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Accelerated growth without prepubertal obesity in nutritionally programmed microswine offspring

Published online by Cambridge University Press:  17 February 2012

E. A. DuPriest
Affiliation:
Department of Medicine, Oregon Health & Science University, Portland, OR, USA Department of Physiology & Pharmacology, Oregon Health & Science University, Portland, OR, USA Research Service, Portland VA Medical Center, Portland, OR, USA Department of Natural Sciences and Health, Warner Pacific College, Portland, OR, USA
P. Kupfer
Affiliation:
Department of Medicine, Oregon Health & Science University, Portland, OR, USA Research Service, Portland VA Medical Center, Portland, OR, USA
B. Lin
Affiliation:
Department of Medicine, Oregon Health & Science University, Portland, OR, USA Research Service, Portland VA Medical Center, Portland, OR, USA
K. Sekiguchi
Affiliation:
Department of Medicine, Oregon Health & Science University, Portland, OR, USA Research Service, Portland VA Medical Center, Portland, OR, USA
J. Q. Purnell
Affiliation:
Department of Medicine, Oregon Health & Science University, Portland, OR, USA
K. E. Saunders
Affiliation:
Department of Comparative Medicine, Oregon Health & Science University, Portland, OR, USA
T. T. Chatkupt
Affiliation:
Department of Comparative Medicine, Oregon Health & Science University, Portland, OR, USA
S. P. Bagby*
Affiliation:
Department of Medicine, Oregon Health & Science University, Portland, OR, USA Department of Physiology & Pharmacology, Oregon Health & Science University, Portland, OR, USA Research Service, Portland VA Medical Center, Portland, OR, USA
*
*Address for correspondence: Dr S. P. Bagby, MD, Professor of Medicine & Physiology/Pharmacology, Division of Nephrology & Hypertension, Oregon Health & Science University, 3303 SW Bond Avenue (CH12R), Portland, OR, USA. (Email [email protected])

Abstract

Poor fetal growth and associated prepubertal growth acceleration are linked to increased risk of cardiometabolic dysfunction in later life, but whether obesity is integral to ‘catch-up’ growth and its ensuing risks are unknown. In microswine offspring exposed to perinatal maternal protein restriction (MPR), we measured body and organ sizes (during MPR); linear growth and weight gain (birth to 5 months of age); feed intake and utilization efficiency (5–14 weeks); and body composition at 6 and 11 weeks of age (by dual-energy X-ray absorptiometry, DEXA). During MPR, low protein offspring (LPO) showed asymmetric growth restriction with reduced body weight (Wt):length (Lth) at birth and elevated heart Wt:liver Wt ratio by 2 weeks of age. In LPO, after slow early postnatal growth (0–5 weeks), subsequent linear growth on ad libitum normal feed was absolutely accelerated (cm/week; P < 0.001) over 6–11 weeks but normal thereafter, whereas absolute weight gain (kg/week) was similar to controls but accelerated relative to lower LPO nadir weights. Concurrently, rates of fat and lean tissue accrual in LPO over 6–11 weeks were similar to normal protein offspring in absolute terms (g/5 weeks) but increased relative to lower mass at 6 weeks, yielding normal lean:Lth but reduced fat:Lth ratios at 11 weeks. LPO had higher relative feed intake (g/kg/meal) in both sexes and higher feed efficiency in females over 5–11 weeks of age. Findings suggest that postnatal linear growth acceleration preserved thinness in juvenile LPO. Given separately reported abnormalities of vascular (Bagby et al., 2011) and adipocyte function in juvenile LPO, (DuPriest et al., 2011) findings demonstrate that perinatal MPR programs catch-up growth and cardiovascular abnormalities independently of obesity.

Type
Original Articles
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2012

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