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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

Adipokines gene expression and protein abundance after LPS injection compared to control. a Relative mRNA abundance of leptin, adiponectin and ZAG. b-d Leptin, adiponectin, and ZAG protein abundance. 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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Fig5: Adipokines gene expression and protein abundance after LPS injection compared to control. a Relative mRNA abundance of leptin, adiponectin and ZAG. b-d Leptin, adiponectin, and ZAG protein abundance. 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: As shown in Fig. 5, mRNA abundances of leptin, adiponectin, and zinc-α2-glycoprotein (ZAG) were not different between control and LPS group. Furthermore, the protein content of leptin remained unchanged after LPS treatment. However, the protein levels of adiponectin and ZAG were significantly increased in the LPS group.Fig. 5


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)

Adipokines gene expression and protein abundance after LPS injection compared to control. a Relative mRNA abundance of leptin, adiponectin and ZAG. b-d Leptin, adiponectin, and ZAG protein abundance. 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

Fig5: Adipokines gene expression and protein abundance after LPS injection compared to control. a Relative mRNA abundance of leptin, adiponectin and ZAG. b-d Leptin, adiponectin, and ZAG protein abundance. 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: As shown in Fig. 5, mRNA abundances of leptin, adiponectin, and zinc-α2-glycoprotein (ZAG) were not different between control and LPS group. Furthermore, the protein content of leptin remained unchanged after LPS treatment. However, the protein levels of adiponectin and ZAG were significantly increased in the LPS group.Fig. 5

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