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Body Fat Distribution and Glucose Homeostasis Is Affected by Perinatal Exposure to High Dietary Advanced Glycation
Zaher Merhi1,2,3, Xiu Quan Du2, Maureen J Charron2,4,5
1Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, Maimonides Medical Center, Brooklyn, New York, USA.
Insights
Maternal high advanced glycation end products (AGEs) diet during pregnancy and lactation impaired offspring growth and glucose metabolism. Perinatal AGEs exposure may contribute to metabolic syndrome development.
Area of Science:
- Metabolic health
- Developmental biology
- Nutritional science
Background:
- Perinatal development is critical for long-term metabolic health.
- Dietary advanced glycation end products (AGEs), common in Western diets, are pro-inflammatory.
- Maternal diet during gestation and lactation can influence offspring metabolic programming.
Purpose of the Study:
- To investigate the impact of perinatal exposure to dietary AGEs on offspring metabolic parameters.
- To assess effects on adiposity and glucose homeostasis in male mice offspring.
Main Methods:
- Female mice were fed low AGE (L-AGE) or high AGE (H-AGE) diets before and during pregnancy/lactation.
- Offspring were monitored for growth, adiposity (Echo MRI), and metabolic function (glucose/insulin tolerance tests).
- Serum leptin levels were also analyzed.
Main Results:
- Offspring from H-AGE dams exhibited lower birth weight and reduced fat mass but higher lean body mass.
- Impaired glucose homeostasis was observed, indicated by higher glucose levels during glucose tolerance tests (GTT) and insulin tolerance tests (ITT).
- Lower serum leptin levels were found in offspring exposed to the H-AGE diet.
Conclusions:
- Perinatal exposure to a maternal diet high in AGEs negatively impacts offspring growth and glucose regulation.
- Dietary AGEs during critical developmental windows may be a significant factor in the etiology of metabolic dysfunction and the metabolic syndrome.
Problem:
Exposures during the perinatal period, a phase of rapid development and growth, may have a profound and sustained effect on metabolic disturbances later in life. The pro-inflammatory advanced glycation end products (AGEs) are widely consumed in the Western diet. The purpose of this study was to determine whether perinatal exposure to these dietary AGEs alters metabolic parameters, in particular adiposity and glucose hemostasis, in male mice offspring.
Methods:
Seven-week-old female CD1 mice were placed before mating and then throughout pregnancy and lactation on either a low AGE (L-AGE; n = 13) or high AGE (H-AGE; n = 13) diet. All offspring in both groups were weaned postnatal day 21 onto normal diet and studied through to 21 weeks of age. The offspring were counted and weighed weekly, starting at birth until 21 weeks of age, to assess the growth curve. At the time of sacrifice, Echo MRI was performed to measure adiposity and to record liver, white epididymal adipose tissue (WAT), and inguinal fat weights. Serum levels of leptin as well as insulin and glucose tolerance tests (ITT and GTT) were compared.
Results:
The Body weight at birth of offspring of dams that were on H-AGE diet was significantly lower compared to the body weight of offspring of dams that were on L-AGE diet. Echo MRI data showed that the offspring of dams that were H-AGE diet had significantly lower fat mass, lower epididymal WAT fat weight, and lower inguinal fat weight but higher lean body mass and similar liver weight. They also had significantly higher glucose levels during GTT and ITT, as well as significantly lower serum leptin levels compared to the offspring of dams that were on the L-AGE diet.
Conclusions:
These results indicate that perinatal exposure to a maternal diet elevated in AGEs causes deficits in perinatal growth and impairment in glucose hemostasis in male mice. These findings suggest that AGEs may represent an important new class of mediators of adiposity and the metabolic syndrome.
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