Undernutrition In Rats Research Articles

Maternal protein restriction during the lactation period disrupts the ontogenetic development of behavioral traits in male Wistar rat offspring.

Neonatal undernutrition in rats results in short- and long-term behavioral and hormonal alterations in the offspring. It is not clear, however, whether these effects are present since the original insult or if they develop at some specific age later in life. Here, we assessed the ontogenetic profile of behavioral parameters associated with anxiety, exploration and memory/learning of Wistar rat offspring that were subjected to protein malnutrition during lactation. Dams and respective litters were separated into two groups: (1) protein-restricted (PR), which received a hypoproteic chow (8% protein) from birth to weaning [postnatal day (PN) 21]; (2) control (C), which received normoproteic chow. Offspring's behaviors, corticosterone, catecholamines, T3 and T4 levels were assessed at PN21 (weaning), PN45 (adolescence), PN90 (young adulthood) or PN180 (adulthood). PR offspring showed an age-independent reduction in the levels of anxiety-like behaviors in the Elevated Plus Maze and better memory performance in the Radial Arm Water Maze. PR offspring showed peak exploratory activity in the Open Field earlier in life, at PN45, than C, which showed theirs at PN90. Corticosterone was reduced in PR offspring, particularly at young adulthood, while catecholamines were increased at weaning and adulthood. The current study shows that considerable age-dependent variations in the expression of the observed behaviors and hormonal levels exist from weaning to adulthood in rats, and that protein restriction during lactation has complex variable-dependent effects on the ontogenesis of the assessed parameters.

Vascular nitrosative stress in hypertension induced by fetal undernutrition in rats

Fetal undernutrition predisposes to hypertension development. Since nitric oxide (NO) is a key factor in blood pressure control, we aimed to investigate the role of NO alterations in hypertension induced by fetal undernutrition in rats. Male and female offspring from dams exposed to undernutrition during the second half of gestation (MUN) were studied at 21 days (normotensive) and 6 months of age (hypertension developed only in males). In aorta, we analyzed total and phosphorylated endothelial NO synthase (eNOS, p-eNOS), 3-nitrotyrosine (3-NT), and Nrf2 (Western blot). In plasma we assessed l-arginine, asymmetric and symmetric dimethylarginine (ADMA, SDMA; LC–MS/MS), nitrates (NOx, Griess reaction), carbonyl groups, and lipid peroxidation (spectrophotometry). In iliac arteries, we studied superoxide anion production (DHE staining, confocal microscopy) and vasodilatation to acetylcholine (isometric tension). Twenty-one-day-old MUN offspring did not show alterations in vascular e-NOS or 3NT expression, plasma l-Arg/ADMA ratio, or NOx. Compared to control group, 6-month-old MUN rats showed increased aortic expression of p-eNOS/eNOS and 3-NT, being Nrf2 expression lower, elevated plasma l-arginine/ADMA, NOx and carbonyl levels, increased iliac artery DHE staining and reduced acetylcholine-mediated relaxations. These alterations in MUN rats were sex-dependent, affecting males. However, females showed some signs of endothelial dysfunction. We conclude that increased NO production in the context of a pro-oxidative environment, leads to vascular nitrosative damage and dysfunction, which can participate in hypertension development in MUN males. Females show a better adaptation, but signs of endothelial dysfunction, which can explain hypertension in ageing.

Slower Growth during Lactation Rescues Early Cardiovascular and Adipose Tissue Hypertrophy Induced by Fetal Undernutrition in Rats.

Low birth weight (LBW) and accelerated growth during lactation are associated with cardiometabolic disease development. LBW offspring from rats exposed to undernutrition during gestation (MUN) develops hypertension. In this rat model, we tested if slower postnatal growth improves early cardiometabolic alterations. MUN dams were fed ad libitum during gestation days 1–10, with 50% of the daily intake during days 11–21 and ad libitum during lactation. Control dams were always fed ad libitum. Pups were maintained with their own mother or cross-fostered. Body weight and length were recorded weekly, and breastmilk was obtained. At weaning, the heart was evaluated by echocardiography, and aorta structure and adipocytes in white perivascular fat were studied by confocal microscopy (size, % beige-adipocytes by Mitotracker staining). Breastmilk protein and fat content were not significantly different between groups. Compared to controls, MUN males significantly accelerated body weight gain during the exclusive lactation period (days 1–14) while females accelerated during the last week; length growth was slower in MUN rats from both sexes. By weaning, MUN males, but not females, showed reduced diastolic function and hypertrophy in the heart, aorta, and adipocytes; the percentage of beige-type adipocytes was smaller in MUN males and females. Fostering MUN offspring on control dams significantly reduced weight gain rate, cardiovascular, and fat hypertrophy, increasing beige-adipocyte proportion. Control offspring nursed by MUN mothers reduced body growth gain, without cardiovascular modifications. In conclusion, slower growth during lactation can rescue early cardiovascular alterations induced by fetal undernutrition. Exclusive lactation was a key period, despite no modifications in breastmilk macronutrients, suggesting the role of bioactive components. Our data support that lactation is a key period to counteract cardiometabolic disease programming in LBW and a potential intervention window for the mother.

