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Lipopolysaccharide challenge significantly influences lipid metabolism and proteome of white adipose tissue in growing pigs.

Guo J, Liu Z, Sun H, Huang Y, Albrecht E, Zhao R, Yang X - Lipids Health Dis (2015)

Bottom Line: The results indicated that LPS significantly increased the expression of toll-like receptor (TLR) 2/4 pathway-related genes and pro-inflammatory factors.In conclusion, LPS challenge can cause acute inflammation in white adipose tissue.The results provide new clues to understand the adipose dysfunction during inflammation.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, 210095, PR China. 451515944@qq.com.

ABSTRACT

Background: White adipose tissue is recognized as a highly active organ, which is closely related to a large number of physiological and metabolic processes besides storing triglycerides. However, little is known regarding the response of adipose tissue to acute inflammation. Therefore, in this study we employed growing pigs to investigate the changes of lipid metabolism and proteome in white adipose tissue after lipopolysaccharide (LPS) stimulation as a model for bacterial infection.

Methods: The expression of lipid metabolism and inflammation related genes was determined by quantitative real-time polymerase chain reaction. Label-free proteomics analysis was used to investigate changes of the protein profile in white adipose tissue and western blot was used to verify changes of selected adipokines.

Results: The results indicated that LPS significantly increased the expression of toll-like receptor (TLR) 2/4 pathway-related genes and pro-inflammatory factors. Lipid metabolism related genes, including acetyl-CoA carboxylase 1 (ACACA), fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD), uncoupling protein 2 (UCP2), and 11 β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), were down-regulated and the lipolytic enzyme activity was decreased after LPS injection. Proteome analysis revealed 47 distinct proteins with > 2-fold changes. The down-regulation of two proteins (cAMP-dependent protein kinase type II-alpha regulatory subunit and β-tubulin) has been verified by western blot analysis. In addition, the abundance of two adipokines (adiponectin and zinc-α2-glycoprotein) was significantly increased after LPS injection.

Conclusion: In conclusion, LPS challenge can cause acute inflammation in white adipose tissue. Concurrently, lipid metabolism was significantly suppressed and the abundance of several proteins changed in white adipose tissue. The results provide new clues to understand the adipose dysfunction during inflammation.

No MeSH data available.


Related in: MedlinePlus

Lipid metabolism gene expression and lipolytic enzymes activity after LPS injection compared to control. a Relative mRNA abundance of ACACA, FASN, SCD, HSL, ATGL, CPT-1A, UCP2, UCP3, and 11β-HSD1. b Lipolytic enzymes activity. Data represent the means ± SEM. Data were considered statistically significant when P < 0.05, n = 6. # represent P < 0.1, *represent P < 0.05, **represent P < 0.01
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Fig2: Lipid metabolism gene expression and lipolytic enzymes activity after LPS injection compared to control. a Relative mRNA abundance of ACACA, FASN, SCD, HSL, ATGL, CPT-1A, UCP2, UCP3, and 11β-HSD1. b Lipolytic enzymes activity. Data represent the means ± SEM. Data were considered statistically significant when P < 0.05, n = 6. # represent P < 0.1, *represent P < 0.05, **represent P < 0.01

Mentions: As shown in Fig. 2, the gene expression of key enzymes of lipogenesis, including acetyl-CoA carboxylase 1 (ACACA), fatty acid synthase (FASN), and stearoyl-CoA desaturase (SCD), decreased after LPS treatment (P < 0.05). The gene expression of key enzymes of lipolysis, including hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL), remained unchanged (P > 0.05). However, as shown in Fig. 2b, the activity of these key enzymes in lipolysis was lower in the LPS injected animals. The gene expression of carnitine palmitoyltransferase-1A (CPT-1A), which is the key enzyme in β-oxidation, was significantly increased in the LPS stimulated group, while the gene expression of uncoupling protein 2 (UCP2) was decreased. The gene expression of 11 β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) showed a trend to lower values in the LPS group.Fig. 2


Lipopolysaccharide challenge significantly influences lipid metabolism and proteome of white adipose tissue in growing pigs.

