Abstract
ContextPubertal timing is under strong genetic control and its early onset associates with several adverse health outcomes in adulthood, including obesity, type 2 diabetes and cardiovascular disease. Recent data indicate strong association between pubertal timing and genetic variants near LIN28B, but it is currently unknown whether the gene contributes to the association between puberty and adult disease.ObjectiveTo elucidate the putative genetic link between early puberty and adult disease risk, we examined the association of two genetic variants near LIN28B with adult body size and metabolic profiles in randomly ascertained adult Finnish males and females.MethodsTwo single nucleotide polymorphisms (SNPs), rs7759938, the lead SNP previously associated with pubertal timing and height, and rs314279, previously also associated with menarcheal age but only partially correlated with rs7759938 (r2 = 0.30), were genotyped in 26,636 study subjects participating in the Finnish population survey FINRISK. Marker associations with adult height, weight, body mass index (BMI), hip and waist circumference, blood glucose, serum insulin and lipid/lipoprotein levels were determined by linear regression analyses.ResultsBoth rs7759938 and rs314279 associated with adult height in both sexes (p = 2×10−6 and p = 0.001). Furthermore, rs314279 associated with increased weight in females (p = 0.001). Conditioned analyses including both SNPs in the regression model verified that rs314279 independently associates with adult female weight, BMI and hip circumference (p<0.005). Neither SNP associated with glucose, lipid, or lipoprotein levels.ConclusionGenetic variants near the puberty-associated gene LIN28B associate with adult weight and body shape in females, suggesting that the gene may tag molecular pathways influencing adult adiposity-related traits.
Highlights
A wealth of epidemiological data show that the overall risk for many adult-onset multi-factorial disorders may correlate with distinct growth patterns during early development [1]
The timing of puberty is strongly regulated by genes and early timing has been associated with an increased risk for various adverse health outcomes, including obesity, type 2 diabetes, cardiovascular disease and hormone dependent cancers [2,3,4,5]
The genetic framework influencing pubertal timing in the general population remains poorly understood, recent genome-wide association (GWA) studies have initiated the identification of puberty-associated genes
Summary
A wealth of epidemiological data show that the overall risk for many adult-onset multi-factorial disorders may correlate with distinct growth patterns during early development [1]. The timing of puberty is strongly regulated by genes and early timing has been associated with an increased risk for various adverse health outcomes, including obesity, type 2 diabetes, cardiovascular disease and hormone dependent cancers [2,3,4,5]. The genetic framework influencing pubertal timing in the general population remains poorly understood, recent genome-wide association (GWA) studies have initiated the identification of puberty-associated genes. Even though variants near the gene have been associated with adult height and 2D:4D digit-length ratio in humans, it has not been implicated in the recent large GWA studies of obesity-related traits or Type 2 diabetes [12,13,14,15]. Epidemiological studies suggest that the genetic influences on body composition in general may become less prominent with increasing age [19]
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