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This study investigated alterations in glucagon receptor-mediated signal transduction in rat livers from 7- to 25-mo-old animals and examined the effects of exercise training on ameliorating these changes. Sixty-six young (4 mo), middle-aged (12 mo), and old (22 mo) male Fischer 344 rats were divided into sedentary and trained (treadmill running) groups. Isolated hepatic membranes were combined with [(125)I-Tyr(10)]monoiodoglucagon and nine concentrations of glucagon to determine maximal binding capacity (B(max)) and dissociation constant (K(d)). No alterations were found in B(max) among groups; however, middle-aged trained animals had significantly higher glucagon affinity (lower K(d); 21.1 +/- 1.8 nM) than did their untrained counterparts (50.2 +/- 7.1 nM). Second messenger studies were performed by measuring adenylyl cyclase (AC) specific activity under basal conditions and with four pharmacological stimulations to assess changes in receptor-dependent, G protein-dependent, and AC catalyst-dependent cAMP production. Age-related declines were observed in the old animals under all five conditions. Training resulted in increased cAMP production in the old animals when AC was directly stimulated by forskolin. Stimulatory G protein (G(s)) content was reduced with age in the sedentary group; however, training offset this decline. We conclude that age-related declines in glucagon signaling capacity and responsiveness may be attributed, in part, to declines in intrinsic AC activity and changes in G protein [inhibitory G protein (G(i))/G(s)] ratios. These age-related changes occur in the absence of alterations in glucagon receptor content and appear to involve both G protein- and AC-related changes. Endurance training was able to significantly offset these declines through restoration of the G(i)/G(s) ratio and AC activity.

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Advocates for civil rights, environmental justice, and movements promoting social justice require data and may lack trust in public authorities, turning instead to academic scientists to help address their questions. Assessing historical exposure to toxic chemicals, especially in situations of a specific industrial source of pollution affecting a community, is critical for informing appropriate public health and policy responses. We describe a community-driven approach to integrate retrospective environmental hazard exposure assessment with community organizing to address concerns about the extent of exposure to toxic metals in a predominantly working-class, Latinx community living near a now-closed lead–acid battery smelter facility. Named the “Truth Fairy Project” by leaders of the community organization East Yard Communities for Environmental Justice, this community–university partnership aimed to assess prenatal and early-life exposures to toxic metals through biomarkers of exposure in baby/deciduous teeth. This partnership integrated community mobilization with empirical research, informing residents about toxic metal exposures and improving the community’s capacity to respond to a public health crisis.