Guo J, Liu Z, Sun H, Huang Y, Albrecht E, Zhao R, Yang X - Lipids Health Dis (2015)

Lipid metabolism gene expression and lipolytic enzymes activity after LPS injection compared to control. a Relative mRNA abundance of ACACA, FASN, SCD, HSL, ATGL, CPT-1A, UCP2, UCP3, and 11β-HSD1. b Lipolytic enzymes activity. Data represent the means ± SEM. Data were considered statistically significant when P < 0.05, n = 6. # represent P < 0.1, *represent P < 0.05, **represent P < 0.01
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4493945&req=5

Fig2: Lipid metabolism gene expression and lipolytic enzymes activity after LPS injection compared to control. a Relative mRNA abundance of ACACA, FASN, SCD, HSL, ATGL, CPT-1A, UCP2, UCP3, and 11β-HSD1. b Lipolytic enzymes activity. Data represent the means ± SEM. Data were considered statistically significant when P < 0.05, n = 6. # represent P < 0.1, *represent P < 0.05, **represent P < 0.01
Mentions: As shown in Fig. 2, the gene expression of key enzymes of lipogenesis, including acetyl-CoA carboxylase 1 (ACACA), fatty acid synthase (FASN), and stearoyl-CoA desaturase (SCD), decreased after LPS treatment (P < 0.05). The gene expression of key enzymes of lipolysis, including hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL), remained unchanged (P > 0.05). However, as shown in Fig. 2b, the activity of these key enzymes in lipolysis was lower in the LPS injected animals. The gene expression of carnitine palmitoyltransferase-1A (CPT-1A), which is the key enzyme in β-oxidation, was significantly increased in the LPS stimulated group, while the gene expression of uncoupling protein 2 (UCP2) was decreased. The gene expression of 11 β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) showed a trend to lower values in the LPS group.Fig. 2

Bottom Line: The results indicated that LPS significantly increased the expression of toll-like receptor (TLR) 2/4 pathway-related genes and pro-inflammatory factors.In conclusion, LPS challenge can cause acute inflammation in white adipose tissue.The results provide new clues to understand the adipose dysfunction during inflammation.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, 210095, PR China. 451515944@qq.com.

ABSTRACT

Background: White adipose tissue is recognized as a highly active organ, which is closely related to a large number of physiological and metabolic processes besides storing triglycerides. However, little is known regarding the response of adipose tissue to acute inflammation. Therefore, in this study we employed growing pigs to investigate the changes of lipid metabolism and proteome in white adipose tissue after lipopolysaccharide (LPS) stimulation as a model for bacterial infection.

Methods: The expression of lipid metabolism and inflammation related genes was determined by quantitative real-time polymerase chain reaction. Label-free proteomics analysis was used to investigate changes of the protein profile in white adipose tissue and western blot was used to verify changes of selected adipokines.

Results: The results indicated that LPS significantly increased the expression of toll-like receptor (TLR) 2/4 pathway-related genes and pro-inflammatory factors. Lipid metabolism related genes, including acetyl-CoA carboxylase 1 (ACACA), fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD), uncoupling protein 2 (UCP2), and 11 β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), were down-regulated and the lipolytic enzyme activity was decreased after LPS injection. Proteome analysis revealed 47 distinct proteins with > 2-fold changes. The down-regulation of two proteins (cAMP-dependent protein kinase type II-alpha regulatory subunit and β-tubulin) has been verified by western blot analysis. In addition, the abundance of two adipokines (adiponectin and zinc-α2-glycoprotein) was significantly increased after LPS injection.

Conclusion: In conclusion, LPS challenge can cause acute inflammation in white adipose tissue. Concurrently, lipid metabolism was significantly suppressed and the abundance of several proteins changed in white adipose tissue. The results provide new clues to understand the adipose dysfunction during inflammation.

No MeSH data available.


Related in: MedlinePlus