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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 OGTT in 6- (A) and 16-week-old (C) offspring rats.Glucose AUC results in 6- (B) and 16-week-old (D) offspring rats. n = 8. Values represent mean ± SD. *p<0.05, **p<0.01 vs. NS; #p<0.05 vs. LPS.
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pone-0111376-g005: The effects of prenatal exposure to LPS/LPS+PDTC on OGTT in 6- (A) and 16-week-old (C) offspring rats.Glucose AUC results in 6- (B) and 16-week-old (D) offspring rats. n = 8. Values represent mean ± SD. *p<0.05, **p<0.01 vs. NS; #p<0.05 vs. LPS.

Mentions: Fasting glucose levels did not significantly differ among the three groups in 6 and 16-week-old offspring. During the OGTT, glucose levels peaked at 30 min and then gradually returned to baseline by 180 min in the three groups of 6-week-old offspring (Figure 5A). The glucose AUC exhibited the same trend (Figure 5B). At 16 weeks, glucose levels peaked at 30 min in the NS and LPS+PDTC groups, whereas the levels, peaked at 60 min in the LPS groups. Moreover, glucose levels in the LPS group were significantly increased compared with the NS (8.93±0.66 mmol/L vs. 6.62±0.52 mmol/L, P<0.01) and LPS+PDTC groups (8.93±0.66 mmol/L vs. 7.47±0.61 mmol/L, P<0.05) at 60 min. In addition, glucose levels in the LPS group were significantly increased compared with the NS group (6.28±0.43 mmol/L vs. 5.16±0.34 mmol/L, P<0.05) at 120 min (Figure 5C). Similarly, the glucose AUC in 16-week-old rat offspring was strikingly increased in the LPS group compared with the NS(P<0.05) and LPS+PDTC groups (P<0.05) (Figure 5D). However, TC, TG, HDL-C and LDL-C levels did not significantly differ among the groups at 6 and 16 weeks (P>0.05) (Figure 6).


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 OGTT in 6- (A) and 16-week-old (C) offspring rats.Glucose AUC results in 6- (B) and 16-week-old (D) offspring rats. n = 8. Values represent mean ± SD. *p<0.05, **p<0.01 vs. NS; #p<0.05 vs. LPS.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0111376-g005: The effects of prenatal exposure to LPS/LPS+PDTC on OGTT in 6- (A) and 16-week-old (C) offspring rats.Glucose AUC results in 6- (B) and 16-week-old (D) offspring rats. n = 8. Values represent mean ± SD. *p<0.05, **p<0.01 vs. NS; #p<0.05 vs. LPS.
Mentions: Fasting glucose levels did not significantly differ among the three groups in 6 and 16-week-old offspring. During the OGTT, glucose levels peaked at 30 min and then gradually returned to baseline by 180 min in the three groups of 6-week-old offspring (Figure 5A). The glucose AUC exhibited the same trend (Figure 5B). At 16 weeks, glucose levels peaked at 30 min in the NS and LPS+PDTC groups, whereas the levels, peaked at 60 min in the LPS groups. Moreover, glucose levels in the LPS group were significantly increased compared with the NS (8.93±0.66 mmol/L vs. 6.62±0.52 mmol/L, P<0.01) and LPS+PDTC groups (8.93±0.66 mmol/L vs. 7.47±0.61 mmol/L, P<0.05) at 60 min. In addition, glucose levels in the LPS group were significantly increased compared with the NS group (6.28±0.43 mmol/L vs. 5.16±0.34 mmol/L, P<0.05) at 120 min (Figure 5C). Similarly, the glucose AUC in 16-week-old rat offspring was strikingly increased in the LPS group compared with the NS(P<0.05) and LPS+PDTC groups (P<0.05) (Figure 5D). However, TC, TG, HDL-C and LDL-C levels did not significantly differ among the groups at 6 and 16 weeks (P>0.05) (Figure 6).

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