Currently, nearly 10% of Americans have type 2 diabetes (T2D), placing it among the most common chronic diseases in the United States.  Growing evidence points to brain neurocircuits that regulate glucose homeostasis as potential targets for developing novel therapeutics to treat T2D. Recent studies have revealed that the brain can induce sustained remission of hyperglycemia in rodent models following intracerebroventricular (icv) injection of fibroblast growth factor 1 (FGF1). FGF1 stimulates the MAPK/ERK signal transduction system, which translates signals from the activation of cell surface receptors into gene expression changes within the cell nucleus. Following FGF1 injection, tanycytes and astrocytes are sites of transcriptional changes related to the ERK pathway. Inhibition of MAPK/ERK signaling blocks FGF1-induced diabetes remission. Like other growth factors, FGF1 requires integrin signaling to elicit the full spectrum of its cellular responses.  The integrin receptor αvβ3, which is implicated in the chronic cellular response to FGF1 is expressed in hypothalamic neurons and tanycytes and is required for FGF1 to induce sustained activation of MAPK/ERK signaling. To determine if integrin signaling in tanycytes is required for FGF1 to induce diabetes remission, we utilized adult, male, diabetic mice expressing either floxed Integrin β3 (ITβ3) or floxed Integrin αV (ITαV). Mice received a single 500µl injection of TAT-cre or heat-inactivated TAT-cre into the 3rd ventricle. TAT-cre administration inactivates the expression of genes encoding either ITβ3 or ITαV. Next, each cohort received a single icv injection of either FGF1 (2 µg) or saline vehicle. Food intake, body weight, and blood glucose measurements were taken daily throughout the investigation.  Our data demonstrates that the ability of icv FGF1 to induce lowering of blood glucose levels is not blocked by knockout of either ITβ3 or ItαV in tanycytes suggesting that integrin signaling isn't required for FGF1 to induce diabetes remission.