Earlier pubertal onset in girls is associated with later-life type 2 diabetes (T2D) risk. Studies have shown that age at menarche (AAM), a marker of girls’ pubertal timing, and T2D are genetically correlated genome-wide. Since both AAM and T2D also correlate with BMI, the biological link between the two traits could be mediated via BMI. As the most recent genome-wide association study (GWAS) for T2D also adjusted for BMI, we queried if AAM and T2D remain correlated after removing the effect of BMI on T2D. Leveraging such large-scale GWAS data, LD Score Regression revealed that the genetic correlation between AAM and T2D (rg (SE)=-0.24 (0.02) P=2.2x10-22) was only partly attenuated after BMI adjustment (rg (SE)=-0.1 (0.03) P=0.0002), suggesting that BMI does not entirely explain the puberty-T2D link. Five of the 13 significant GWAS-implicated loci associated with both AAM and T2D do not associate with BMI, further supporting that BMI is not the only mediator between the two traits. Given that causal effector genes are unknown at most GWAS loci, identification of target genes at these shared loci should provide key biological insights. To implicate effector genes, we first identified all SNPs in LD with the sentinel SNPs. We then extracted the subsets of proxy SNPs in open chromatin, determined by ATAC-seq, in primary cells or cell lines relevant to this trait area beta cells (EndoC-βH1), adipose (SGBS and MSC-derived adipocytes), and—given recent findings in both AAM and BMI studies—brain (neural precursors, microglia, astrocytes and hypothalamic neurons). Using high resolution Capture-C, we detected consistent physical contacts between open-proxy SNPs and candidate effector genes. Our results support direct SNP-to-gene promoter contacts for at least four of these shared loci (one not associated with BMI) including TSPAN3 at ‘AC046168.1’ and TFAP2D at ‘TFAP2B’, along with leads at the ‘MTCH2/CELF1’ and ‘MAP2K5’ loci. Follow-up experiments are needed to determine the physiological roles of implicated target genes. Disclosure D.L. Cousminer: None. R. Mishra: None. M.A. Argenziano: None. E. Manduchi: None. K.M. Hodge: None. C. Su: None. M. Leonard: None. S. Lu: None. J.A. Pippin: None. M. Johnson: None. A.D. Wells: Research Support; Self; GlaxoSmithKline plc. A. Chesi: None. B.F. Voight: None. S.F. Grant: None. Funding American Diabetes Association (1-17-PDF-077 to D.L.C.); National Institutes of Health