Fish oil supplementation during adolescence attenuates metabolic programming of perinatal maternal high-fat diet in adult offspring. Issue 12 (28th June 2019)

• Record Type: Journal Article
• Authors: Souza, Aline F. P.; Souza, Luana L.; Oliveira, Lorraine S.; Cordeiro, Aline; Souza, Eliete; Kluck, George E. G.; Atella, Georgia C.; Trevenzoli, Isis H.; Pazos-Moura, Carmen C.
• Is Part Of: British journal of nutrition. Volume 121:Issue 12(2019)
• Page Start: 1345
• Page End: 1356
• Publication Date: 2019-06-28
• Subjects: Maternal high-fat diet, -- Fish oil intake, -- Adolescence, -- Metabolic programming and reprogramming; Nutrition -- Periodicals; 572.4
• DOI: 10.1017/S0007114519000771
• Languages: English
• ISSNs: 0007-1145

Abstract

Abstract: Perinatal maternal high-fat diet (HFD) increases susceptibility to obesity and fatty liver diseases in adult offspring, which can be attenuated by the potent hypolipidaemic action of fish oil (FO), an n -3 PUFA source, during adult life. Previously, we described that adolescent HFD offspring showed resistance to FO hypolipidaemic effects, although FO promoted hepatic molecular changes suggestive of reduced lipid accumulation. Here, we investigated whether this FO intervention only during the adolescence period could affect offspring metabolism in adulthood. Then, female Wistar rats received isoenergetic, standard (STD: 9 % fat) or high-fat (HFD: 28·6 % fat) diet before mating, and throughout pregnancy and lactation. After weaning, male offspring received the standard diet; and from 25 to 45 d old they received oral administration of soyabean oil or FO. At 150 d old, serum and hepatic metabolic parameters were evaluated. Maternal HFD adult offspring showed increased body weight, visceral adiposity, hyperleptinaemia and decreased hepatic pSTAT3/STAT3 ratio, suggestive of hepatic leptin resistance. FO intake only during the adolescence period reduced visceral adiposity and serum leptin, regardless of maternal diet. Maternal HFD promoted dyslipidaemia and hepatic TAG accumulation, which was correlated with reduced hepatic carnitine palmitoyl transferase-1a content, suggesting lipid oxidation impairment. FO intake did not change serum lipids; however, it restored hepatic TAG content and hepatic markers of lipid oxidation to STD offspring levels. Therefore, we concluded that FO intake exclusively during adolescence programmed STD offspring and reprogrammed HFD offspring male rats to a healthier metabolic phenotype in adult life, reducing visceral adiposity, serum leptin and hepatic TAG content in offspring adulthood.