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Fructose induced endotoxemia in pediatric nonalcoholic Fatty liver disease.

Jin R, Willment A, Patel SS, Sun X, Song M, Mannery YO, Kosters A, McClain CJ, Vos MB - Int J Hepatol (2014)

Bottom Line: In a 24-hour feeding study, endotoxin levels in NAFLD adolescents increased after fructose beverages (consumed with meals) as compared to healthy children.Similarly, endotoxin was significantly increased after adolescents consumed fructose beverages for 2 weeks and remained high although not significantly at 4 weeks.In conclusion, these data provide support for the concept of low level endotoxemia contributing to pediatric NAFLD and the possible role of fructose in this process.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, School of Medicine, Emory University, 2015 Uppergate Drive NE, Atlanta, GA 30322, USA.

ABSTRACT
In preclinical studies of fructose-induced NAFLD, endotoxin appears to play an important role. We retrospectively examined samples from three pediatric cohorts (1) to investigate whether endotoxemia is associated with the presence of hepatic steatosis; (2) to evaluate postprandial endotoxin levels in response to fructose beverage in an acute 24-hour feeding challenge, and (3) to determine the change of fasting endotoxin amounts in a 4-week randomized controlled trial comparing fructose to glucose beverages in NAFLD. We found that adolescents with hepatic steatosis had elevated endotoxin levels compared to obese controls and that the endotoxin level correlated with insulin resistance and several inflammatory cytokines. In a 24-hour feeding study, endotoxin levels in NAFLD adolescents increased after fructose beverages (consumed with meals) as compared to healthy children. Similarly, endotoxin was significantly increased after adolescents consumed fructose beverages for 2 weeks and remained high although not significantly at 4 weeks. In conclusion, these data provide support for the concept of low level endotoxemia contributing to pediatric NAFLD and the possible role of fructose in this process. Further studies are needed to determine if manipulation of the microbiome or other methods of endotoxin reduction would be useful as a therapy for pediatric NAFLD.

No MeSH data available.


Related in: MedlinePlus

Postprandial plasma endotoxin levels in response to (a) fructose and (b) glucose beverages given with breakfast, lunch, and dinner. The solid line represents 7 children without NAFLD and the dashed line shows the response in 8 children with biopsy-proven NAFLD. Baseline values were set as reference (1.0) and the following time points represent the ratio to baseline. *P < 0.05 when comparing NAFLD and non-NAFLD subjects at given time point.
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fig2: Postprandial plasma endotoxin levels in response to (a) fructose and (b) glucose beverages given with breakfast, lunch, and dinner. The solid line represents 7 children without NAFLD and the dashed line shows the response in 8 children with biopsy-proven NAFLD. Baseline values were set as reference (1.0) and the following time points represent the ratio to baseline. *P < 0.05 when comparing NAFLD and non-NAFLD subjects at given time point.

Mentions: Next, we evaluated postprandial endotoxin levels in samples from a group of 15 adolescents, 8 of whom had histologically confirmed NAFLD and 7 matched healthy adolescents. Their baseline characteristics are summarized in Table 2. In response to fructose beverages (consumed with meals), adolescents with NAFLD had an acute increase of plasma endotoxin levels after 1, 3, and 5 hours (P < 0.05 for all) comparing to non-NAFLD subjects. This resulted in an elevation of 9-h IAUC of postprandial endotoxin in NAFLD compared to their healthy controls (mean ± SE: 6.85 ± 1.49 versus 2.50 ± 0.87, P = 0.026). The biggest differences were seen after breakfast and lunch and less variation was seen overnight; thus their 23-h IAUC comparison (mean ± SE: 15.11 ± 3.83 versus 10.19 ± 4.23, P = 0.23) did not reach statistical significance (Figure 2(a)). In contrast, no significant difference of postprandial endotoxin in response to glucose beverages (consumed with meals) was observed between adolescents with and without NAFLD (Figure 2(b)).


