A short region on human chromosome 16 increases risk of being underweight
01.09.2011
Duplications of a short region on chromosome 16 are associated with an increased risk of being underweight, according to a report in Nature this week.
Deletion of this same section has previously been associated with obesity, indicating a possible opposing causal link between being underweight and being obese.
Extremes at either end of the weight scale pose important health risks. Although a number of genetic variants have been associated with obesity, little is known about the genetic basis of being underweight.
Jacques Beckmann and colleagues show that carriers of duplications of the locus 16p11.2 have notably lower postnatal weight and BMI compared with a reference population.
Each of the observed associated characteristics is opposite of those reported in carriers of deletions at this locus. Moreover, these traits correlate with changes in transcript levels for genes within the duplication but not within the adjacent regions.
The authors conclude that severe obesity and being underweight could have mirror aetiologies, possibly through contrasting effects on energy balance.
International research group includes scientists from University of Lausanne (Switzerland), University of Tartu Institute of Molecular and Cell Biology, UT Estonian Genome Project and UT Clinic's United Lab's Centre of Genetics.
Additional information: Katrin Männik, researcher, phone +372 510 4789, kmannik [ät] ebc [dot] ee
Anneli Miljan
UT Press Officer
737 5683, 515 0184
avalik [ät] ut [dot] ee
www.ut.ee
Deletion of this same section has previously been associated with obesity, indicating a possible opposing causal link between being underweight and being obese.
Extremes at either end of the weight scale pose important health risks. Although a number of genetic variants have been associated with obesity, little is known about the genetic basis of being underweight.
Jacques Beckmann and colleagues show that carriers of duplications of the locus 16p11.2 have notably lower postnatal weight and BMI compared with a reference population.
Each of the observed associated characteristics is opposite of those reported in carriers of deletions at this locus. Moreover, these traits correlate with changes in transcript levels for genes within the duplication but not within the adjacent regions.
The authors conclude that severe obesity and being underweight could have mirror aetiologies, possibly through contrasting effects on energy balance.
International research group includes scientists from University of Lausanne (Switzerland), University of Tartu Institute of Molecular and Cell Biology, UT Estonian Genome Project and UT Clinic's United Lab's Centre of Genetics.
Additional information: Katrin Männik, researcher, phone +372 510 4789, kmannik [ät] ebc [dot] ee
Anneli Miljan
UT Press Officer
737 5683, 515 0184
avalik [ät] ut [dot] ee
www.ut.ee