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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

The protein abundance of PRKAR2A and TUBB after LPS injection compared to control. a The protein abundance of PRKAR2A. b The protein abundance of TUBB. Representative parts of western blots are shown above the graph. 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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Fig4: The protein abundance of PRKAR2A and TUBB after LPS injection compared to control. a The protein abundance of PRKAR2A. b The protein abundance of TUBB. Representative parts of western blots are shown above the graph. 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: Table 1 specifies 47 proteins which showed at least a 2-fold change between the two groups. The proteins were classified into 7 categories based on their function (Fig. 3a). In Fig. 3b, the heat map of the 47 distinct proteins is shown. The volcano plot and radar chart are shown in Additional file 1: Figure S1 and Additional file 2: Figure S2. The results indicate that cAMP-dependent protein kinase type II-alpha regulatory subunit (PRKAR2A) and β-tubulin (TUBB) were significantly down-regulated following the administration of LPS. The results could be confirmed by western blot analysis (Fig. 4).Table 1


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)

The protein abundance of PRKAR2A and TUBB after LPS injection compared to control. a The protein abundance of PRKAR2A. b The protein abundance of TUBB. Representative parts of western blots are shown above the graph. 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

Fig4: The protein abundance of PRKAR2A and TUBB after LPS injection compared to control. a The protein abundance of PRKAR2A. b The protein abundance of TUBB. Representative parts of western blots are shown above the graph. 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: Table 1 specifies 47 proteins which showed at least a 2-fold change between the two groups. The proteins were classified into 7 categories based on their function (Fig. 3a). In Fig. 3b, the heat map of the 47 distinct proteins is shown. The volcano plot and radar chart are shown in Additional file 1: Figure S1 and Additional file 2: Figure S2. The results indicate that cAMP-dependent protein kinase type II-alpha regulatory subunit (PRKAR2A) and β-tubulin (TUBB) were significantly down-regulated following the administration of LPS. The results could be confirmed by western blot analysis (Fig. 4).Table 1

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