Understanding weight-related differences in functional connectivity provides key insight into neurocognitive factors implicated in obesity. Here, we sampled three groups from human connectome project data: 1) 47 pairs of BMI-discordant twins (n=94; average BMI-discordancy 6.7 3.1 kg/m2), 2) 47 pairs of gender and BMI matched BMI-discordant, unrelated individuals, and 3) 47 pairs of BMI-similar twins to test for body mass dependent differences in between network functional connectivity. Across BMI discordant samples, three networks appeared to be highly sensitivity to weight status; specifically, a network compromised of gustatory processing regions, a visual processing network, and the default mode network (DMN). Further, individuals with a lower BMI relative to their twin had stronger connectivity between striatal/thalamic and prefrontal networks (pFWE = 0.04) in the BMI-discordant twin sample. Cortical-striatal-thalamic networks underlie regulation of hedonically motivated behaviors. Stronger connectivity may facilitate increased regulation of decision-making when presented with highly rewarding, energy-dense foods. We also observed that individuals with a higher BMI than their twin had stronger connectivity between cerebellar and insular networks (pFWE = 0.04). Increased cerebellar-insula connectivity is associated with caloric deprivation and, in high BMI individuals, is associated compromised satiation signaling, thereby increasing risk for postprandial food intake. Connectivity patterns observed in the BMI-discordant twin sample were not see in a BMI-similar sample, providing evidence that the results are specific to BMI discordance. Beyond the involvement of gustatory and visual networks and the DMN, little overlap in results were seen between the two BMI-discordant samples. This may be a function of the higher study design sensitivity in the BMI-discordant twin sample, relative to the more generalizable results in the unrelated sample. These findings demonstrate that distinct connectivity patterns can represent weight variability, adding to mounting evidence that implicates atypical brain functioning with the accumulation and/or maintenance of elevated weight.