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Coenzyme Q10 prevents hepatic fibrosis, inflammation, and oxidative stress in a male rat model of poor maternal nutrition and accelerated postnatal growth.
- Source :
- American Journal of Clinical Nutrition; 2/1/2016, Vol. 103 Issue 2, p579-588, 10p, 3 Charts, 5 Graphs
- Publication Year :
- 2016
-
Abstract
- Background: It is well established that low birth weight and accelerated postnatal growth increase the risk of liver dysfunction in later life. However, molecular mechanisms underlying such developmental programming are not well characterized, and potential intervention strategies are poorly defined. Objectives: We tested the hypotheses that poor maternal nutrition and accelerated postnatal growth would lead to increased hepatic fibrosis (a pathological marker of liver dysfunction) and that postnatal supplementation with the antioxidant coenzyme Q<subscript>10</subscript> (CoQ<subscript>10</subscript>) would prevent this programmed phenotype. Design: A rat model of maternal protein restriction was used to generate low-birth-weight offspring that underwent accelerated postnatal growth (termed "recuperated"). These were compared with control rats. Offspring were weaned onto standard feed pellets with or without dietary CoQ<subscript>10</subscript> (1 mg/kg body weight per day) supplementation. At 12 mo, hepatic fibrosis, indexes of inflammation, oxidative stress, and insulin signaling were measured by histology, Western blot, ELISA, and reverse transcriptase-polymerase chain reaction. Results: Hepatic collagen deposition (diameter of deposit) was greater in recuperated offspring (mean ± SEM: 12 ± 2 µm) than in controls (5 ± 0.5 mm) (P < 0.001). This was associated with greater inflammation (interleukin 6: 38% ± 24% increase; P < 0.05; tumor necrosis factor a: 64% ± 24% increase; P < 0.05), lipid peroxidation (4-hydroxynonenal, measured by ELISA: 0.30 ± 0.02 compared with 0.19 ± 0.05 µg/mL per mg protein; P < 0.05), and hyperinsulinemia (P < 0.05). CoQ<subscript>10</subscript> supplementation increased (P < 0.01) hepatic CoQ<subscript>10</subscript> concentrations and ameliorated liver fibrosis (P < 0.001), inflammation (P < 0.001), some measures of oxidative stress (P < 0.001), and hyperinsulinemia (P < 0.01). Conclusions: Suboptimal in utero nutrition combined with accelerated postnatal catch-up growth caused more hepatic fibrosis in adulthood, which was associated with higher indexes of oxidative stress and inflammation and hyperinsulinemia. CoQ<subscript>10</subscript> supplementation prevented liver fibrosis accompanied by downregulation of oxidative stress, inflammation, and hyperinsulinemia. [ABSTRACT FROM AUTHOR]
- Subjects :
- BLOOD sugar analysis
LIVER disease prevention
FIBROSIS
ANALYSIS of variance
ANIMAL experimentation
ANTHROPOMETRY
COLLAGEN
DIETARY supplements
ENZYME-linked immunosorbent assay
HISTOLOGICAL techniques
HUMAN growth
HYPERINSULINISM
INFLAMMATION
INSULIN
INTERLEUKINS
LIVER
LONGITUDINAL method
MALNUTRITION in pregnancy
LIPID peroxidation (Biology)
POLYMERASE chain reaction
PROBABILITY theory
RATS
RESEARCH funding
STAINS & staining (Microscopy)
STATISTICS
TUMOR necrosis factors
UBIQUINONES
WESTERN immunoblotting
DATA analysis
OXIDATIVE stress
REVERSE transcriptase polymerase chain reaction
DATA analysis software
DESCRIPTIVE statistics
IN vivo studies
METABOLISM
PREVENTION
Subjects
Details
- Language :
- English
- ISSN :
- 00029165
- Volume :
- 103
- Issue :
- 2
- Database :
- Complementary Index
- Journal :
- American Journal of Clinical Nutrition
- Publication Type :
- Academic Journal
- Accession number :
- 112739589
- Full Text :
- https://doi.org/10.3945/ajcn.115.119834