Maternal Undernutrition in Rats Affects Hippocampal Development through Inhibition of Neurogenin 1

Maternal Undernutrition in Rats Affects Hippocampal Development through Inhibition of Neurogenin 1

Blood cell transcriptomic-based early biomarkers of adverse programming effects of gestational calorie restriction and their reversibility by leptin supplementation.

The challenge of preventing major chronic diseases requires reliable, early biomarkers. Gestational mild undernutrition in rats is enough to program the offspring to develop later pathologies; the intake of leptin, a breastmilk component, during lactation may reverse these programming effects. We used these models to identify, in peripheral blood mononuclear cells (PBMCs), transcriptomic-based early biomarkers of programmed susceptibility to later disorders, and explored their response to neonatal leptin intake. Microarray analysis was performed in PBMCs from the offspring of control and 20% gestational calorie-restricted dams (CR), and CR-rats supplemented with physiological doses of leptin throughout lactation. Notably, leptin supplementation normalised 218 of the 224 mRNA-levels identified in PBMCs associated to undernutrition during pregnancy. These markers may be useful for early identification and subsequent monitoring of individuals who are at risk of later diseases and would specifically benefit from the intake of appropriate amounts of leptin during lactation.

Metabolic programming of adipose tissue structure and function in male rat offspring by prenatal undernutrition.

BackgroundA number of different pathways to obesity with different metabolic outcomes are recognised. Prenatal undernutrition in rats leads to increased fat deposition in adulthood. However, the form of obesity is metabolically distinct from obesity induced through other pathways (e.g. diet-induced obesity). Previous rat studies have shown that maternal undernutrition during pregnancy led to insulin hyper-secretion and obesity in offspring, but not to systemic insulin resistance. Increased muscle and liver glycogen stores indicated that glucose is taken up efficiently, reflecting an active physiological function of these energy storage tissues. It is increasingly recognised that adipose tissue plays a central role in the regulation of metabolism and pathophysiology of obesity development. The present study investigated the cell size and endocrine responsiveness of subcutaneous and visceral adipose tissue from prenatally undernourished rats. We aimed to identify whether these adipose tissue depots contribute to the altered energy metabolism observed in these offspring.MethodsAdipocyte size was measured in both subcutaneous (ScAT) and retroperitoneal adipose tissue (RpAT) in male prenatally ad libitum fed (AD) or prenatally undernourished (UN) rat offspring. Metabolic responses were investigated in adipose tissue explants stimulated by insulin and beta3 receptor agonists ex vivo. Expression of markers of insulin signalling was determined by Western blot analyses. Data were analysed by unpaired t-test or Two Way ANOVA followed by Fisher’s PLSD post-hoc test, where appropriate.ResultsAdipocytes in offspring of undernourished mothers were larger, even at a lower body weight, in both RpAT and ScAT. The insulin response of adipose tissue was reduced in ScAT, and statistically absent in RpAT of UN rats compared with control. This lack of RpAT insulin response was associated with reduced expression of insulin signalling pathway proteins. Adrenergic receptor-driven lipolysis was observed in both adipose depots; however insulin failed to express its anti-lipolytic effect in RpAT in both, AD and UN offspring.ConclusionsMetabolic dysregulation in offspring of undernourished mothers is mediated by increased adipocyte size and reduced insulin responsiveness in both ScAT and especially in RpAT. These functional and morphological changes in adipocytes were accompanied by impaired activity of the insulin signalling cascade highlighting the important role of different adipose tissue depots in the pathogenesis of metabolic disorders.

