Objective: Disruption of satiety signaling may lead to increased caloric intake and obesity. Uroguanylin, the intestinal hormone, travels as a precursor to the central nervous system where it activates guanylyl cyclase C (GUCY2C) and stimulates pro-satiety neurons. Rodent studies have demonstrated that (1) GUCY2C-knockout mice over-eat and have increased weight gain vs. wild-type mice; and (2) hyper-caloric obesity diminishes uroguanylin expression. We measured circulating plasma pro-uroguanylin, along with other gastrointestinal peptides and inflammatory markers, in human adolescents with and without obesity, as a pilot study. We hypothesized that adolescents with obesity would have less circulating pro-uroguanylin than adolescents without obesity have. Methods: We recruited 24 adolescents (age 14-17) with and without obesity (BMI >95% or BMI
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