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Perinatal Semaglutide Treatment Improves Maternal Health and Mitigates Offspring Metabolic Dysfunction in a Mouse
Insights
Maternal semaglutide treatment during pregnancy improved mother and offspring metabolic health in a mouse model. This suggests potential for GLP-1 therapies to reduce childhood metabolic risks like obesity and fatty liver disease.
Area of Science:
- Metabolic disease research
- Developmental biology
- Pharmacology
Background:
- Rising rates of childhood obesity, type 2 diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD) are linked to early-life exposures.
- Maternal obesity and insulin resistance during critical developmental periods can program offspring for lifelong metabolic risk.
Purpose of the Study:
- To evaluate the safety and metabolic effects of semaglutide, a GLP-1 receptor agonist (GLP-1 RA), in dams fed a high-fat diet (HFD) from preconception through lactation.
- To assess the impact of maternal semaglutide treatment on metabolic outcomes in both dams and their offspring.
Main Methods:
- Administered semaglutide to dams on HFD or standard diet from preconception through lactation.
- Assessed maternal body composition, glucose metabolism, and reproductive parameters.
- Evaluated offspring metabolic health, including glucose homeostasis and hepatic steatosis, at 18 weeks of age after weaning to a standard diet.
Main Results:
- Semaglutide improved maternal body composition and glucose metabolism in HFD-fed dams, with lasting effects post-treatment.
- Maternal HFD impaired offspring glucose homeostasis and promoted hepatic steatosis, which were ameliorated by maternal semaglutide treatment.
- Metabolic improvements in dams and offspring occurred without adverse effects on conception or fetal viability.
Conclusions:
- Perinatal GLP-1 receptor agonism with semaglutide can improve maternal metabolic health in an obesity model.
- Maternal semaglutide treatment mitigates adverse metabolic programming in offspring exposed to HFD during development.
- These findings support further investigation of GLP-1-based therapies to reduce metabolic dysfunction and risk in children.
Abstract:
Early-life exposures during critical periods of development significantly impact lifelong metabolic risk and likely contribute to the rising rates of obesity, type 2 diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD) in children. Here, we evaluated the safety and metabolic effects of semaglutide, a GLP-1 receptor agonist (GLP-1 RA), administered from preconception through lactation in dams fed a high-fat diet (HFD) or standard diet, and assessed metabolic outcomes in dams and their offspring. Offspring were weaned to a standard diet. We found that semaglutide improved body composition and glucose metabolism in HFD-fed dams during pregnancy. These maternal changes persisted 10 weeks after weaning despite discontinuation of semaglutide treatment. HFD exposure impaired glucose homeostasis and promoted hepatic steatosis in offspring at 18 weeks. These effects were ameliorated by maternal semaglutide treatment. Importantly, metabolic improvements in dams and offspring occurred without adverse effects on conception rate or fetal viability. These findings suggest that GLP-1 RA during the perinatal period can improve maternal and offspring metabolic health in a mouse model of obesity and support further investigation of GLP-1-based therapies to mitigate maternal metabolic dysfunction and improve metabolic risk in children.
Article Highlights:
Rates of obesity, type 2 diabetes, and fatty liver disease are rising in children, in part due to maternal obesity and insulin resistance that program offspring metabolic risk during the perinatal period.We asked whether the GLP-1 receptor agonist (GLP-1 RA), semaglutide, administered during critical developmental windows could prevent adverse outcomes in offspring using a diet-induced mouse model of maternal obesity.Semaglutide, given to dams from preconception through lactation, improved maternal metabolism and ameliorated metabolic dysfunction in offspring caused by maternal high-fat diet.These findings highlight a potential role for perinatal GLP-1 receptor agonism to improve maternal metabolic health and reduce metabolic risk in offspring.
