Exposure to undernutrition in fetal life determines fat distribution, locomotor activity and food intake in ageing rats

Abstract

Objective: To assess the long-term impact of undernutrition during specific periods of fetal life, upon central adiposity, control of feeding behaviour and locomotor activity. Design: Pregnant rats were fed a control or low-protein (LP) diet, targeted to early (LPE), mid (LPM) or late (LPL) pregnancy or throughout gestation (LPA). The offspring were studied at 9 and 18 months of age. Measurements: Adiposity was assessed by measuring weight of abdominal fat depots relative to body weight. Locomotor activity was assessed using an infrared sensor array system in both light and dark conditions. Hypothalamic expression of mRNA for galanin and the galanin 2 receptor (Gal2R) was determined using real-time PCR. Results: At 9 months, male rats exposed to LP in utero had less fat in the gonadal depot, but were of similar body weight to controls. By 18 months, the males of groups LPA and LPM had more abdominal and less subcutaneous fat. Females deposited more fat centrally than males between 9 and 18 months of age, and this was more marked in groups LPA and LPL. Food intake was greater in LPM males. Among females hypophagia was noted in groups LPA and LPL. Expression of galanin and Gal2R were unaffected by maternal diet. Total locomotor activity was reduced in LPE males and all LP females in the light but not in the dark. Conclusion: Locomotor activity and feeding behaviour in aged rats are subject to prenatal programming influences. Fetal undernutrition does not programme obesity in rats without postnatal dietary challenge.

Early life determinants of physical activity and sedentary time: Current knowledge and future research

“…Animal experiments imply that under-nutrition in fetal life, followed by postnatal weight gain, is associated with reduced motor activity (65,66) and increased sedentary behavior (67). Some human data tend to support these observations.…”

Perinatal nutrient restriction induces long-lasting alterations in the circadian expression pattern of genes regulating food intake and energy metabolism

“…Many epidemiological studies have indeed demonstrated that infants born small for gestational age are more prone to develop obesity, hypertension and type 2 diabetes in adulthood. [27][28][29] Experimental studies have further corroborated that rodents and other animal species submitted to protein or calorie restriction during gestation and/or suckling exhibit hyperphagia, [30][31][32][33] insulin resistance, 34,35 reduced leptin sensitivity, 36,37 hepatic steatosis, 38 elevated blood pressure 39,40 and hyperlipidemia. 35,37,38 These observations have been explained by the thrifty phenotype hypothesis, also called metabolic programming or the developmental origins of disease.…”

Epigenetic changes in early life and future risk of obesity

“…In some studies, this nutritional constraint is continued during lactation. Offspring from PR dams show a number of features of human cardio-metabolic disease, including hypertension, 34 increased fat deposition and altered feeding behaviour, [35][36][37] impaired glucose homeostasis, dyslipidaemia, 38 vascular dysfunction, 35,39 impaired immunity 40 and increased susceptibility to oxidative stress. 41 The phenotype of the offspring, however, does vary according to the exact composition of the diet.…”