In recent years, the evolutionarily conserved gene LIN28B
has been convincingly associated with both timing of puberty and growth in height in humans 
. Highlighting its pleiotropic effects, the locus has also been associated with finger-length ratio 
. Mice over-expressing the homologous gene, LIN28A
, recapitulate the same phenotypes as observed in human GWA-studies, including increased growth in length and delayed onset of puberty 
. Additionally, overexpression of LIN28B
in muscle tissue renders mice under high fat diet resistant to weight gain through increased peripheral glucose uptake and insulin sensitivity 
. The extent to which LIN28B
may impact on adiposity and energy metabolism in humans is currently unknown. This study, including 26,636 adult study subjects from the homogenous population of Finland, identified evidence supporting that genetic variation near LIN28B
impacts body weight, BMI and hip circumference predominantly in females.
In the current study, we chose to genotype two genetic markers located upstream of LIN28B
, rs7759938 and rs314279. The former has been robustly associated with pubertal timing and adult height. The latter, here associating with female body size and male insulin levels, appears to be less well studied. The pair-wise correlation of rs314279 with rs7759938 (the lead SNP associating with AAM) is only 0.30, and a large meta-analysis including 87,802 women reported evidence also for association between rs314279 and AAM. The finding may indicate the presence of two independent effects at the LIN28B
region influencing the trait. Nonetheless, this has not been confirmed. Many of the cohorts participating in the meta-analysis study of AAM were lacking data for the marker rs314279, and conditioned analyses interrogating the independent effect of that marker were not carried out 
. It is possible that rs314279 is poorly covered by large GWA studies in general and that limited data availability might explain why previous GWA studies of BMI, in contrast to our study, have not detected association between BMI and this particular marker 
. More importantly, in our study the impact of rs314279 on body size appeared stronger when adjusting for the partially correlated rs7759938, but in previous GWA-studies of BMI this model has not been assessed in detail. Finally, whereas our study targets a single, homogenous population, the GWA studies are mostly based on meta-analysis of multiple distinct study cohorts. Therefore, the discrepancy in results might in part originate from a population specific effect, although the accumulated data from association studies of common genetic variants show little evidence for variation in phenotype response between different populations of European descent. Nonetheless, even if our study sample is large, we do acknowledge that further replication studies are needed to verify the findings.
So far only one other study has suggested that genetic variants near LIN28B
may affect adult BMI 
. In that study the effect of rs314276 on BMI was evaluated, and the authors found evidence for an age-dependent interaction between the SNP and BMI, in females. Even though rs314276 is completely correlated with one of the markers in the current study, rs7759938, we could not replicate the previous finding. In our study we did not find any evidence for genotype by age interaction at any of the tested marker loci. Of note, the two studies differ by study design, the former being a longitudinal study of a birth cohort and our study representing a cross-sectional study including individuals born between 1923 and 1982. Thus it is possible that varying environmental influences may have prevented detection of an existing age interaction in our study. The disparate results could also be due to differences in the LD-structure between the study populations. Finally, given the power needed to robustly show gene-environment interactions, the results reported in the previous study may represent a false positive effect. Thus, further targeted replication studies are required to elucidate the detailed contribution of LIN28B
to human body shape and adiposity.
In conclusion, this study shows that genetic variants near LIN28B in addition to influencing height growth also associate with female body shape. These data support the accumulating evidence linking LIN28B-mediated pathways with adult adiposity-related traits.