Olfactory Discrimination in Adult Male Rats Undernourished during the Pre- and Neonatal Period

In the neonatal rat, the olfactory system is a fundamental channel to locate and recognize the mother, to survive and develop early social behavior, and to distinguish related or unrelated members of a litter. Perinatal undernutrition in rats alters the neuronal organization and functioning of the olfactory system and its ascending relays, possibly affecting odor discrimination. In this study we compared the frequency and time spent visiting the source of urine obtained from unrelated female subjects and amyl acetate odors vs water in adult perinatally underfed rats. Each test initiated with one daily presentation during three consecutive aliquots of deionized water (10 μl) placed on a filter paper for 2 min, separated by 1-min intervals for habituation. The water presentations were followed by three exposures to an odor, all at the same dilution (either 1:1 or 1:80) for dishabituation. Control (C) and undernourished (U) subjects display similar, significant habituation/dishabituation responses, except that the U subjects showed greater increases in the frequency and duration of visits to undiluted and diluted urine and amyl acetate cues compared to the controls. These findings are similar to previous studies showing that adult rats investigate novel odors longer than the familiar ones. Thus, perinatal undernutrition appears to interfere with the foundation of the olfactory development causing long-term olfactory discrimination deficits as revealed by the increased frequency and duration of visits to the source of odors that may be relevant for social behavior.

Pre-weaning undernutrition alters the expression levels of reactive oxygen species enzymes but not their activity levels or lipid peroxidation in the rat brain

It has been hypothesised that the increased life span commonly observed in rodents that have had their diet restricted after weaning may be related to its effects on the anti-oxidant defence systems. However, undernutrition during the gestation and pre-weaning period is known to have long-term deleterious effects on a rodent's growth and development, and it has been suggested that this may reduce their life span. We have now examined some of the anti-oxidant defence system in rats that have been undernourished from conception until 21 postnatal days-of-age, followed in some cases by a period of nutritional rehabilitation until 62 days of age. We found that such undernutrition could modulate the mRNA expression of Cu/ZnSOD and catalase in some brain regions. However, only catalase showed any undernutrition-induced change of enzyme activity level. There was some evidence that undernourished (but not control) rats had an age-related increase in the level of lipid peroxidation between 21 and 62 days of age, although the group × age interaction was not statistically significant. There was no significant change in the level of reduced glutathione induced by the pre-weaning period of undernutrition. If ROS and the extent of oxidative damage are truly implicated in the determination of life span, our results indicate that this is unlikely to be markedly affected by the relatively small changes we have observed in the anti-oxidant defence systems induced by undernutrition of rats from conception until weaning.

Protective effect of selenium on protein-undernutrition-induced brain damage in rats

The effect of ad libitum ingestion of selenium (Se) in drinking water (0.15 mg SeO2/L) for 3 wk on the brain weight, total brain protein, glutathione (GSH) level, catalase activity, and lipid peroxidation in the brain of protein-undernourished (PU) rats was investigated, in an attempt to determine whether antioxidants alone can reverse some of the neuropathological changes associated with protein undernutrition in rats. Feeding on a normal diet (16% casein) by well-fed rats or a low-protein diet (5% casein) by PU rats and Se-treated PU rats lasted 14 wk. Se-treated PU rats were given Se in drinking water during the last 3 wk of the experiment. Results show that protein undernutrition induced significant reductions (p < 0.001) in brain weight, total brain protein, and catalase activity (p < 0.05) while it induced a significant increase (p < 0.05) in lipid peroxidation when compared with well-nourished rats; but no significant effect was observed for the GSH level. However, the ingestion of Se in drinking water by PU rats for 3 wk resulted in significant increases (p < 0.05) in brain weight, catalase activity, and total brain protein but induced a significant reduction (p < 0.05) in lipid peroxidation when compared with PU rats given water. The values obtained for Se-treated PU rats are comparable with those obtained for well-nourished rats. The GSH level was, however, not affected by Se ingestion. We suggest that Se, by inducing increases in the concentration of certain proteins, including catalase, in the brain, abolished some of the pathological changes associated with protein undernutrition in the brain, and appears as a promising antioxidant in the prevention and management of pro-oxidant-induced brain damage.

