Perinatal maternal high‐fat diet promotes alterations in hepatic lipid metabolism and resistance to the hypolipidemic effect of fish oil in adolescent rat offspring. Issue 11 (25th July 2016)

• Record Type: Journal Article
• Authors: Oliveira, Lorraine S.; Souza, Luana L.; Souza, Aline F. P.; Cordeiro, Aline; Kluck, George E. G.; Atella, Georgia C.; Trevenzoli, Isis H.; Pazos‐Moura, Carmen C.
• Is Part Of: Molecular nutrition & food research. Volume 60:Issue 11(2016)
• Page Start: 2493
• Page End: 2504
• Publication Date: 2016-07-25
• Subjects: Adolescence -- Fish oil -- Hepatic cholesterol metabolism -- Hepatic triglycerides metabolism -- Liver -- Maternal high‐fat diet -- Metabolic programming; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201600171
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : In adolescent offspring from maternal standard diet, fish oil (FO) increases serum docosahexanoic acid and eicosapentanoic acid and modulates key mechanisms of hepatic lipid metabolism, reducing serum and hepatic cholesterol and triglyceride content. In adolescent offspring from maternal high‐fat diet (HFD), the low serum n ‐3 PUFA concentration and hepatic molecular changes, as ABCG8, SREBP‐1, and acetyl CoA carboxylase (ACC) expression, may disturb the FO effect, contributing to the resistance to a hypolipidemic FO effect. Abstract : Scope: Maternal high‐fat diet (HFD) promotes obesity and metabolic disturbances in offspring at weaning and adult life. We investigated metabolic consequences of maternal HFD in adolescent rat offspring and the potential benefic effects of fish oil (FO) ( n ‐3 polyunsaturated fatty acid source). Methods and results: Female rats received isocaloric, standard diet (STD: 9% fat) or HFD (28.6%) before mating, and throughout pregnancy and lactation. After weaning, male offspring received standard diet and, from 25th to 45th day, received oral administration of soybean oil (SO) or FO. HFD offspring showed higher body weight and adiposity, which was not attenuated by FO. In STD offspring, FO reduced serum triglyceride and cholesterol, as expected, but not in HFD offspring. Liver of HFD offspring groups showed increased free cholesterol and FO‐treated HFD group showed lower expression of Abcg8, suggesting decreased cholesterol biliary excretion. HFD offspring presented higher hepatic expression of lipogenic markers, Srebf1 mRNA and acetyl CoA carboxylase (ACC). Serum n ‐3 PUFA were decreased in FO‐treated HFD compared to FO‐treated STD offspring, which may explain the reduced hypolipidemic FO effect. Conclusion: Maternal HFD impaired the ability of FO to reduce adiposity and serum lipids in adolescent offspring, suggesting a potential predisposition to future development of metabolic disorders