout mice gained significantly more weight as compared to their wild-type counterparts in response to 12 weeks high fat diet feeding (1.5-fold; P < .01 for genotype). Plasma free cholesterol levels were ~2-fold higher (P < .001) in SR-BI knockout mice of both genders, whilst plasma cholesteryl ester and triglyceride concentrations were only significantly elevated in males. Strikingly, the exacerbated obesity in SR-BI knockout mice was paralleled by a better glucose handling. In contrast, only SR-BI knockout mice developed atherosclerotic lesions in the aortic root, with a higher predisposition in females. Biochemical and histological studies in male mice revealed that SR-BI deficiency was associated with a reduced hepatic steatosis degree as evident from the 29% lower (P < .05) liver triglyceride levels. Relative mRNA expression levels of the glucose uptake transporter GLUT4 were increased (+47%; P < .05), whilst expression levels of the metabolic PPARgamma target genes CD36, HSL, ADIPOQ and ATGL were reduced 39%–58% (P < .01) in the context of unchanged PPARgamma expression levels in SR-BI knockout gonadal white adipose tissue. In conclusion, we have shown that SR-BI deficiency is associated with a decrease in adipocyte PPARgamma activity and a concomitant uncoupling of obesity development from hepatic steatosis and glucose intolerance development in high fat diet-fed mice.     

Modest hypoxia significantly reduces triglyceride content and lipid droplet size in 3T3-L1 adipocytes

Background

A previous study has demonstrated that endurance training under hypoxia results in a greater reduction in body fat mass compared to exercise under normoxia. However, the cellular and molecular mechanisms that underlie this hypoxia-mediated reduction in fat mass remain uncertain. Here, we examine the effects of modest hypoxia on adipocyte function.

Methods

Differentiated 3T3-L1 adipocytes were incubated at 5% O₂ for 1 week (long-term hypoxia, HL) or one day (short-term hypoxia, HS) and compared with a normoxia control (NC).

Results

HL, but not HS, resulted in a significant reduction in lipid droplet size and triglyceride content (by 50%) compared to NC (p < 0.01). As estimated by glycerol release, isoproterenol-induced lipolysis was significantly lowered by hypoxia, whereas the release of free fatty acids under the basal condition was prominently enhanced with HL compared to NC or HS (p < 0.01). Lipolysis-associated proteins, such as perilipin 1 and hormone-sensitive lipase, were unchanged, whereas adipose triglyceride lipase and its activator protein CGI-58 were decreased with HL in comparison to NC. Interestingly, such lipogenic proteins as fatty acid synthase, lipin-1, and peroxisome proliferator-activated receptor gamma were decreased. Furthermore, the uptake of glucose, the major precursor of 3-glycerol phosphate for triglyceride synthesis, was significantly reduced in HL compared to NC or HS (p < 0.01).

Conclusion

We conclude that hypoxia has a direct impact on reducing the triglyceride content and lipid droplet size via decreased glucose uptake and lipogenic protein expression and increased basal lipolysis. Such an hypoxia-induced decrease in lipogenesis may be an attractive therapeutic target against lipid-associated metabolic diseases.     

Expression of key myogenic,fibrogenic and adipogenic genes in Longissimus thoracis and Masseter muscles in cattle

Adipogenesis, myogenesis and fibrogenesis are related processes that can contribute to meat quality. Therefore, extending the knowledge of these processes would facilitate the identification of molecular markers that predict intramuscular fat accretion. The main purpose of this work, based on previous results, was to further study the expression of key genes related to adipogenic, myogenic, fibrogenic processes and some cytokines in Longissimus thoracis (LT) and Masseter (MS) muscles of Pirenaica and Holstein young bulls. Longissimus thoracis and MS muscles from Pirenaica (n = 4) and Spanish Holstein (n = 4) were sampled for proximate analysis, determination of adipocyte size distribution and expression of key candidate genes. Fat percentage was lower in LT than in MS muscle in Pirenaica young bulls (P = 0.023) and was higher in LT muscle in Holstein than in Pirenaica young bulls (P = 0.007). Gene expression analysis revealed that the mRNA level of myogenic differentiation 1 (MYOD) was higher in LT than in MS muscles in both groups of animals (P < 0.001) and that myostatin (MSTN) expression was also higher in LT than in MS muscle in Holstein bulls (P = 0.001). On the other hand, MSTN and PPARG showed higher expression in LT and MS in Pirenaica young bulls (P = 0.026), while the expression of fatty acid-binding protein 4 (FABP4) was higher in Holstein young bulls, also in both muscles (P < 0.001). The results suggested that the development of intramuscular adipose depot was directly related to the expression of adipogenic genes, such as FABP4, but inversely related to the expression of the cytokine MSTN and the myogenic gene MYOD, genes which showed a muscle-specific expression.     