In utero undernutrition in rats induces increased vascular smooth muscle content in the offspring

We hypothesized that undernutrition in utero alters the structure of conduit and resistance vessels early in development. We studied a rodent model in which dams were 50% food restricted from day 10 of gestation to term. Vascular smooth muscle content and vascular caliber in the offspring were examined by quantitative histologic methods and by Western blot analysis. Maternal food restriction induced a significant increase in the smooth muscle content of 1-day- and 2-month-old offspring aortas and mesenteric arterioles of different luminal diameters. Histologic data were confirmed by Western blot analysis that showed greater expression of smooth muscle alpha-actin in 1-day-old food restriction aortas. The increase in vascular smooth muscle in the aortas was determined to be the result of cellular hypertrophy. These results demonstrate that the vascular smooth muscle is altered in food-restriction offspring and that this may be a mechanism for the programming of offspring hypertension.

Maternal undernutrition reduces aortic wall thickness and elastin content in offspring rats without altering endothelial function

Epidemiological studies suggest a link between fetal/early infant nutrition and adult coronary artery disease. In the present study, we examined the effects of altering nutrition during gestation, lactation and juvenile life on aortic structure and function in rats. Wistar rat dams were fed either a control or low-protein diet throughout pregnancy, or a low-protein diet for the final 7 days of gestation only. At 21 days post-partum, male pups were weaned on to a control, low-protein or high-fat diet. At 12 weeks, the offspring rats were killed. In 46 rats, aortic sections were mounted and stained to assess media thickness and elastin content. In a further 38 rats, aortic rings were suspended in an organ bath and vascular reactivity was tested with dose-response curves to the endothelium-dependent dilator acetylcholine and the endothelium-independent dilator sodium nitroprusside. Rats exposed to maternal protein restriction while in utero had a significantly decreased aortic wall thickness compared with control rats (P=0.005). Total elastin content of the aorta was also decreased by both maternal low-protein (P=0.02) and early postnatal low-protein (P=0.01) diets. Neither maternal nor postnatal low-protein or high-fat diets, however, resulted in any significant changes in arterial dilator function. In conclusion, fetal undernutrition in rats, induced via a maternal low-protein diet, causes a decrease in aortic wall thickness and elastin content without altering aortic dilator function. These changes in vascular structure may amplify aging-related changes to the vasculature and contribute to the pathophysiology of the putative link between impaired fetal growth and adult cardiovascular disease.

Intrauterine Undernutrition in Rats Interferes with Leukocyte Migration, Decreasing Adhesion Molecule Expression in Leukocytes and Endothelial Cells

Experimental and epidemiologic data have shown that malnutrition predisposes individuals to infections. Immune responses are compromised, particularly in undernourished children. Therefore, we investigated the migratory capacity of leukocytes, using the intravital microscopy technique, in male Wistar rats (8-9 wk of age) that were undernourished in utero after their dams were fed 50% less food than the amount consumed by control dams. The number of leukocytes rolling along the venular endothelium, sticking after stimulation with leukotriene B4, tumor necrosis factor-alpha (TNF-alpha) or zymosan-activated plasma, or migrating after TNF-alpha stimulation was significantly reduced in the undernourished rat offspring. Compared with nourished rat offspring, undernourished offspring had significantly reduced numbers of circulating leukocytes, higher blood pressure, and higher leukocyte rolling velocity (V(WBC)), as well as a higher ratio between V(WBC) and RBC velocity (V(RBC)). Endothelial P-selectin and intercellular adhesion molecule-1 (ICAM-1) expression, analyzed by immunohistochemistry, and basal leukocyte L-selectin expression, analyzed by flow cytometry, were significantly reduced in the undernourished rat offspring. Because the groups did not differ in leukocyte CD11/18 expression, endothelial expression of platelet-endothelial cell adhesion molecule-1, or venular blood flow velocity and, consequently, venular shear rate, we conclude that intrauterine undernutrition in rats reduces leukocyte migration, downregulates endothelial expression of P-selectin and ICAM-1, as well as leukocyte expression of L-selectin, while reducing leukocyte counts. The higher V(WBC) and V(WBC)/V(RBC) ratio may also play a role in this reduced leukocyte migration. Our data suggest that this phenomenon is involved in the increased predisposition to infections in undernourished subjects.

Glucose uptake and glucose transporter proteins in skeletal muscle from undernourished rats.

