Editing Maternal effect (section)

===High fat diets during gestation correlated with metabolic syndrome===
High fat diets in utero are believed to cause metabolic syndrome. [[Metabolic syndrome]] is a set of symptoms including obesity and insulin resistance that appear to be related.  This syndrome is often associated with type II diabetes as well as hypertension and atherosclerosis.  Using mice models, researchers have shown that high fat diets in utero cause modifications to the [[adiponectin]] and leptin genes that alter gene expression; these changes contribute to metabolic syndrome.  The adiponectin genes regulate glucose metabolism as well as fatty acid breakdown; however, the exact mechanisms are not entirely understood.  In both human and mice models, adiponectin has been shown to add insulin-sensitizing and anti-inflammatory properties to different types of tissue, specifically muscle and liver tissue.  Adiponectin has also been shown to increase the rate of fatty acid transport and oxidation in mice, which causes an increase in fatty acid metabolism.<ref name="care.diabetesjournals.org">{{cite journal |vauthors=Chandran M, Phillips SA, Ciaraldi T, Henry RR |title=Adiponectin: more than just another fat cell hormone? |journal=Diabetes Care |volume=26 |issue=8 |pages=2442–50 |year=2003 |pmid=12882876 |doi=10.2337/diacare.26.8.2442 |doi-access=free }}</ref>  With a high fat diet during gestation, there was an increase in methylation in the promoter of the adiponectin gene accompanied by a decrease in acetylation. These changes likely inhibit the transcription of the adiponectin genes because increases in methylation and decreases in acetylation usually repress transcription.  Additionally, there was an increase in methylation of the leptin promoter, which turns down the production of the leptin gene.  Therefore, there was less adiponectin to help cells take up glucose and break down fat, as well as less leptin to cause a feeling of satiety.  The decrease in these hormones caused fat mass gain, glucose intolerance, hypertriglyceridemia, abnormal adiponectin and leptin levels, and hypertension throughout the animal's lifetime.  However, the effect was abolished after three subsequent generations with normal diets. This study highlights the fact that these epigenetic marks can be altered in as many as one generation and can even be completely eliminated over time.<ref>{{cite journal |vauthors=Masuyama H, Mitsui T, Nobumoto E, Hiramatsu Y |title=The Effects of High-Fat Diet Exposure In Utero on the Obesogenic and Diabetogenic Traits Through Epigenetic Changes in Adiponectin and Leptin Gene Expression for Multiple Generations in Female Mice |journal=Endocrinology |volume=156 |issue=7 |pages=2482–91 |year=2015 |pmid=25853666 |doi=10.1210/en.2014-2020 |doi-access=free }}</ref>  This study highlighted the connection between high fat diets to the adiponectin and leptin in mice.  In contrast, few studies have been done in humans to show the specific effects of high fat diets in utero on humans.  However, it has been shown that decreased adiponectin levels are associated with obesity, insulin resistance, type II diabetes, and coronary artery disease in humans.  It is postulated that a similar mechanism as the one described in mice may also contribute to metabolic syndrome in humans.<ref name="care.diabetesjournals.org"/>