The arapaima is the largest of the extant air-breathing freshwater fishes. Their respiratory gas bladder is arguably the most striking of all the adaptations to living in the hypoxic waters of the Amazon basin, in which dissolved oxygen can reach 0 ppm (0 mg/l) at night. As obligatory air-breathers, arapaima have undergone extensive anatomical and physiological adaptations in almost every organ system. These changes were evaluated using magnetic resonance and computed tomography imaging, gross necropsy, and histology to create a comprehensive morphological assessment of this unique fish. Segmentation of advanced imaging data allowed for creation of anatomically accurate and quantitative 3D models of organs and their spatial relationships. The deflated gas bladder [1.96% body volume (BV)] runs the length of the coelomic cavity, and encompasses the kidneys (0.35% BV). It is compartmentalized by a highly vascularized webbing comprising of ediculae and inter-edicular septa lined with epithelium acting as a gas exchange surface analogous to a lung. Gills have reduced surface area, with severe blunting and broadening of the lamellae. The kidneys are not divided into separate regions, and have hematopoietic and excretory tissue interspersed throughout. The heart (0.21% BV) is encased in a thick layer of lipid rich tissue. Arapaima have an unusually large telencephalon (28.3% brain volume) for teleosts. The characteristics that allow arapaima to perfectly exploit their native environment also make them easy targets for overfishing. In addition, their habitat is at high risk from climate change and anthropogenic activities which are likely to result is fewer specimens living in the wild, or achieving their growth potential of up to 4.5 m in length.

Background and Hypothesis: Hyperglycemia is a major source of disease and morbidity among the adult population. Prior studies correlate long-term high fat diet (HFD) mediated hyperglycemia with bone fragility and muscle weakness. Furthermore, the mechanism driving hyperglycemia between sexes are unknown. Our group previously showed that HFDs induced insulin resistance in male mice and glucose intolerance in female mice. This establishes the need to study the impact of long-term HFDs on the bones and muscles using an older cohort of both male and female mice. For that, we hypothesized a long-term HFD mediated hyperglycemia will change bone and muscle structures and impair their functions in adult male and female mice. Experimental Design or Project Methods: 22-week C57Bl6 mice were fed either a HFD or low fat diet (LFD) for 25 weeks. After euthanasia, bones and muscles were harvested and evaluated using MicroCT, histology, and mechanical testing. Statistical analysis was performed using GraphPad Prism with p<0.05 considered significant. Results: MicoCT data saw significant reductions to cortical thickness (p<0.05), bone mineral density (p<0.001), and increases to medullary area (p<0.05) among HFD males and females compared to LFD. HFD-males also experienced significant increase in cortical porosity (P<0.001) whereas no changes were noted in HFDfemales. Trabecular bone volume was relatively unchanged. HFD increased cortical osteoclast surface (p<0.001) for both sexes. Bone histology saw increased marrow adiposity among HFD-females (p<0.05). Muscle histology exhibited HFD-related reductions in myofiber diameter (p<0.001) for both sexes. Mechanical testing demonstrated reduced young’s modulus (p<0.05) and yield stress (p<0.05) among HFD mice, despite non-significant differences in ultimate strength. Conclusion and Potential Impact: The changes associated with a long-term HFD differed between sexes but still led to functional impairments of bone and muscle for both sexes, emphasizing the importance of looking further into the mechanisms responsible for these changes. This can potentially translate to the clinic in the treatment of musculoskeletal complications associated with HFDs.