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Visceral adipocytes and associated macrophages produce and release excessive amounts of biologically active inflammatory cytokines via the portal and systemic vascular system, which induce insulin resistance in insulin target tissues such as fat, liver, and muscle. Free fatty acids (FFAs) absorbed via the portal system or released from adipocytes also induce insulin resistance. In this report, we show that phenylmethimazole (C10) blocks basal IL6 and leptin production as well as basal Socs-3 expression in fully differentiated 3T3L1 cells (3T3L1 adipocytes) without affecting insulin-stimulated AKT signaling. In addition, C10 inhibits palmitate-induced IL6 and iNos up-regulation in both 3T3L1 adipocytes and RAW 264.7 macrophages, LPS-induced NF-kB and IFN-b activation in 3T3L1 cells, and LPS-induced iNos, Ifn-b, Il1b, Cxcl10, and Il6 expression in RAW 264.7 macrophages. C10 also blocks palmitate-induced Socs-3 up-regulation and insulin receptor substrate-1 (IRS-1) serine 307 phosphorylation in 3T3L1 adipocytes. Additionally, we show for the first time that although palmitate increases IRS-1 serine 307 phosphorylation in 3T3L1 adipocytes, AKT serine 473 phosphorylation is enhanced, not reduced, by palmitate. These results suggest that through inhibition of FFA-mediated signaling in adipocytes and associated macrophages, as well as possibly other insulin target cells/tissues (i.e. non-immune cells), C10 might be efficacious to prevent or reverse cytokine-induced insulin resistance seen in obesity-related insulin resistance and type 2 diabetes mellitus.

Coastal species encounter numerous physiological stressors ranging from daily fluctuations in salinity and temperature to anthropogenic contaminants, yet the effects of such stressor combinations on aquatic organisms remain largely unknown. Exposure to environmental contaminants, such as polychlorinated biphenyls (PCBs), can disrupt physiological processes, and while physiological responses to salinity change are well understood, the combined effects of salinity change and contaminants on these processes are unknown. Marine and brackish water turtles are often simultaneously exposed to both stressors. We exposed male, eight-month-old diamondback terrapins to one of four salinity treatments (0, 10, 20, and 30 parts per thousand) in the presence and absence of the anthropogenic stressor 3,3',4,4',5-pentachlorobiphenyl (PCB 126, 20 microg/g via intraperitoneal injection) and monitored growth (carapace length and mass) and metabolic rate for six months. Exposure to PCB 126 significantly reduced growth (p < 0.0001), lowered standard metabolic rates (SMRs; p < 0.0001), and altered respiratory pattern (p < 0.0001). Salinity stress reduced growth (p < 0.0001) and altered the respiratory pattern (p < 0.0001) but had no overall effect on metabolic rate (p = 0.33). No interactive effects of PCBs and salinity were seen on either growth or metabolic rate. Our data indicate terrapins may be able to cope with some effects of salinity change through physiological adjustments but are less able to cope with PCBs. We show that PCB 126 disrupts the ecophysiological mechanisms that affect life history traits and thus ultimately could alter population structure and dynamics. The present study enriches our understanding of the environmental toxicology of reptiles and aids in the interpretation of health conditions documented in field-collected turtles contaminated with PCBs.

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Developmental exposure of turtles and other reptiles to endocrine-disrupting chemicals (EDCs), including bisphenol A (BPA) and ethinyl estradiol (EE), can stimulate partial to full gonadal sex-reversal in males. We have also recently shown that in ovo exposure to either EDC can induce similar sex-dependent behavioral changes typified by improved spatial learning and memory or possibly feminized brain responses. Observed behavioral changes are presumed to be due to BPA- and EE-induced brain transcriptomic alterations during development. To test this hypothesis, we treated painted turtles () at developmental , incubated at 26°C (male-inducing temperature), with) BPA (1 ng/µl), ) EE (4 ng/µl), or) vehicle ethanol (control group). Ten months after hatching and completion of the behavioral tests, juvenile turtles were euthanized, brains were collected and frozen in liquid nitrogen, and RNA was isolated for RNA-Seq analysis. Turtles exposed to BPA clustered separately from EE-exposed and control individuals. More transcripts and gene pathways were altered in BPA vs. EE individuals. The one transcript upregulated in both BPA- and EE-exposed individuals was the mitochondrial-associated gene, ND5, which is involved in oxidative phosphorylation. Early exposure of turtles to BPA increases transcripts linked with ribosomal and mitochondrial functions, especially bioenergetics, which has been previously linked with improved cognitive performance. In summary, even though both BPA and EE resulted in similar behavioral alterations, they diverge in the pattern of neural transcript alterations with early BPA significantly upregulating several genes involved in oxidative phosphorylation, mitochondrial activity, and ribosomal function, which could enhance cognitive performance.

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Aquatic organisms encounter a number of contaminants in their environments. Here, we report polycyclic aromatic hydrocarbon (PAH) concentrations detected in diamondback terrapin eggs collected from the Patuxent River, Maryland, one year after an oil spill. Data suggested a geographic difference in egg hydrocarbon concentrations. However, at one year after the oil spill, most PAH concentrations detected were low, were not correlated with the extent of shoreline oiling, and thus likely represent current background levels. Future research should investigate the route of egg PAH exposure and include studies of embryotoxicity.