The Role of Hypothalamic Inflammation in Dim Light at Night and High Fat Diet Induced Metabolic Disturbance

The prevalence of obesity and metabolic disorders is rapidly increasing worldwide. This increase in metabolic dysfunction correlates with increased exposure to artificial light at night (LAN). LAN disrupts the biological clock of living organisms, which controls circadian regulation of energy homeostasis and is important for proper metabolic functioning in humans and animals. Mice housed with dim LAN (dLAN) have previously been reported to develop symptoms of metabolic syndrome. In industrialized societies exposure to LAN and calorie rich diet often occur in tandem and may contribute to the increasing obesity epidemic. Thus, despite the association in humans between light at night and obesity, I have used mice to establish a causative relationship among light at night, high calorie food, and metabolic syndrome. I hypothesized that dLAN combined with a high fat diet (HFD) exacerbates metabolic dysfunction. Fifty four mice were assigned to four groups; (1) standard light-dark (LD) cycle/standard chow, (2) standard LD/HFD, (3) dLAN/standard chow, or (4) dLAN/HFD. After 4 experimental weeks hypothalamic and white adipose tissue was collected for qPCR and immunohistochemical analyses. dLAN and HFD each increased body and fat pad mass compared to LD and standard chow, respectively. Both variables also altered glucose levels and daytime food intake. dLAN and HFD each elevated TNFα and MAC1 in white adipose tissue. However, dLAN did not increase gene expression of TNFα, POMC, or MAC1 in the hypothalamus. These results indicate that central nervous system inflammation is not a primary mechanism driving light induced weight gain. Further understanding of the mechanisms through which dLAN contributes to inflammation and obesity is important for characterizing and treating metabolic disorders.