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Maternal undernutrition leads to endothelial dysfunction in adult male rat offspring independent of postnatal diet

Maternal undernutrition leads to endothelial dysfunction in adult male rat offspring independent of postnatal diet
Maternal undernutrition leads to endothelial dysfunction in adult male rat offspring independent of postnatal diet
Increasing evidence suggests a role for prenatal environment in the onset of cardiovascular and metabolic disease in later life. In the rat, undernutrition in utero and a postnatal high-fat diet gives rise to a phenotype similar to the metabolic syndrome. As endothelial dysfunction is a feature of both CVD and the metabolic syndrome we investigated the impact of maternal undernutrition and/or postnatal high-fat on endothelial function. Virgin Wistar rats were mated and randomly assigned to groups to receive food either ad libitum (control) or at 30 % of ad libitum intake throughout gestation. At postnatal day 250, a cohort from each group was challenged with a high-fat diet (D12451, 45 % energy from fat; Research Diets, Inc., New Brunswick, NJ, USA) for the remainder of the study. At 1 year of age, small mesenteric arteries were dissected and mounted on a wire myograph and responses to phenylephrine, endothelin, acetylcholine, leptin and sodium nitroprusside assessed. Vasoconstriction to endothelin was significantly enhanced in all groups compared with controls (-log effective concentration equal to 50 % of the maximal response (pEC50); P < 0.001). Endothelium-dependent vasodilatation to acetylcholine was significantly blunted in all groups compared with controls (% maximum response; P < 0.01), while dilatation to leptin and sodium nitroprusside was similar in all groups. These data demonstrate that both maternal undernutrition and postnatal high fat lead to vascular alterations and suggest that maternal undernutrition alone is at least as detrimental to offspring endothelial function as a long-term exposure to a high-fat diet in the offspring
later life, leptin, diet, exposure, adult, disease, maternal undernutrition, maternal, health, syndrome, environment, developmental origins, rats, phenotype, cohort, male
0007-1145
27-33
Torrens, Christopher
15a35713-0651-4249-8227-5901e2cfcd22
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Gluckman, Peter D.
ef2e8b92-0b76-4a12-bd7c-01b0674f94d3
Vickers, Mark H.
6e05d089-9742-44f5-b4e1-3a505027d10c
Torrens, Christopher
15a35713-0651-4249-8227-5901e2cfcd22
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Gluckman, Peter D.
ef2e8b92-0b76-4a12-bd7c-01b0674f94d3
Vickers, Mark H.
6e05d089-9742-44f5-b4e1-3a505027d10c

Torrens, Christopher, Hanson, Mark A., Gluckman, Peter D. and Vickers, Mark H. (2008) Maternal undernutrition leads to endothelial dysfunction in adult male rat offspring independent of postnatal diet. British Journal of Nutrition, 101 (1), 27-33. (doi:10.1017/S0007114508988760). (PMID:18492297)

Record type: Article

Abstract

Increasing evidence suggests a role for prenatal environment in the onset of cardiovascular and metabolic disease in later life. In the rat, undernutrition in utero and a postnatal high-fat diet gives rise to a phenotype similar to the metabolic syndrome. As endothelial dysfunction is a feature of both CVD and the metabolic syndrome we investigated the impact of maternal undernutrition and/or postnatal high-fat on endothelial function. Virgin Wistar rats were mated and randomly assigned to groups to receive food either ad libitum (control) or at 30 % of ad libitum intake throughout gestation. At postnatal day 250, a cohort from each group was challenged with a high-fat diet (D12451, 45 % energy from fat; Research Diets, Inc., New Brunswick, NJ, USA) for the remainder of the study. At 1 year of age, small mesenteric arteries were dissected and mounted on a wire myograph and responses to phenylephrine, endothelin, acetylcholine, leptin and sodium nitroprusside assessed. Vasoconstriction to endothelin was significantly enhanced in all groups compared with controls (-log effective concentration equal to 50 % of the maximal response (pEC50); P < 0.001). Endothelium-dependent vasodilatation to acetylcholine was significantly blunted in all groups compared with controls (% maximum response; P < 0.01), while dilatation to leptin and sodium nitroprusside was similar in all groups. These data demonstrate that both maternal undernutrition and postnatal high fat lead to vascular alterations and suggest that maternal undernutrition alone is at least as detrimental to offspring endothelial function as a long-term exposure to a high-fat diet in the offspring

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More information

Published date: 2008
Keywords: later life, leptin, diet, exposure, adult, disease, maternal undernutrition, maternal, health, syndrome, environment, developmental origins, rats, phenotype, cohort, male
Organisations: Faculty of Medicine, Dev Origins of Health & Disease

Identifiers

Local EPrints ID: 70557
URI: http://eprints.soton.ac.uk/id/eprint/70557
ISSN: 0007-1145
PURE UUID: 3c3557bf-0d9c-4f90-a475-5f4fa88f4c00
ORCID for Mark A. Hanson: ORCID iD orcid.org/0000-0002-6907-613X

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Date deposited: 10 Feb 2010
Last modified: 29 Oct 2019 01:56

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Contributors

Author: Christopher Torrens
Author: Mark A. Hanson ORCID iD
Author: Peter D. Gluckman
Author: Mark H. Vickers

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