An alternative hypothesis to explain our findings is that variants in TCF7L2 disrupt adipogenesis and/or adipocyte function by altering the transcriptional regulation of PPARG leading to deposition of triglycerides in peripheral tissues (i.e., liver and muscle) and resulting in insulin resistance or that the defect on insulin secretion would be exacerbated by acute free fatty acid (FFA)-induced insulin resistance [19, 21, 22]. Here, TCF7L2 is linked to Insulin resistance.