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Hofer, M. J.

Publications and source records attributed to Hofer, M. J..

2 recordsLinked to original sources

High fat diet consumption and social instability stress impair stress adaptation and maternal care in C57Bl/6 mice

Poor maternal diet and psychosocial stress represent two environmental factors that can significantly impact maternal health during pregnancy. While various mouse models have been developed to study the relationship between maternal health and offspring development, few incorporate multiple sources of stress that mirror the complexity of human experiences. Maternal high-fat diet (HF) models in rodents are well-established, whereas maternal psychosocial stress models are still emerging. The social instability stress (SIS) paradigm, serves as a chronic and unpredictable form of social stress. To evaluate the combined effects of a poor maternal diet and social stress on maternal health and behaviour, we developed a novel maternal stress model in adult female C57Bl/6 mice. We observed that all HF+ mice demonstrated rapid weight gain, elevated fasting blood glucose levels and impaired glucose tolerance independent of the presence (+) or absence (-) of SIS. Behavioural testing revealed anxiety-like behaviors remained across all groups prior to pregnancy. However, we did observe a trend of poorer nest quality among all HF+ mice compared to HF-mice following nest building testing. Unlike the other HF+ and HF-stress groups, which exhibited significantly reduced plasma ACTH and corticosterone levels following SIS exposure, we did not observe this reduction in HF+/SIS+ females. In addition, HF+/SIS+ females demonstrated significant postpartum maternal neglect, resulting in fewer numbers of live offspring. These findings suggest that prolonged maternal HF diet consumption, coupled with SIS, places a significant burden on the maternal stress response system, resulting in reduced parental investment and negative postpartum behaviour towards offspring.

animal behavior and cognition↗

Virally induced lipid droplets are a platform for innate immune signalling complexes

Lipid droplets (LDs) are upregulated by host cells in the face of pathogen infection, however, the reason for this phenomenon remains largely unknown. Here, we demonstrate that virally induced LDs house a distinct and dynamic proteome containing key antiviral signalling pathway members, including the essential pattern recognition receptor; RIG-I, key adaptor proteins; STAT1 and STAT2 and prominent interferon inducible proteins; viperin and MX1. Changes in the LD proteome were underpinned by specific key changes in the lipidome of virally driven LDs, particularity in the phospholipid membrane. Following virus infection, key antiviral proteins formed complex protein-protein interactions on the LD surface, positioning this organelle as a key antiviral signalling platform for the first time. It is clear that dynamic regulation of both the proteome and the lipidome of LDs occurs rapidly following viral infection towards the initiation of a successful innate immune response.

immunology↗