Fructose induced endotoxemia in pediatric nonalcoholic Fatty liver disease.

Jin R, Willment A, Patel SS, Sun X, Song M, Mannery YO, Kosters A, McClain CJ, Vos MB - Int J Hepatol (2014)

Postprandial plasma endotoxin levels in response to (a) fructose and (b) glucose beverages given with breakfast, lunch, and dinner. The solid line represents 7 children without NAFLD and the dashed line shows the response in 8 children with biopsy-proven NAFLD. Baseline values were set as reference (1.0) and the following time points represent the ratio to baseline. *P < 0.05 when comparing NAFLD and non-NAFLD subjects at given time point.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4195259&req=5

fig2: Postprandial plasma endotoxin levels in response to (a) fructose and (b) glucose beverages given with breakfast, lunch, and dinner. The solid line represents 7 children without NAFLD and the dashed line shows the response in 8 children with biopsy-proven NAFLD. Baseline values were set as reference (1.0) and the following time points represent the ratio to baseline. *P < 0.05 when comparing NAFLD and non-NAFLD subjects at given time point.
Mentions: Next, we evaluated postprandial endotoxin levels in samples from a group of 15 adolescents, 8 of whom had histologically confirmed NAFLD and 7 matched healthy adolescents. Their baseline characteristics are summarized in Table 2. In response to fructose beverages (consumed with meals), adolescents with NAFLD had an acute increase of plasma endotoxin levels after 1, 3, and 5 hours (P < 0.05 for all) comparing to non-NAFLD subjects. This resulted in an elevation of 9-h IAUC of postprandial endotoxin in NAFLD compared to their healthy controls (mean ± SE: 6.85 ± 1.49 versus 2.50 ± 0.87, P = 0.026). The biggest differences were seen after breakfast and lunch and less variation was seen overnight; thus their 23-h IAUC comparison (mean ± SE: 15.11 ± 3.83 versus 10.19 ± 4.23, P = 0.23) did not reach statistical significance (Figure 2(a)). In contrast, no significant difference of postprandial endotoxin in response to glucose beverages (consumed with meals) was observed between adolescents with and without NAFLD (Figure 2(b)).

Bottom Line: In a 24-hour feeding study, endotoxin levels in NAFLD adolescents increased after fructose beverages (consumed with meals) as compared to healthy children.Similarly, endotoxin was significantly increased after adolescents consumed fructose beverages for 2 weeks and remained high although not significantly at 4 weeks.In conclusion, these data provide support for the concept of low level endotoxemia contributing to pediatric NAFLD and the possible role of fructose in this process.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, School of Medicine, Emory University, 2015 Uppergate Drive NE, Atlanta, GA 30322, USA.

ABSTRACT
In preclinical studies of fructose-induced NAFLD, endotoxin appears to play an important role. We retrospectively examined samples from three pediatric cohorts (1) to investigate whether endotoxemia is associated with the presence of hepatic steatosis; (2) to evaluate postprandial endotoxin levels in response to fructose beverage in an acute 24-hour feeding challenge, and (3) to determine the change of fasting endotoxin amounts in a 4-week randomized controlled trial comparing fructose to glucose beverages in NAFLD. We found that adolescents with hepatic steatosis had elevated endotoxin levels compared to obese controls and that the endotoxin level correlated with insulin resistance and several inflammatory cytokines. In a 24-hour feeding study, endotoxin levels in NAFLD adolescents increased after fructose beverages (consumed with meals) as compared to healthy children. Similarly, endotoxin was significantly increased after adolescents consumed fructose beverages for 2 weeks and remained high although not significantly at 4 weeks. In conclusion, these data provide support for the concept of low level endotoxemia contributing to pediatric NAFLD and the possible role of fructose in this process. Further studies are needed to determine if manipulation of the microbiome or other methods of endotoxin reduction would be useful as a therapy for pediatric NAFLD.

No MeSH data available.


Related in: MedlinePlus