Maternal obesity at conception programs obesity in the offspring.

Arkansas Children's Nutrition Center, 1212 Marshall Street, Little Rock, AR 72202, USA.
AJP Regulatory Integrative and Comparative Physiology (Impact Factor: 3.28). 02/2008; 294(2):R528-38. DOI: 10.1152/ajpregu.00316.2007
Source: PubMed

ABSTRACT Risk of obesity in adult life is subject to programming during gestation. To examine whether in utero exposure to maternal obesity increases the risk of obesity in offspring, we developed an overfeeding-based model of maternal obesity in rats utilizing intragastric feeding of diets via total enteral nutrition. Feeding liquid diets to adult female rats at 220 kcal/kg(3/4) per day (15% excess calories/day) compared with 187 kcal/kg(3/4) per day for 3 wk caused substantial increase in body weight gain, adiposity, serum insulin, leptin, and insulin resistance. Lean or obese female rats were mated with ad libitum AIN-93G-fed male rats. Exposure to obesity was ensured to be limited only to the maternal in utero environment by cross-fostering pups to lean dams having ad libitum access to AIN-93G diets throughout lactation. Numbers of pups, birth weight, and size were not affected by maternal obesity. Male offspring from each group were weaned at postnatal day (PND)21 to either AIN-93G diets or high-fat diets (45% fat calories). Body weights of offspring from obese dams did not differ from offspring of lean dams when fed AIN-93G diets through PND130. However, offspring from obese dams gained remarkably greater (P < 0.005) body weight and higher % body fat when fed a high-fat diet. Body composition was assessed by NMR, X-ray computerized tomography, and weights of adipose tissues. Adipose histomorphometry, insulin sensitivity, and food intake were also assessed in the offspring. Our data suggest that maternal obesity at conception leads to fetal programming of offspring, which could result in obesity in later life.

  • [Show abstract] [Hide abstract]
    ABSTRACT: A commercial pig spends nearly half of its life in utero and its nutrition during this time can influence birth weight and postnatal growth. We hypothesised that postnatal growth is increased in pigs raised by sows with a high backfat depth and high level of energy intake during gestation compared with sows with a low backfat depth and low level of energy intake during gestation. This was tested in a 2×3 factorial design experiment with 2 factors for gilt backfat depth (Thin and Fat) and 3 factors for gestation feed allowance (Restricted, Control and High). Between d 25 and d 90 of gestation, Thin gilts (n=68; 12±0.6 mm P2 backfat) and Fat gilts (n=72; 19±0.6 mm P2 backfat) were randomly allocated, as individuals, to a gestation diet (6.19 g/kg lysine, 13.0 MJ DE/kg) at the following feed allowances: 1.8 kg/day (Restricted); 2.5 kg/day (Control) and 3.5 kg/day (High). For the remainder of gestation and during lactation all gilts were treated similarly. At weaning (day 28), 155 piglets were sacrificed and 272 were individually housed and followed through to slaughter (day 158). At day 80 of gestation, fasted Thin Restricted gilts had lower serum IGF-1 concentrations than Thin High or Thin Control fed gilts (P<0.001). Pigs born from Fat gilts had greater backfat depths (P<0.05), a lower lean meat yield (P<0.05) and were heavier (P<0.05) at slaughter than pigs born from Thin gilts. Gilt gestation feed allowance had only transitory effects on average daily gain and feed conversion efficiency and had no effect on pig weight at slaughter (P>0.05) or lean meat yield (P>0.05). In conclusion, gilts with a backfat depth of ~19 mm at insemination produced pigs that were heavier and fatter at ~158 days of age than those born from gilts with ~12 mm backfat depth at insemination. Maternal body condition during gestation had a more predominant influence on growth parameters of the offspring, such as weight at slaughter and backfat depth, than did feed level during gestation.
    animal 02/2014; 8(2):236-44. · 1.65 Impact Factor
  • Source
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The adverse effects on offspring of diabetic and/or obese mothers can be passed to the next generation. However, the mechanisms behind this are still unclear. Epigenetics may play a key role during this process. To confirm the hypothesis, we investigated the DNA methylation of several imprinted genes in spermatozoa of offspring from diabetic and/or obese mothers utilizing streptozotocin (STZ)- and high-fat-diet (HFD)-induced mouse models. We found that the DNA methylation of Peg3 was significantly increased in spermatozoa of offspring of obese mothers compared to that in spermatozoa of offspring of normal mothers. The DNA methylation of H19 was significantly higher in spermatozoa of offspring of diabetic mothers than that in spermatozoa of offspring of non-diabetic mothers. These results indicate that pre-gestational diabetes and/or obesity can alter DNA methylation in offspring spermatozoa.
    Reproductive Biology and Endocrinology 01/2014; 12(1):29. · 2.14 Impact Factor


Available from
May 21, 2014