title: Dim light at night exaggerates weight gain and inflammation associated with a high-fat diet in male mice.
abstract: Elevated nighttime light exposure is associated with symptoms of metabolic syndrome. In industrialized societies, high-fat diet (HFD) and exposure to light at night (LAN) often cooccur and may contribute to the increasing obesity epidemic. Thus, we hypothesized that dim LAN (dLAN) would provoke additional and sustained body mass gain in mice on a HFD. Male mice were housed in either a standard light/dark cycle or dLAN and fed either chow or HFD. Exposure to dLAN and HFD increase weight gain, reduce glucose tolerance, and alter insulin secretion as compared with light/dark cycle and chow, respectively. The effects of dLAN and HFD appear additive, because mice exposed to dLAN that were fed HFD display the greatest increases in body mass. Exposure to both dLAN and HFD also change the timing of food intake and increase TNFα and MAC1 gene expression in white adipose tissue after 4 experimental weeks. Changes in MAC1 gene expression occur more rapidly due to HFD as compared with dLAN; after 5 days of experimental conditions, mice fed HFD already increase MAC1 gene expression in white adipose tissue. HFD also elevates microglia activation in the arcuate nucleus of the hypothalamus and hypothalamic TNFα, IL-6, and Ikbkb gene expression. Microglia activation is increased by dLAN, but only among chow-fed mice and dLAN does not affect inflammatory gene expression. These results suggest that dLAN exaggerates weight gain and peripheral inflammation associated with HFD.
authors.affiliation: Department of Neuroscience, Wexner Medical Center, The Ohio State University, 636 Biomedical Research Tower, 460 West 12th Avenue, Columbus, Ohio 43210. fonken.1@osu.edu.
authors.forename: Laura K
authors.initials: LK
authors.lastname: Fonken
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Lieberman
authors.forename: Zachary M
authors.initials: ZM
authors.lastname: Weil
authors.forename: Randy J
authors.initials: RJ
authors.lastname: Nelson
mesh_terms: D052436:Adipose Tissue, White / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001069:Appetite Regulation / Q000528:radiation effects*; D001111:Arcuate Nucleus of Hypothalamus / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D001522:Behavior, Animal / Q000528:radiation effects; D039481:CD11b Antigen / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D002940:Circadian Rhythm; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects*; D005247:Feeding Behavior / Q000528:radiation effects; D005786:Gene Expression Regulation; D018149:Glucose Intolerance / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D051550:I-kappa B Kinase / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D007333:Insulin Resistance; D008029:Lighting / Q000009:adverse effects*; D008297:Male; D051379:Mice; D017628:Microglia / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D009765:Obesity / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D015430:Weight Gain
chemical_list: D039481:CD11b Antigen; D016207:Cytokines; D009419:Nerve Tissue Proteins; D051550:I-kappa B Kinase; C496562:Ikbkb protein, mouse