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While there are still many questions about TCF7L2 left unanswered, it has been shown that TCF7L2 is essential to the production of proglucagon via the intestinal cells (not the glucagon produced in the alpha cells of the pancreas).[ref] Genetic variants in TCF7L2 are associated with impaired glucose stimulation of insulin secretion and GLP-1.[ref] GLP1R (glucagon-like peptide 1 receptor) receives the signal from GLP-1, and variants in GLP1R have associations with altered BMI, weight, and insulin resistance

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Despite this, there was no association between the duration of treatment and the dose administered