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Nutrients 2017, 9(9), 1041; doi:10.3390/nu9091041

Developmental Programming of Obesity and Liver Metabolism by Maternal Perinatal Nutrition Involves the Melanocortin System

1
Institute for Liver and Digestive Health, University College London, London NW3 2PF, UK
2
Division of Women’s Health, Faculty of Life Sciences & Medicine, King’s College London, London SE1 7EH, UK
3
Department of Pathology, University College London, London WC1E 6JJ, UK
4
Center for Translational Medicine, International Clinical Research Center (FNUSA-ICRC), Brno 65691, Czech Republic
5
Department of Gastroenterology and Hepatology, Guy’s and St Thomas’ Hospital, NHS Foundation Trust, London SE1 7EH, UK
*
Authors to whom correspondence should be addressed.
Received: 30 July 2017 / Revised: 14 September 2017 / Accepted: 15 September 2017 / Published: 20 September 2017
(This article belongs to the Special Issue Precision Nutrition and Metabolic Syndrome Management)
View Full-Text   |   Download PDF [1997 KB, uploaded 20 September 2017]   |  

Abstract

Maternal obesity predisposes offspring to metabolic dysfunction and Non-Alcoholic Fatty Liver Disease (NAFLD). Melanocortin-4 receptor (Mc4r)-deficient mouse models exhibit obesity during adulthood. Here, we aim to determine the influence of the Mc4r gene on the liver of mice subjected to perinatal diet-induced obesity. Female mice heterozygous for Mc4r fed an obesogenic or a control diet for 5 weeks were mated with heterozygous males, with the same diet continued throughout pregnancy and lactation, generating four offspring groups: control wild type (C_wt), control knockout (C_KO), obese wild type (Ob_wt), and obese knockout (Ob_KO). At 21 days, offspring were genotyped, weaned onto a control diet, and sacrificed at 6 months old. Offspring phenotypic characteristics, plasma biochemical profile, liver histology, and hepatic gene expression were analyzed. Mc4r_ko offspring showed higher body, liver and adipose tissue weights respect to the wild type animals. Histological examination showed mild hepatic steatosis in offspring group C_KO. The expression of hepatic genes involved in regulating inflammation, fibrosis, and immune cell infiltration were upregulated by the absence of the Mc4r gene. These results demonstrate that maternal obesogenic feeding during the perinatal period programs offspring obesity development with involvement of the Mc4r system. View Full-Text
Keywords: obesity; developmental programming; Non-Alcoholic Fatty Liver Disease; maternal nutrition; intra-abdominal fat obesity; developmental programming; Non-Alcoholic Fatty Liver Disease; maternal nutrition; intra-abdominal fat
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Cordero, P.; Li, J.; Nguyen, V.; Pombo, J.; Maicas, N.; Novelli, M.; Taylor, P.D.; Samuelsson, A.-M.; Vinciguerra, M.; Oben, J.A. Developmental Programming of Obesity and Liver Metabolism by Maternal Perinatal Nutrition Involves the Melanocortin System. Nutrients 2017, 9, 1041.

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