Reductions in caloric intake and early postnatal growth prevent glucose intolerance and obesity associated with low birthweight

Jimenez-Chillaron, Jose; Hernández-Valencia, Marcelino; Lightner, Amy L.; Faucette, Ryan; Reamer, C.; Przybyla, R.; Ruest, S.; Barry, Kristen; Otis, Jessica P.; Patti, Mary‐Elizabeth

doi:10.1007/s00125-006-0311-7

Cited by 154 publications

(104 citation statements)

References 44 publications

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“…Body composition Since growth curves suggested that undernourished mice had undergone postnatal catch-up growth, often accompanied by increased adiposity [18], we performed DEXA at 12, 16, 20 and 24 weeks. Fat mass (as percentage of body weight) at 24 weeks was significantly higher in the undernourished group than in controls (control: 20.3±4.8%; undernourished: 27.9±4.1%; p= 0.001) (Fig.…”

Section: Birthweight and Growth Parametersmentioning

confidence: 99%

In utero undernutrition reduces diabetes incidence in non-obese diabetic mice

et al. 2007

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Aims/hypothesis Observational studies in humans suggest that low birthweight may decrease the risk of type 1 diabetes, but the mechanism is unknown. We hypothesised that antenatal undernutrition would decrease the incidence of type 1 diabetes in non-obese diabetic (NOD) mice. Materials and methods A 40% restriction of energy intake was applied to pregnant NOD dams from day 12.5 to day 18.5 of gestation, resulting in intrauterine growth retardation of offspring. All mice were fed a standard diet after weaning. Control and undernourished female offspring were followed to assess diabetes incidence. Male NOD mice were treated with cyclophosphamide to accelerate development of diabetes. Glucose homeostasis, body composition and pancreatic histology were compared in control and undernourished offspring. Results Mean birthweight was lower in undernourished than in control mice (p=0.00003). At 24 weeks of age, the cumulative incidence of spontaneous diabetes in female mice was 73% in control and 48% in undernourished mice (p=0.003). In cyclophosphamide-treated male mice, antenatal undernutrition also tended to reduce the development of diabetes (p=0.058). Maternal leptin levels were lower in undernourished dams on day 18.5 of pregnancy (p=0.039), while postnatal leptin levels were significantly higher in undernourished offspring at 4, 20 and 27 weeks of life (p<0.05). Beta cell mass was similar in both groups (control = 0.4 mg; undernourished = 0.54 mg; p=0.24). Histological evidence of apoptosis at 20 weeks was greater in control than in undernourished mice (control = 6.3± 1.4%; undernourished = 4.2±0.3%, p=0.05). Conclusions/interpretation Antenatal undernutrition reduces the incidence of diabetes in NOD mice, perhaps via alterations in apoptosis.

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Section: Birthweight and Growth Parametersmentioning

confidence: 99%

In utero undernutrition reduces diabetes incidence in non-obese diabetic mice

et al. 2007

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“…Calorie restriction (50% of normal intake) of mice late in gestation did not affect body weight or food intake in offspring of either gender, but increased the relative body fat content in males at 6 months of age (24). No diffe rence was found in the body weight of 15-week-old rat offspring of either gender from dams fed a low-protein diet or a control diet during the entire gestation (25).…”

Section: Discussionmentioning

confidence: 85%

Prenatal essential fatty acid deficiency in mice results in long-term gender-specific effects on body weight and glucose metabolism

Pálsdóttir¹

2011

Mol Med Report

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Abstract. Essential fatty acids are important for normal growth and development in early life. However, the long-term effects of prenatal essential fatty acid deficiency (EFAD) on the adult metabolism remain to be determined. The aim of this study was to investigate the effects of an EFAD diet given to mice during late gestation on body weight and body composition, and metabolism in the adult offspring. Pregnant dams were given an EFAD or a control diet during the last 10 days of gestation. After delivery, all mice were fed normal chow and the body weight of the offspring was measured weekly. Furthermore, food intake, energy expenditure and intraperitoneal glucose tolera nce were analysed in the adult offspring in addition to body composition (analysed by dual-energy X-ray absorptiometry), plasma levels of leptin, triglycerides and cholesterol. The body weight was lower in the EFAD offspring as compared to the controls during the first 4 weeks of age, and remained lower in the females throughout the study. Lean body mass and plasma leptin levels were also lower in the female EFAD offspring as compared to the controls. Male EFAD offspring were found to have higher fasting glucose and insulin levels as well as higher insulin levels during the glucose tolerance test compared to the controls. However, no differences were found in blood lipids, food intake or energy expenditure between EFAD and control mice of either gender. These results demonstrate that an EFAD diet given during the last 10 days of gestation results in long-term gender-specific effects on body weight and insulin sensitivity in the adult offspring. IntroductionMaternal nutritional status during pregnancy and lactation is a significant factor in the adult health of the offspring. The combination of inadequate nutrition early in life and overnutrition later in life is thought to increase the risk of obesity and associated metabolic disorders such as type 2 diabetes (1). Essential fatty acids are required for normal growth and development in early life, and deficiency in humans results in growth retardation during the neonatal period (2). Low plasma levels of essential fatty acids have been observed in children with malnutrition (3-5), and in preterm infants (6). However, essential fatty acid deficiency (EFAD) in humans rarely occurs in isolation, but is common in general undernutrition or in dietary protein deficiency. Therefore, experimental animal models are useful to separate the specific long-term effects of EFAD from those of undernutrition and protein malnutrition.Adult rats subjected to EFAD from perinatal life and onwards had decreased body weight, but increased insulin levels before and during a glucose tolerance test to which these rats were subjected (7). In diabetes-prone BB rats, an EFAD diet commencing at 10 weeks of age reduced the incidence of autoimmune diabetes, and this reduction was associated with the depletion of omega-6 fatty acids (8). Metabolites of omega-6 fatty acids, such as prostaglandin E 2, are known to suppress glucose-...

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“…Epigenetic changes occur most often during gestation, neonatal development, puberty, and old age [9]. However, animal studies and human epidemiologic data suggest that long-term epigenetic changes that manifest in disease phenotypes are especially critical during the prenatal and neonatal stages as well as during times of 'dietary transition' in adulthood [32][33][34][35].…”

Section: Epigenetic Mechanisms That Impact Disease Developmentmentioning

confidence: 99%