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Effects of maternal obesity on fasting metabolism in newborn rats
1Department of Pediatrics, Case Western Reserve University, Rainbow Babies and Children's Hospital, Cleveland, OH 44106.
Insights
Maternal obesity in rats leads to neonatal hypoglycemia in pups. Obese mothers had pups with altered hepatic glycogen and triglyceride stores, suggesting impaired energy mobilization after birth.
Area of Science:
- Perinatal Medicine
- Neonatal Metabolism
- Endocrinology
Background:
- Maternal obesity is a known risk factor for infant hypoglycemia.
- Neonatal metabolic adaptations are crucial for survival after birth.
- Animal models are essential for studying complex maternal-fetal health issues.
Purpose of the Study:
- To investigate the impact of maternal obesity on neonatal metabolic adaptations in rat pups.
- To examine hepatic glycogen and triglyceride stores in offspring of obese versus lean mothers.
- To understand the mechanisms behind neonatal hypoglycemia in pups born to obese mothers.
Main Methods:
- Induction of obesity in female Sprague-Dawley rats using a cafeteria diet prior to and during pregnancy.
- Comparison of maternal weight gain, food consumption, and pup parameters (weight, litter size) between obese and lean groups.
- Assessment of hepatic glycogen and triglyceride content in fetuses and pups after varying fasting periods.
Main Results:
- Obese mothers exhibited significantly higher pre-pregnancy weight and weight gain during gestation.
- Pups born to obese mothers showed hypoglycemia after fasting (150 and 180 min) compared to controls.
- Increased fetal hepatic glycogen and triglyceride stores were observed in pups of obese mothers.
- Hepatic glycogen stores declined minimally post-birth in pups of obese mothers, remaining higher than controls.
- Hepatic triglyceride stores were mobilized during fasting in pups of obese mothers, unlike controls where they increased.
Conclusions:
- Maternal obesity results in augmented fetal hepatic glycogen and triglyceride stores in rat pups.
- Neonatal hypoglycemia in offspring of obese mothers may stem from attenuated hepatic glycogen mobilization.
- This study highlights the significant impact of maternal metabolic status on neonatal energy homeostasis.
Abstract:
Maternal obesity is a risk factor for subsequent fasting hypoglycemia in human infants after birth. To investigate further this problem, we employed an animal model of obesity to study neonatal extrauterine metabolic adaptations in pups of obese and lean rats. Female Sprague-Dawley rats were fed a 'cafeteria diet' to induce obesity prior to and during pregnancy. Prior to mating, the cafeteria fed rats were significantly heavier (449 v. 345 g, P less than 0.001) than the controls. Furthermore, weight gain during pregnancy and weight at term were also significantly greater in the obese rats even though they consumed less food during pregnancy. Pup weights and the number of pups per litter were similar between the two groups. Pups born to obese mothers demonstrated hypoglycemia after being fasted for 150 and 180 min when compared with control pups. Hepatic glycogen stores were increased in the fetus of pups born to obese mothers. Glycogen content in pups born to obese mothers declined minimally after birth and remained greater than hepatic glycogen values in control pups throughout the study. In addition to increased fetal storage of glycogen, fetal hepatic triglyceride content was augmented in pups of obese rats. These triglyceride stores declined and were mobilized during fasting after birth. In contrast, hepatic triglyceride content increased after birth among control rats. These results suggest that maternal obesity results in augmented fetal hepatic tissue stores of both glycogen and triglycerides. Hypoglycemia among pups of excessively obese mothers may be due to attenuated mobilization of hepatic glycogen.(ABSTRACT TRUNCATED AT 250 WORDS)