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Yaghootkar, H.* ; Lamina, C.* ; Scott, R.A.* ; Dastani, Z.* ; Hivert, M.F.* ; Warren, L.L.* ; Stancáková, A.* ; Buxbaum, S.G.* ; Lyytikäinen, L.P.* ; Henneman, P.* ; Wu, Y.* ; Cheung, C.Y.* ; Pankow, J.S.* ; Jackson, A.U.* ; Gustafsson, S.* ; Zhao, J.H.* ; Ballantyne, C.M.* ; Xie, W.* ; Bergman, R.N.* ; Boehnke, M.* ; el Bouazzaoui, F.* ; Collins, F.S.* ; Dunn, S.H.* ; Dupuis, J.* ; Forouhi, N.G.* ; Gillson, C.* ; Hattersley, A.T.* ; Hong, J.* ; Kähönen, M.* ; Kuusisto, J.* ; Kedenko, L.* ; Kronenberg, F.* ; Doria, A.* ; Assimes, T.L.* ; Ferrannini, E.* ; Hansen, T.* ; Häring, H.-U. ; Knowles, J.W.* ; Lindgren, C.M.* ; Nolan, J.J.* ; Paananen, J.* ; Pedersen, O.* ; Quertermous, T.* ; Smith, U.* ; Lehtimäki, T.* ; Liu, C.T.* ; Loos, R.J.* ; McCarthy, M.I.* ; Morris, A.D.* ; Vasan, R.S.* ; Spector, T.D.* ; Teslovich, T.M.* ; Tuomilehto, J.* ; van Dijk, K.W.* ; Viikari, J.S.* ; Zhu, N.* ; Langenberg, C.* ; Ingelsson, E.* ; Semple, R.K.* ; Sinaiko, A.R.* ; Palmer, C.N.* ; Walker, M.* ; Lam, K.S.* ; Paulweber, B.* ; Mohlke, K.L.* ; van Duijn, C.M.* ; Raitakari, O.T.* ; Bidulescu, A.* ; Wareham, N.J.* ; Laakso, M.* ; Waterworth, D.M.* ; Lawlor, D.A.* ; Meigs, J.B.* ; Richards, J.B.* ; Frayling, T.M.*

Mendelian randomization studies do not support a causal role for reduced circulating adiponectin levels in insulin resistance and type 2 diabetes.

Diabetes 62, 3589-3598 (2013)

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Adiponectin is strongly inversely associated with insulin resistance and type 2 diabetes, but its causal role remains controversial. We used a Mendelian randomization approach to test the hypothesis that adiponectin causally influences insulin resistance and type 2 diabetes. We used genetic variants at the ADIPOQ gene as instruments to calculate a regression slope between adiponectin levels and metabolic traits (up to 31,000 individuals) and a combination of instrumental variables and summary statistics-based genetic risk scores to test the associations with gold-standard measures of insulin sensitivity (2,969 individuals) and type 2 diabetes (15,960 case subjects and 64,731 control subjects). In conventional regression analyses, a 1-SD decrease in adiponectin levels was correlated with a 0.31-SD (95% CI 0.26-0.35) increase in fasting insulin, a 0.34-SD (0.30-0.38) decrease in insulin sensitivity, and a type 2 diabetes odds ratio (OR) of 1.75 (1.47-2.13). The instrumental variable analysis revealed no evidence of a causal association between genetically lower circulating adiponectin and higher fasting insulin (0.02 SD; 95% CI -0.07 to 0.11; N = 29,771), nominal evidence of a causal relationship with lower insulin sensitivity (-0.20 SD; 95% CI -0.38 to -0.02; N = 1,860), and no evidence of a relationship with type 2 diabetes (OR 0.94; 95% CI 0.75-1.19; N = 2,777 case subjects and 13,011 control subjects). Using the ADIPOQ summary statistics genetic risk scores, we found no evidence of an association between adiponectin-lowering alleles and insulin sensitivity (effect per weighted adiponectin-lowering allele: -0.03 SD; 95% CI -0.07 to 0.01; N = 2,969) or type 2 diabetes (OR per weighted adiponectin-lowering allele: 0.99; 95% CI 0.95-1.04; 15,960 case subjects vs. 64,731 control subjects). These results do not provide any consistent evidence that interventions aimed at increasing adiponectin levels will improve insulin sensitivity or risk of type 2 diabetes.

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