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Prenatal exposure to lipopolysaccharide results in local RAS activation in the adipose tissue of rat offspring.

Gao M, Zhang X, Chen X, Mi C, Tang Y, Zhou J, Li X - PLoS ONE (2014)

Bottom Line: Adult metabolic syndrome may originate in part during fetal or early life.Moreover, each component of the RAS was changed and was shown to be activated.PDTC, an inhibitor of NF-κB, could reverse the influence of the stimulus during pregnancy.

View Article: PubMed Central - PubMed

Affiliation: Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, China.

ABSTRACT

Background: Adult metabolic syndrome may originate in part during fetal or early life. This study was designed to investigate the effects of prenatal exposure to lipopolysaccharide (LPS) on adipose development and local renin-angiotensin system (RAS) activation in rat offspring.

Methods: Pregnant rats were randomly divided into three groups (n = 8 in each), including an NS group (pregnant rats were only treated with 0.5 ml normal saline from the 8th to the 14th day of gestation); an LPS group (pregnant rats were injected intraperitoneally with 0.79 mg/kg LPS on the 8th, 10th and 12th days of pregnancy); and an LPS+pyrrolidine dithiocarbamate (PDTC) group (identical to the LPS group except that 100 mg/kg PDTC was administered from the 8th to the 14th day of gestation).

Results: Prenatal exposure to LPS resulted in increased blood pressure, adipose coefficient and body weight in rat offspring. Specifically, during the infancy of the offspring rats, the LPS stimulus promoted the differentiation of adipose cells, diminishing their diameters and proportions while simultaneously increasing cell number. In contrast, once the rats were grown, adipose cell differentiation was inhibited, and the diameters and proportions of the cells were increased. Moreover, each component of the RAS was changed and was shown to be activated. PDTC, an inhibitor of NF-κB, could reverse the influence of the stimulus during pregnancy.

Conclusion: Prenatal exposure to LPS in rats results in increased blood pressure, adipose coefficient, body weight and activation of adipose RAS in offspring.

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Related in: MedlinePlus

The effects of prenatal exposure to LPS/LPS+PDTC on ACE, AT1, and AT2 protein expression in adipose tissue in 6- (A) and 16-week-old (B) offspring rats.ACE expression at 6 weeks (C), AT1 expression at 6 weeks (D), AT2 expression at 6 weeks (E), ACE expression at 16 weeks (F), AT1 expression at 16 weeks (G), AT2 expression at 16 weeks (H). n = 6 per group. Values represent mean ± SD. *p<0.05, **p<0.01 vs. NS; #p<0.05 vs. LPS.
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pone-0111376-g009: The effects of prenatal exposure to LPS/LPS+PDTC on ACE, AT1, and AT2 protein expression in adipose tissue in 6- (A) and 16-week-old (B) offspring rats.ACE expression at 6 weeks (C), AT1 expression at 6 weeks (D), AT2 expression at 6 weeks (E), ACE expression at 16 weeks (F), AT1 expression at 16 weeks (G), AT2 expression at 16 weeks (H). n = 6 per group. Values represent mean ± SD. *p<0.05, **p<0.01 vs. NS; #p<0.05 vs. LPS.

Mentions: ACE and AT1R protein expression in the adipose tissue of the LPS group was higher than in the control group at 6 and 16 weeks of age, but it only reached significance at 16 weeks. PDTC treatment clearly reduced ACE protein expression at 16 weeks of age. Similarly, at 6 weeks, AT2R protein expression in the adipose tissue of the LPS group was lower than in the NS group, and PDTC treatment increased the expression level, but the differences were not significant. At 16 weeks of age, AT2R showed significantly increased expression in the offspring of the LPS group (P<0.05), and PDTC treatment mitigated the increase in AT2R protein expression (P<0.05) (Figure 9).


Prenatal exposure to lipopolysaccharide results in local RAS activation in the adipose tissue of rat offspring.

Gao M, Zhang X, Chen X, Mi C, Tang Y, Zhou J, Li X - PLoS ONE (2014)

The effects of prenatal exposure to LPS/LPS+PDTC on ACE, AT1, and AT2 protein expression in adipose tissue in 6- (A) and 16-week-old (B) offspring rats.ACE expression at 6 weeks (C), AT1 expression at 6 weeks (D), AT2 expression at 6 weeks (E), ACE expression at 16 weeks (F), AT1 expression at 16 weeks (G), AT2 expression at 16 weeks (H). n = 6 per group. Values represent mean ± SD. *p<0.05, **p<0.01 vs. NS; #p<0.05 vs. LPS.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4216013&req=5

pone-0111376-g009: The effects of prenatal exposure to LPS/LPS+PDTC on ACE, AT1, and AT2 protein expression in adipose tissue in 6- (A) and 16-week-old (B) offspring rats.ACE expression at 6 weeks (C), AT1 expression at 6 weeks (D), AT2 expression at 6 weeks (E), ACE expression at 16 weeks (F), AT1 expression at 16 weeks (G), AT2 expression at 16 weeks (H). n = 6 per group. Values represent mean ± SD. *p<0.05, **p<0.01 vs. NS; #p<0.05 vs. LPS.
Mentions: ACE and AT1R protein expression in the adipose tissue of the LPS group was higher than in the control group at 6 and 16 weeks of age, but it only reached significance at 16 weeks. PDTC treatment clearly reduced ACE protein expression at 16 weeks of age. Similarly, at 6 weeks, AT2R protein expression in the adipose tissue of the LPS group was lower than in the NS group, and PDTC treatment increased the expression level, but the differences were not significant. At 16 weeks of age, AT2R showed significantly increased expression in the offspring of the LPS group (P<0.05), and PDTC treatment mitigated the increase in AT2R protein expression (P<0.05) (Figure 9).

Bottom Line: Adult metabolic syndrome may originate in part during fetal or early life.Moreover, each component of the RAS was changed and was shown to be activated.PDTC, an inhibitor of NF-κB, could reverse the influence of the stimulus during pregnancy.

View Article: PubMed Central - PubMed

Affiliation: Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, China.

ABSTRACT

Background: Adult metabolic syndrome may originate in part during fetal or early life. This study was designed to investigate the effects of prenatal exposure to lipopolysaccharide (LPS) on adipose development and local renin-angiotensin system (RAS) activation in rat offspring.

Methods: Pregnant rats were randomly divided into three groups (n = 8 in each), including an NS group (pregnant rats were only treated with 0.5 ml normal saline from the 8th to the 14th day of gestation); an LPS group (pregnant rats were injected intraperitoneally with 0.79 mg/kg LPS on the 8th, 10th and 12th days of pregnancy); and an LPS+pyrrolidine dithiocarbamate (PDTC) group (identical to the LPS group except that 100 mg/kg PDTC was administered from the 8th to the 14th day of gestation).

Results: Prenatal exposure to LPS resulted in increased blood pressure, adipose coefficient and body weight in rat offspring. Specifically, during the infancy of the offspring rats, the LPS stimulus promoted the differentiation of adipose cells, diminishing their diameters and proportions while simultaneously increasing cell number. In contrast, once the rats were grown, adipose cell differentiation was inhibited, and the diameters and proportions of the cells were increased. Moreover, each component of the RAS was changed and was shown to be activated. PDTC, an inhibitor of NF-κB, could reverse the influence of the stimulus during pregnancy.

Conclusion: Prenatal exposure to LPS in rats results in increased blood pressure, adipose coefficient, body weight and activation of adipose RAS in offspring.

Show MeSH
Related in: MedlinePlus