Growth performance,nutrient digestibility,blood parameters,and carcass characteristics by lambs fed an oregano and cobalt blend

Shifting ruminal fermentation via feeding a blend of oregano (Organum vulgare L.) essential oils and Co-lactate (EOC; Rum-A-Fresh, Ralco, Inc. Marshall, MN) could improve lamb growth and carcass performance. Eighteen Suffolk × Little Han Tail F1 male lambs (20.3 ± 0.23 kg BW and approximately 3 months old) were randomly assigned using a completely random design to one of three treatments. Treatments were (1) EOC0: basal ration without EOC, (2) EOC4: basal ration plus 4 g/d EOC, and (3) EOC7: basal ration plus 7 g/d EOC. Initial and 24 d BW was similar (P > 0.10), but at 48 and 72 d, lambs fed EOC7 demonstrated greater (P = 0.01) BW compared with EOC0 fed lambs, while lambs fed EOC4 were intermediate and similar (P > 0.05). Average daily gains (ADGs) for 0–24 and 0–72 d were greater (P < 0.05) for lambs fed EOC4 and EOC7 compared with lambs fed EOC0, while DM intake was similar (P > 0.10). Feed conversions for 0–24 d were improved (P < 0.02) for lambs fed EOC4 and EOC7 compared with lambs fed EOC0. However, 0–72-d feed conversions were greater (P < 0.01) for lambs fed EOC7 compared to lambs fed EOC0, with lambs fed EOC4 being intermediate and similar (P > 0.05). DM, NDF, and ADF digestibilities were similar (P > 0.10) among treatments, while CP digestibility was greater (P < 0.01) for lambs fed EOC4 and EOC7 compared with lambs fed EOC0. Carcass weight and dressing percentages were improved (P < 0.01) for lambs fed EOC7 compared with lambs fed EOC0 and EOC4. Head width was greater (P > 0.01) for lambs fed EOC7 compared with lambs fed EOC0 and EOC4, while rump width was greater (P > 0.01) for lambs fed EOC4 and EOC7 compared with lambs fed EOC0. Plasma triglyceride and cholesterol concentrations were lower (P < 0.05) for lambs fed EOC4 and EOC7 compared with lambs fed EOC0, while albumin, total serum protein, and glucose concentrations were greater (P < 0.05) for lambs fed EOC4 and EOC7 compared with lambs fed EOC0. Feeding an EOC blend as an alternative antibiotic growth promoter at 4 and 7 g/d linearly improved lamb growth performance, feed conversions, frame growth, carcass weights, dressing percentages, and immunity.     

MiR-130a 在猪皮下脂肪细胞分化中的调节作用

为研究miR-130a对猪皮下脂肪细胞分化的影响及可能机制,本试验分离猪皮下脂肪前体细胞,诱导分化为成熟脂肪细胞,检测脂肪细胞分化过程中脂滴变化及miR-130a及其可能靶基因TNF α和PPARγ的表达模式.同时合成miR-130a mimics及inhibitor 对细胞进行转染,并以乱序序列作为阴性对照（NC）.细胞转染24 h后进行诱导分化,连续诱导8 d,检测各处理细胞的聚脂情况及甘油三酯含量变化,荧光定量PCR检测脂肪细胞分化相关基因的表达变化.结果显示,猪皮下脂肪前体细胞分化过程中脂滴逐渐变大增多,miR-130a、TNF α和PPARγ的表达模式具有一定的相似性.转染结果显示,相对于对照组,miR 130a mimics转染组细胞脂滴减少变小,甘油三酯含量降低（P<0.05）,脂肪细胞分化相关基因LPL、PPARγ、adiponectin、FASN和葡萄糖转运相关基因GLUT1,GLUT4以及JNK通路上的PDE3B的表达均比对照组显著下调（P<0.01）;而miR-130a inhibitor转染组细胞则脂滴增多,甘油三酯含量提高（P<0.05）,但大部分分化相关基因的表达与对照组无显著差异,提示miR-130a可能不只通过单一的靶基因影响脂肪细胞分化.其结果为后续深入研究miR-130a调节猪脂肪细胞分化的通路及机制奠定基础.     

