Int. J. Devl Neuroscience 29 (2011) 785–793 Contents lists available at SciVerse ScienceDirect International Journal of Developmental Neuroscience j our na l ho me p age: www.elsevier.com/locate/ijdevneu Exposure to maternal consumption of cafeteria diet during the lactation period programmes feeding behaviour in the rat Thomas M. Wright a , Kevin C.F. Fone b , Simon C. Langley-Evans c , Jörg-Peter W. Voigt a,∗ a School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, Loughborough LE12 5RD, United Kingdom b School of Biomedical Sciences, Queen’s Medical Centre, University of Nottingham, Sutton Bonington, Loughborough LE12 5RD, United Kingdom c School of Biosciences, University of Nottingham, Sutton Bonington, Loughborough LE12 5RD, United Kingdom a r t i c l e i n f o Article history: Received 4 August 2011 Received in revised form 29 September 2011 Accepted 30 September 2011 Keywords: Nutritional programming Behavioural satiety sequence Appetite Obesity Lactation a b s t r a c t Lactational overfeeding programmes obesity in the adult rat, and also impacts on adult emotional behaviour. The present study investigated the impact of exposing the lactating female to a hypercaloric diet on structural aspects of feeding behaviour in the adult offspring as measured by the behavioural sati- ety sequence (BSS). Lactating Wistar rats were fed a hypercaloric cafeteria diet (CD) in addition to chow. Controls were fed on chow only. All offspring were chow fed after weaning. BSS was tested in 12–15 week old offspring. At 20 weeks of age, monoamine neurotransmitter levels were measured in selected brain regions. When exposed to a palatable 1-h test meal, offspring responded with the same latency to feed, regardless of lactational diet. Total food intake during the test was unaffected by lactational diet. Control offspring showed a normal BSS pattern. Male CD offspring displayed shorter feeding bouts (P < 0.05) with an overall higher bout frequency (P < 0.001) and their latency to rest was delayed (P < 0.001). Overall eat- ing frequency (P < 0.05), but not duration was increased in male CD offspring. Although the transition from feeding to resting was not affected by lactational CD, CD males fed for longer at the beginning of the test meal and were more active towards the end. CD females displayed an increased number of feeding bouts (P < 0.05) and they spent more time eating (P < 0.05). Resting latency was delayed (P < 0.05) and overall time spent resting was shortened (P < 0.01). Frequency of eating was increased in the middle of the test meal. The onset of satiety as indicated by the transition point between eating and resting was delayed in CD females (P < 0.001). In both sexes, hypothalamic 5-hydroxytryptamine (5-HT) was increased (P < 0.05 in females, P < 0.01 in males) and 5-HT turnover was reduced by lactational CD (P < 0.001 in females, P < 0.01 in males). Lactational CD led also to an increase in dopamine (DA) (P < 0.01). Hypothalamic DA metabolism (DOPAC + HVA/DA ratio) was overall lower in females than in males (P < 0.01). This study indi- cates a programming effect of lactational CD on feeding behaviour and brain monoaminergic neurons. © 2011 ISDN. Published by Elsevier Ltd. All rights reserved. 1. Introduction Many aspects of metabolic and physiological function are influ- enced by the early-life experiences of the individual. A robust body of epidemiological evidence has demonstrated associations between low weight or thinness at birth and risk of cardiovas- cular disease (Barker et al., 1989; Fall et al., 1995) and type 2 diabetes (Barker et al., 1993; Phillips et al., 1994) and between exposure to famine during fetal life and risk of later obesity (Ravelli et al., 1976). Such findings have given rise to the hypothesis that maternal nutritional status may be one of a number of factors ∗ Corresponding author. Tel.: +44 0115 951 6408. E-mail address: peter.voigt@nottingham.ac.uk (J.-P.W. Voigt). that programme long-term risk of conditions, such as cardiovas- cular disease and type 2 diabetes (Gluckman and Hanson, 2008; Langley-Evans and Jackson, 1996; Langley-Evans and McMullen, 2010). This hypothesis has received strong support from studies of small and large animal species, which demonstrate that exposure to maternal undernutrition in pregnancy impacts upon fetal growth determines metabolic and physiological function and hence disease risk in adult offspring (Langley-Evans and McMullen, 2010). Inter- estingly, alongside these disease-related outcomes of early-life programming there is evidence that exposure to maternal protein restriction, or a limited maternal food supply, influences feeding behaviour in rats (Bellinger et al., 2004, 2006; Langley-Evans et al., 2005). Differences in appetite appear related to programming of hypothalamic expression of serotonin receptors and orexigenic and anorexogenic peptides (Lopes de Souza et al., 2008; Orozco-Solis et al., 2009). 0736-5748/$36.00 © 2011 ISDN. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.ijdevneu.2011.09.007