Metabolic Syndrome Linked to Prenatal Nicotine Exposure
Rat model shows prenatal nicotine exposure associated with early pancreatic and fat tissue changes, followed by metabolic syndrome later
WEDNESDAY, Nov. 26 (HealthDay News) -- Prenatal nicotine exposure directly leads to early pancreatic changes and subsequent metabolic syndrome, according to a report published in the December issue of Endocrinology.
Emmanuel Somm, Ph.D., of the Geneva University Hospitals in Switzerland, and colleagues used a rat model to mimic prenatal nicotine exposure. After birth, histological changes were measured in pancreatic and adipose tissue, while metabolic changes were measured later in life. The investigators also challenged the rats with glucose and insulin tolerance tests.
Early in life, several tissue changes were observed in rats with prenatal nicotine exposure, the researchers report. A decrease in both the number and size of pancreatic islet cells were observed at one week, accompanied by decreases in pancreatic-specific genes as well as hormones such as insulin and glucagon. As the rats began to wean, they exhibited an increase in expression of genes involved in adipose tissue formation, with concomitant increases in epididymal white adipose tissue, the investigators found. As the rats grew into adulthood, they exhibited several metabolic alterations indicative of metabolic syndrome, including increased body weight, elevated levels of fat deposition, heightened cold intolerance and reduced physical activity. Additionally, the rats became glucose intolerant and insulin resistant, the report indicates.
"We conclude that these early alterations in the pancreas might be due to a direct effect of fetal toxicity," the authors write, adding that the results "prove a direct association between fetal nicotine exposure and offspring metabolic syndrome."