Evaluation of physiological and molecular responses to acute heat stress in two chicken breeds

High environmental temperatures are a foremost concern affecting poultry production; thus, understanding and controlling such conditions are vital to successful production and welfare of poultry. In view of this, a completely randomized design with a 2 × 2 factorial arrangement involving two local strains (Kirin chicken (KC) and Three-yellow chicken (TYC)) and two temperature groups (normal/control = 30 ± 2 °C and acute heat stress (AHS) = 35 ± 1 °C for 8-h with 70% humidity) was used to assess the main regulatory factors such as heat shock protein (HSP70) gene, cytokine genes (IL-1β, IL-6, IL-10), muscle development gene (IGF-1) and tissue histopathological changes. At 56 days old, the temperatures of the comb (CT), feet (FT), eyelid (ET) and rectal (RT) from each group were taken thrice at 0, 2, 4 and 8-h during AHS, and 1 and 3-h recovery period after AHS. At 80 days old, the slaughter weight was also analyzed. The CT and ET of the AHS groups increased during the 8-h trial, while the RT of both strains decreased significantly at 4 h but increased at 8 h in the TYC group. All temperature recordings dropped in the AHS groups of both strains during the recovery period. The results revealed that the mRNA expression of HSP70 in the liver was higher in the heat-stressed group of both strains compared to the control. The expression of HSP70 was shown in the AHS-KC group to be significantly high compared to the control (P < 0.05). Moreover, the IGF1 gene in the liver, breast muscle and leg muscle was downregulated in the AHS-TYC group compared to the control (P < 0.05), although that in the AHS-KC was downregulated in the breast muscle. The mRNA expression of spleen IL-1β significantly decreased in the AHS-TYC group (P < 0.01), whereas that of the AHS-KC had no significant difference (P > 0.05). The mRNA expression of spleen IL-6 and IL-10 was increased in the AHS-KC group but did not exhibit obvious changes in the AHS-TYC. Correspondingly, the histopathological examinations revealed tissue injury in the AHS groups of both strains, with the TYC strain experiencing more severe changes. The final live and carcass weights showed a significant enhancement in the treatments (P < 0.01 and P < 0.05, respectively) and treatment × strain interaction (P < 0.05) with breast muscle rate significantly reducing among the treatments (P < 0.01) at 80 days. In conclusion, the differential response to AHS after physiological, molecular and immune response portrays KC to have better thermal tolerance than the TYC.     

Effects of 5-aminolevulinic acid on the inflammatory responses and antioxidative capacity in broiler chickens challenged with lipopolysaccharide

5-Aminolevulinic acid (5-ALA) is an intermediate in haem biosynthesis and has anti-apoptotic, anti-inflammatory, antioxidant, and other pharmacological effects. This study aimed to investigate the effect of dietary supplementation with 5-ALA on growth performance, antioxidant capacity, and inflammatory response of the lipopolysaccharide (LPS)-challenged broiler chickens. The experiment was designed as a 2 × 2 factorial arrangement with dietary 5-ALA (0 or 60 mg/kg) and LPS (injection of saline or 0.5 mg/kg BW) levels as treatments. A total of 240 one-day-old Arbor Acres broilers were distributed into four treatments consisting of six replicates of 10 birds. All the experimental broilers were intraperitoneally injected with LPS or sterile saline at 16, 18, and 20 days of age. Our results showed that dietary 5-ALA supplementation reduced (P < 0.05) the feed to gain before broilers were stimulated with LPS (days 1–15). LPS challenge decreased (P < 0.05) the catalase (CAT), total superoxide dismutase activities and increased the content of malondialdehyde (MDA) in the serum of broiler chickens. However, 5-ALA supplementation had a tendency to increase (P = 0.08) the activity of CAT and decreased (P < 0.05) the content of MDA. LPS challenge showed higher (P < 0.05) interleukin (IL)-1β, IL-6, and IL-10 concentrations in the serum, whereas dietary 5-ALA supplementation decreased (P < 0.05) the levels of IL-1β and IL-6. Additionally, dietary 5-ALA supplementation significantly attenuated (P < 0.05) the upregulation of mRNA expression levels of hepatic toll-like receptor 4 (TLR4), IL-1β, and IL-2 induced by LPS challenge. Moreover, dietary 5-ALA supplementation also enhanced the mRNA expression of 5-aminolevulinate dehydratase, ferrochelatase, and haem oxygenase-1 (HO-1) as compared to the unsupplemented groups. In conclusion, our results suggested that supplementation of 60 mg/kg 5-ALA exhibited LPS-induced anti-inflammatory and antioxidant properties by enhancing the HO-1 expression and inhibiting the TLR4/NF-κB signalling pathway.     

