	Hyperglycemia during pregnancy is thought to cause epigenetic changes in the leptin gene of newborns leading to a potential increased risk for obesity and heart disease. Leptin is sometimes known as the “satiety hormone” because it is released by fat cells to inhibit hunger. By studying both animal models and human observational studies, it has been suggested that a leptin surge in the perinatal period plays a critical role in contributing to long-term risk of obesity. The perinatal period begins at 22 weeks gestation and ends a week after birth.[34] DNA methylation near the leptin locus has been examined to determine if there was a correlation between maternal glycemia and neonatal leptin levels. Results showed that glycemia was inversely associated with the methylation states of LEP gene, which controls the production of the leptin hormone. Therefore, higher glycemic levels in mothers corresponded to lower methylation states in LEP gene in their children. With this lower methylation state, the LEP gene is transcribed more often, thereby inducing higher blood leptin levels. These higher blood leptin levels during the perinatal period were linked to obesity in adulthood, perhaps due to the fact that a higher “normal” level of leptin was set during gestation. Because obesity is a large contributor to heart disease, this leptin surge is not only correlated with obesity but also heart disease.