Undernutrition in rats impairs secretion of insulin but maintains glucose normotolerance, because muscle tissue presents an increased insulin-induced glucose uptake. We studied glucose transporters in gastrocnemius muscles from food-restricted and control anesthetized rats under basal and euglycemic hyperinsulinemic conditions. Muscle membranes were prepared by subcellular fractionation in sucrose gradients. Insulin-induced glucose uptake, estimated by a 2-deoxyglucose technique, was increased 4- and 12-fold in control and food-restricted rats, respectively. Muscle insulin receptor was increased, but phosphotyrosine-associated phosphatidylinositol 3-kinase activity stimulated by insulin was lower in undernourished rats, whereas insulin receptor substrate-1 content remained unaltered. The main glucose transporter in the muscle, GLUT-4, was severely reduced albeit more efficiently translocated in response to insulin in food-deprived rats. GLUT-1, GLUT-3, and GLUT-5, minor isoforms in skeletal muscle, were found increased in food-deprived rats. The rise in these minor glucose carriers, as well as the improvement in GLUT-4 recruitment, is probably insufficient to account for the insulin-induced increase in the uptake of glucose in undernourished rats, thereby suggesting possible changes in other steps required for glucose metabolism.

Long-Term Modification of the Excretion of Prostaglandin E2 by Fetal Exposure to a Maternal Low Protein Diet in the Rat

Prenatal exposure to maternal undernutrition in both humans and animals is associated with long-term changes in the structure, physiological functions and metabolism of key tissues and organs. This phenomenon, termed programming, is implicated in the aetiology of cardiovascular disease. Using an established rat model of hypertension programmed by prenatal protein restriction, assessment was made of the long-term influence of maternal diet upon prostaglandin metabolism. Pregnant rats were fed isoenergetic diets containing 18% casein (control) or 9% casein (low protein) from conception until littering. The offspring of these pregnancies were studied at day 20 of gestation, full-term gestation and at 4, 7 or 12 weeks postnatal age. Prostaglandin E₂ concentrations in plasma were similar in control and low-protein diet-exposed rats at 4 weeks of age. Urinary prostaglandin E₂ excretion was, however, significantly increased by prenatal undernutrition in rats at both 4 and 12 weeks postnatal age. The principal enzyme of prostaglandin E₂ degradation, 15-hydroxyprostaglandin dehydrogenase (PGDH) exhibited significantly lower activity in the kidneys of 4-week-old rats exposed to a maternal low-protein diet. This effect was transient and absent by 12 weeks postnatal age. There was also some evidence of an altered developmental profile of PGDH activity in the lungs of low-protein diet-exposed rats. These data are consistent with the long-term programming effects of the maternal diet upon renal prostaglandin metabolism. In the rat, increased local prostaglandin E₂ concentrations associated with impaired degradation may contribute to increased renovascular resistance and hypertension.

Undernutrition of rats during early life does not affect the total number of cortical neurons

Undernutrition during early life is known to cause deficits and distortions in brain structure. However, it remains uncertain whether this includes a diminution of the total numbers of neurons. Recent advances in stereological techniques have made it possible to obtain unbiased estimates of total numbers of cells in well-defined biological structures. Rats were undernourished from day 16 of gestation to 30 postnatal days of age by standardized procedures. These rats and well-fed control rats were anaesthetized and killed by intracardiac perfusion with fixatives at 70 days of age. The left cerebral hemisphere from each animal was embedded in Paraplast and serially sectioned. The sections were analyzed via the Cavalieri principle to obtain the total cortical volume and by the "disector" method to estimate the numerical density of neurons in the cortex. These values were later used to compute estimates of the total number of cortical neurons for each animal. Well-fed control rats had 26.9 million cortical neurons, while the previously undernourished animals had 24.8 million. The difference between these two groups was not statistically significant. It therefore appears that undernutrition of rats during early postnatal life does not affect the total numbers of neurons in the cerebral cortex.

Influence of early undernutrition in rats on their body fat and RNA content in VMH neurons

The RNA content of the ventromedial hypothalamus (VMH) and lateral hypothalamic area (LHA) neurons, and the epididymal, retroperitoneal, and liver fat content of 150-day-old male rats submitted to neonatal undernutrition, were investigated. The neonatal undernutrition was carried out by two different ways. First, by reducing the litters to two pups per nest from birth to weaning. The pups from normal litters (eight pups/nest) served as controls. Secondly, by separating half of the pups (four pups) from normal litters for 8 h daily during the first 5 postnatal days. The remaining nonseparated pups served as their controls. The data show that both groups of early undernourished pups had a significantly increased RNA content in the VMH neurons (RNA content in the LHA neurons was unchanged) and a significantly decreased epididymal, retroperitoneal, and liver fat content in comparison with their controls. The results indicate that early undernutrition leads to a permanent increase in the functional activity of VMH and alteration in fat metabolism in rats.