Bovine colostrum promoted ileal health in newborn lambs at 24 h after birth: insight from intestinal morphology and innate immunity

The contribution of colostrum to passive immunity transfer and intestinal protection in newborn ruminants is well known; however, it is currently unclear how colostrum intake affects intestinal innate immunity. We investigated the effects of bovine colostrum intake on ileal morphology, expression of genes involved in intestinal innate immunity, and serum concentrations of inflammatory cytokines in newborn lambs. Twenty-seven newborn male Hu lambs were used, of which 18 were bottle-fed either bovine colostrum (C24h; n = 9) or bovine mature milk (M24h; n = 9) within the first 2 h after birth at an intake of approximately 8% of BW; the remaining nine lambs did not receive any feeding (N24h). Blood and ileal tissue samples were collected after the lambs were slaughtered at 24 h after birth. Ileal villus height and villus height-to-crypt depth ratio were significantly higher in C24h than those in N24h and M24h lambs (P < 0.01). Messenger RNA (mRNA) abundance of toll-like receptor (TLR)-2, TLR3, TLR4, TLR6, TLR7, TLR8 and tumour necrosis factor alpha in the ileum was lower in C24h than that in N24h lambs (P < 0.05). Moreover, C24h lambs had a lower TLR3 mRNA abundance (P < 0.01) and a trend of lower TLR6 (P = 0.06) and interleukin 1 beta (P = 0.08) expression compared with those in M24h lambs. We also observed strong positive correlations of tumour necrosis factor alpha expression with that of TLR2 (r = 0.71; P < 0.001), TLR4 (r = 0.88; P < 0.001) and TLR8 (r = 0.83; P < 0.001). Interestingly, the expression of barrier-related molecules, including mucin-13, lysozyme, claudin (CLDN)-1, CLDN2, CLDN4, CLDN7, CLDN12, occludin, zonula occluden-1 and junctional adhesion molecule-1, was consistently lower in C24h lambs than that in N24h and M24h lambs (P < 0.05). These results indicated that the beneficial roles of colostrum intake on intestinal protection in newborn lambs were associated with low TLR expression, which was reflected by improved intestinal development and reduced inflammatory response. Further studies using fluorescence in situ hybridisation and immunohistochemical methods are needed to further explore the mechanisms underlying the lower expression of intestinal barrier-related molecules due to colostrum feeding.     

Lipid metabolism and identification of biomarkers in asthma by lipidomic analysis

BackgroundLipids participate in many important biological functions through energy storage, material transport, signal transduction, and molecular recognition processes. Studies have reported that asthmatic patients have abnormal lipid metabolism. However, there are limited studies on the characterization of lipid metabolism in asthmatic patients by lipidomics.MethodsWe characterized the plasma lipid profile of 28 healthy controls and 33 outpatients with asthma (18 mild, 15 moderate) by liquid chromatography mass spectrometry/mass spectrometry-based lipidomics.ResultsWe determined 1338 individual lipid species in the plasma. Significant changes were identified in ten lipid species in asthmatic patients than in healthy controls (all P < 0.05). Phosphatidylethanolamine (PE) (18:1p/22:6), PE (20:0/18:1), PE (38:1), sphingomyelin (SM) (d18:1/18:1), and triglyceride (TG) (16:0/16:0/18:1) positively correlated with the severity of asthma (all P < 0.05). Phosphatidylinositol (PI) (16:0/20:4), TG (17:0/18:1/18:1), phosphatidylglycerol (PG) (44:0), ceramide (Cer) (d16:0/27:2), and lysophosphatidylcholine (LPC) (22:4) negatively correlated with the severity of asthma (all P < 0.05). Correlation analysis showed a significant correlation between all ten lipid species (all P < 0.05). From the area under the curve of the receiver operating characteristic curve analysis, PE (38:1) was the major lipid metabolite that distinguished asthmatic patients from healthy controls, and may be considered a potential lipid biomarker. PE (20:0/18:1) and TG (16:0/16:0/18:1) might be related to IgE levels in asthmatic patients.ConclusionsOur results indicated the presence of abnormal lipid metabolism, which correlated with the severity and IgE levels in asthmatic patients.