Diabetes risk linked to body weight
The development of insulin resistance is influenced more by current body weight than by birth weight, says study.health and fitness Updated: Dec 25, 2007 11:13 IST
In adults, the development of insulin resistance, a precursor to diabetes, is influenced more by current body weight than by birth weight, results of a study in twins suggests.
The results also suggest that the postnatal (after delivery) growth pattern is potentially more important in terms of later development of insulin resistance than fetal growth.
"Previous research has shown that those who are small at birth are more likely to experience rapid weight gain in childhood, which is strongly related to obesity and increased insulin resistance in adulthood," Dr Paula Skidmore of the University of East Anglia, Norwich, England, notes in a written statement."Our data show that this postnatal weight gain and current body size are the chief influencers of insulin resistance," she adds.
How the body metabolises glucose (sugar) and insulin are thought to be programmed in the womb, Skidmore and colleagues explain. And low birth weight, as a proxy for an adverse fetal environment, has been linked to high insulin levels. However, it is not clear whether this inverse relationship is a strictly "in the womb" effect.
The investigators studied relationships between birth weight, body mass index (BMI) and change in body size over the life course and insulin resistance in 1194 female twins aged 18 to 74 years.
They failed to find any significant relationship between a person's weight at birth and the development of insulin resistance, the investigators report.
However, there was a significant positive relationship between insulin resistance and current weight; insulin resistance increased as current BMI increased.
This association was mediated equally through both individual effects and shared environment influences of the twins. There was no evidence that relationships between birth weight, BMI and change in body size and insulin resistance were mediated by genetic makeup.
SOURCE: Journal of Clinical Endocrinology & Metabolism, online December 2007.