Obese
Pregnant Moms May Mean Fat Offspring
The
number of overweight and obese Americans continues to grow rapidly.
Today, 50 percent of adults are overweight and up to 20 percent
are obese. While the number of overweight/obese children is at
an all time high, the steady increase of overweight infants --
individuals under 11 months old -- is alarming.
Research studies have found
that pregnant women who are overweight/obese are more likely to
give birth to heavier babies, and the risk of overweight children
becoming obese adults is nearly nine times greater than for children
who are not overweight. Studies also show that greater body-weight
at birth and weight gain early in life increases the risk of becoming
overweight or obese as an adult. Inheritance studies show that
a child's body mass index (BMI) correlates more closely with the
mother's BMI than with it's father's, suggesting that an interaction
of both genetic and intrauterine influences, may contribute to
later-life obesity risk in the offspring.
Armed with these and other
data, a team of researchers from the USDA-Arkansas Children's
Nutrition Center has examined whether the subtle effects of fetal
exposure to the mother's obesity can have a latent effect on the
offspring. In a new report, investigators studied whether fetal
exposure to gestational obesity leads to a self-reinforcing viscious
cycle of excessive weight gain and body fat which passes from
mother to child. The results of the new study suggest they do.
The
study is entitled, "Maternal Obesity at Conception Programs
Obesity in the Offspring." It was conducted by the research
team of Kartik Shankar, Amanda Harrell, Xiaoli Liu, Janet M. Gilchrist,
Martin J.J. Ronis and Thomas M. Badger, all of the Arkansas Children's
Nutrition Center, Little Rock, AR. Their findings appear in the
online edition of the American Journal of Physiology -- Regulatory,
Integrative and Comparative Physiology (doi:10.1152/ajpregu.00316.2007).
The journal is one of 11 published each month by the American
Physiological Society (APS; http://www.the-aps.org/).
To test the theory that obesity
in adulthood may be subject to programming during fetal development,
the researchers developed an overfeeding model which was used
in rats. The model allowed the investigators to replicate many
of the metabolic and hormonal features of overweight human individuals.
They were also able to exclude parental genetic influences, match
gestational weight gain, limit the exposure of maternal obesity
in utero, and control lactation efficiency, all of which can be
difficult confounding variables in studies with human subjects.
Virgin
female rats were fed liquid diets via enteral nutrition at one
of two caloric levels: (1) the caloric level recommended by the
National Research Council (187 kcal/kg3/4/day) or (2) a level
of 15 percent overfeeding (220 kcal/kg3/4/day). In the preliminary
experiments, the rats consuming the normal caloric intake had
weight gains similar to controls while those being fed the obesegenic
diet had become substantially overweight. Body weights were monitored
three times a week and body composition was analyzed non-invasively
on a regular basis.
To examine the long-term gestational
effects of maternal obesity on the offspring, lean (n=7) and obese
(n=15) rats were allowed to mate with normal (lean) male rats
for a period of one week. Following mating, all female rats (lean
and obese) received respective diets at 15 percent excess calories
per day in order to ensure adequate caloric intake for pregnancy.
Maternal body weights were monitored three times a week and all
rats gave birth naturally. Offspring born to lean or obese rats
were raised by surrogates who were fed regular rodent diets to
ascertain the pups' obesity exposure was limited only during gestation.
The male offspring from each
group were weaned from the surrogate mother at 21 days after birth
and fed (by giving unlimited access to) either a normal diet or
a high-fat diet. The pups' body weight, body composition and other
factors were analyzed for 130 days. At day 130 additional samples
were taken and analyzed, to include organ weights, glucose and
triglyceride levels, fat cell size, body composition and hormones.
The
researchers found the following:
•
at birth, the weight of the offspring from both groups was similar.
The number and size of pups and the ratio of males to females
did not differ significantly.
•
the amount of calories the pups consumed (relative to their body-weight)
at the 60- and 120-day mark suggested that both groups consumed
the same amount of calories, indicating no effect of maternal
obesity on the offspring's food intake.
•
when both the lean and obese offspring were fed a control diet,
their body weights remained similar. However, when both groups
were fed a high-fat diet, the obese offspring gained remarkably
more weight, suggesting that exposure to maternal obesity led
to programming of increased susceptibility to obesity in the offspring,
which was revealed following an obesegenic challenge despite a
normal birth weight.
•
when both groups were fed a control diet, obese offspring had
a ~ 1.6 times greater fat ratio compared to their lean offspring
counterparts. Further, obese offspring fed a high-fat diet had
a 26 percent greater percent fat ratio and a 60 percent increase
in subcutaneous fat mass vs. lean offspring.
•
high fat feeding significantly increased serum glucose, triglyceride,
insulin and leptin levels in both groups. Strikingly, the serum
insulin and leptin levels increased by 2.2 and 2.3 fold in obese
offspring compared to lean offspring fed the same diet.
These
findings add to the existing body of evidence showing that both
maternal obesity and genetic background influence offspring's
susceptibility to obesity. It goes further, to highlight the role
of post-natal obesegenic diet as a determinant in revealing subtle
programming imposed by maternal obesity. The results also demonstrate
that high levels of adiposity (body fat) occur in the offspring
of obese mothers despite consuming similar calories as their lean-offspring
counterparts and that offspring obesity is associated with insulin
resistance.
The "programming"
of susceptibility to obesity occurs in the absence of changes
in birth weights and other fetal outcomes.
According to Dr. Kartik Shankar
of the Arkansas Children's Nutrition Center, "The mother's
body composition at conception has important implications for
the metabolism and risk of obesity in the offspring in later years.
Not only do these findings help us appreciate the reasons for
the rapid rise in obesity, this novel model will allow us to understand
the underlying mechanisms and should provide fertile opportunity
for translational type research." |