Postnatal undernutrition slows development of bronchiolar epithelium in rats.

The lung's small conducting airways are sites of dysfunction early in the course of chronic lung diseases that are prevalent in humans; furthermore, there is evidence that aspects of childhood environment may adversely influence small airway function in adulthood. Because there is considerable early postnatal morphological maturation of the bronchiolar epithelium in rats, these considerations led to the present study in which we assessed the effect of early postnatal undernutrition in rats on the anatomic development of the bronchiolar epithelium. We found undernutrition, produced by increasing rat litter size shortly after birth, led to delayed development of the mitochondria and rough endoplasmic reticulum of bronchiolar Clara cells. Of particular interest, underfeeding resulted in considerably diminished mitosis by Clara cells, decreased nuclear numerical density of bronchiolar ciliated cells, evidence of diminished conversion of Clara cells to ciliated cells, and an abnormal cellular composition of the small airway epithelium that persisted well beyond the period of underfeeding. We conclude that early neonatal events can have long-term effects on the bronchiolar epithelium.

Different methods for producing neonatal undernutrition in rats cause different brain changes in the face of equivalent somatic growth parameters.

Similar degrees of undernutrition were induced in neonatal rat pups using a modified Slob technique and a large-litter manipulation. From birth, large litters and Slob litters were comprised of 20 and 10 pups, respectively. On days 2, 4 and 6, half of the pups in the Slob group were cross-fostered to nonlactating foster aunts, while the remaining half of each litter (controls), as well as the large-litter rats were cross-fostered to a lactating dam. On day 10, undernourished Slob and large-litter pups showed similar body weight and body length deficits compared with controls, but differences between the two undernourished groups emerged when regional brain weight and nucleic acids and proteins were examined. The acute intermittent undernutrition of the modified Slob technique had more severe consequences than the large-litter manipulation for brain growth and development. Therefore, two methods of inducing early postnatal undernutrition may yield equivalent somatic effects, but very different brain growth parameters.

Amphetamine-induced activity after fetal alcohol exposure and undernutrition in rats

Behavioral responses to amphetamine were examined in 28- and 42-day-old rats whose mothers consumed a liquid diet consisting of 35% ethanol-derived calories (EDC) during pregnancy. Offspring of pair-fed (0% EDC) and ad lib chow (LC) dams were included as controls. Animals received 0.0, 0.5, 1.0, or 2.0 mg/kg/ml d-amphetamine prior to single 2-hr tests in automated activity monitors. At 28 days of age, when there were no differences in activity after saline injection, 35% EDC males were more active (measured by distance traveled) than LC and 0% EDC males following treatment with 2.0 mg/kg amphetamine. Thirty-five percent EDC females exhibited brief reductions in activity relative to LC females but were not different from 0% EDC females at 28 days of age following 2.0 mg/kg amphetamine. When treated with 1.0 mg/kg amphetamine, 28-day-old 0% EDC males were less active than LC and 35% EDC males, who did not differ from each other at this dose. At 42 days of age, animals from both liquid diet groups were less active than LC controls following 2 mg/kg amphetamine. These results suggest that both prenatal alcohol exposure and undernutrition may influence the postnatal functional status of catecholamine systems but that the nature of those functional changes varies with type of prenatal insult, sex and age of the animal at testing.

Early life undernutrition in rats. 3. Motor performance in adulthood.

1. A detailed investigation was made of the motor performance of rats which had impaired cerebellar and muscular growth resulting from early-life undernutrition. 2. Developing rats were growth-retarded by underfeeding their mothers during pregnancy and lactation. They were fed ad lib. from 25 d of age. 3. Adult male previously-undernourished (PU) and well-fed control rats were given tests of motor behaviour commencing at 5 months of age. They were required to run backwards to maintain their position on a revolving drum. Aspects of the test situation were varied systematically: visual environment, interval between trials, test duration and drum speed. 4. PU rats had a 29% body-weight deficit compared with controls at 5 months. 5. There was nio evidence of impaired motor performance by the PU rats under any for the test conditions.