Leptin exposure could increase type 2 diabetes development in children

A hormone secreted by fat cells that is crucial to maintaining energy balance in the body could help explain how type 2 diabetes develops, particularly in children of obese mothers.
Leptin is one of the many hormonal factors that is crucial for the regulation of insulin secretion and blood glucose levels.
In this new study, researchers at The Saban Research Institute of Children’s Hospital Los Angeles (CHLA) report that leptin stops the prenatal development of neuronal connections between the brain and the pancreas.
The scientists used mouse models to create direct connections between the brain and pancreatic beta cells. As they examined the factors influencing these connections during embryonic development, they found that leptin receptors were highly expressed in the brain stem.
“We showed that exposure of the embryonic mouse brain to leptin during a key developmental period resulted in permanent alternations in the growth of neurons from the brain stem to the pancreas, resulting in long-term disturbances to the balance of insulin levels in the adult mouse,” said Sebastien G. Bouret, PhD, researcher in the developmental neuroscience program at CHLA.
The scientists then injected a single dose of leptin directly in the brain of mouse embryos during mid-gestation. This resulted in a permanent reduced connectivity between brain stem and pancreas.
Bouret explained: “This breakdown in communication from the brain to the pancreas resulted in impaired glucose regulatio, or homeostasis, in the adult mouse.
“This study reveals an unanticipated regulatory role for the leptin hormone known to be produced by fat cells. Because babies of obese moms have high levels of lepti, it might put them at a higher risk for type 2 diabetes and obesity.”
While the study shows that a high level of leptin appears to be a factor in the development of type 2 diabetes in children, a child’s diet is the most important factor in reducing this risk.
The findings appear in the journal Cell Reports.