Diet choice exaggerates food hoarding, intake and pup survival across reproduction Diane E. Day a , Eric M. Mintz a , Timothy J. Bartness a,b, * a Department of Biology, Neurobiology and Behavior Program, Center for Behavioral Neuroscience, Georgia State University, Atlanta, GA 30303, USA b Department of Psychology, Neuropsychology and Behavioral Neuroscience Program, Georgia State University, Atlanta, GA 30303, USA Received 30 April 2001; received in revised form 25 July 2001; accepted 4 October 2001 Abstract Siberian hamsters increase food intake and hoarding during pregnancy and lactation, perhaps to compensate for large decreases in body fat (  50%). We tested the effects of diet choice on these responses in pregnant, lactating and virgin hamsters housed in a simulated burrow system. Hamsters were offered pellet chow (PC) or a choice of sunflower seeds (SS), rabbit chow (RC) and PC. Pregnant or lactating PC-fed hamsters had increased food intake and hoard size compared with virgins, effects exaggerated by diet self-selection. The pregnancy-induced increases and lactation-induced decreases in body mass were enhanced and diminished by diet self-selection, respectively. Pregnant self- selecting hamsters ate relatively more carbohydrate and less fat and hoarded less carbohydrate and more fat than their virgin counterparts (protein not affected). Lactating and virgin self-selecting hamsters both ate and hoarded relatively more carbohydrate than protein or fat compared with PC-fed hamsters but were not different from each other. Litter and pup sizes were similar at birth, but pups from self-selecting mothers had decreased lipid content (50%) compared with pups from PC-fed mothers, whereas at weaning they were heavier but not fatter. Only lactating PC-fed mothers cannibalized their pups (  60% eaten, 8/10 litters). The pregnancy-induced increased eating and hoarding of carbohydrate may have helped meet immediate energy needs sparing dwindling lipid reserves, whereas the decreased fetal lipid investment may have helped conserve energy in anticipation of the increased demands of lactation. The diet-induced exaggerated caloric intake and food hoard size of lactating hamsters may have promoted pup growth and survival. D 2002 Elsevier Science Inc. All rights reserved. Keywords: Body mass; White adipose tissue; Carcass composition; Food preference; Fat pad specific; Lipid mobilization 1. Introduction Species-specific strategies have evolved to help mam- mals meet the energetic demands of routine physiological and behavioral responses as well as the extremely high energetic demands of pregnancy and lactation (for review, see Refs. [23,24,29,38]). These reproductively related energy demands are particularly difficult to meet by small mammals because of their high metabolic rates combined with their high surface/volume ratios [17], two energetically costly traits. As a result, a variety of physiological and behavioral strategies have evolved to contend with these energetically expensive reproductive conditions [8]. For example, laboratory rats (Rattus norvegicus) increase both body mass [fat; white adipose tissue (WAT)] and food intake during pregnancy and lactation [20]. In contrast, both Syrian (Mesocricetus auratus) [14,22] and Siberian (Phodopus sungorus) [3,31] hamsters decrease body mass (fat) during pregnancy and lactation but differ somewhat in their food intake responses during these reproductive conditions. Spe- cifically, Syrian hamsters increase food intake during lacta- tion but not during pregnancy [14,41], whereas Siberian hamsters increase food intake under both conditions [3,31]. Additional energy savings come from the pregnancy- and lactation-induced decreases in energy expenditure seen by virtually all small rodent species (for reviews, see Refs. [3,38]). As a supplement to, or in place of, storage of excess energy in WAT during pregnancy, some species store excess energy externally in the form of a food hoard to cache their calories [3,7,39]. Siberian hamsters increase both food 0031-9384/02/$ – see front matter D 2002 Elsevier Science Inc. All rights reserved. PII:S0031-9384(01)00655-2 * Corresponding author. Department of Biology, Georgia State University, 24 Peachtree Center Avenue NE, University Plaza, Atlanta, GA 30303-3083, USA. Tel.: +1-404-651-2766; fax: +1-404-651-2509. E-mail address: bartness@gsu.edu (T.J. Bartness). Physiology & Behavior 75 (2002) 143 – 157