Aims/hypothesis Exposure to sunlight has the potential to suppress metabolic dysfunction and obesity. We previously demonstrated that regular exposure to low-doses of ultraviolet radiation (UVR) reduced weight gain and signs of diabetes in male mice fed a high-fat diet, in part via release of nitric oxide from skin. Here, we explore further mechanistic pathways through which lowdose UVR exerts these beneficial effects. Methods We fed mice with a luciferase-tagged Ucp1 gene (which encodes uncoupling protein-1 [UCP-1]), referred to here as the Ucp1 luciferase transgenic mouse ('Thermomouse') a high-fat diet and examined the effects of repeated exposure to low-dose UVR on weight gain and development of metabolic dysfunction as well as UCP-1-dependent thermogenesis in interscapular brown adipose tissue (iBAT). Results Repeated exposure to low-dose UVR suppressed the development of glucose intolerance and hepatic lipid accumulation via dermal release of nitric oxide while also reducing circulating IL-6 (compared with mice fed a high-fat diet only). Dietary nitrate supplementation did not mimic the effects of low-dose UVR. A single low dose of UVR increased UCP-1 expression (by more than twofold) in iBAT of mice fed a low-fat diet, 24 h after exposure. However, in mice fed a high-fat diet, there was no effect of UVR on UCP-1 expression in iBAT (compared with mock-treated mice) when measured at regular intervals over 12 weeks. More extensive circadian studies did not identify any substantial shifts in UCP-1 expression in mice exposed to low-dose UVR, although skin temperature at the interscapular site was reduced in UVR-exposed mice. The appearance of cells with a white adipocyte phenotype ('whitening') in iBAT induced by consuming the high-fat diet was suppressed by exposure to low-dose UVR in a nitric oxide-dependent fashion. Significant shifts in the expression of important core gene regulators of BAT function Gursimran K. Dhamrait and Kunjal Panchal contributed equally to this study.

ObjectiveTo investigate the associations between interpregnancy intervals (IPIs) and developmental vulnerability in children’s first year of full-time school (age 5).DesignRetrospective cohort study using logistic regression. ORs were estimated for associations with IPIs with adjustment for child, parent and community sociodemographic variables.SettingWestern Australia (WA), 2002–2015.Participants34 574 WA born singletons with a 2009, 2012 or 2015 Australian Early Development Census (AEDC) record.Main outcome measureThe AEDC measures child development across five domains; Physical Health and Wellbeing, Social Competence, Emotional Maturity, Language and Cognitive Skills (school-based) and Communication Skills and General Knowledge. Children with scores <10th percentile were classified as developmentally vulnerable on, one or more domains (DV1), or two or more domains (DV2).Results22.8% and 11.5% of children were classified as DV1 and DV2, respectively. In the adjusted models (relative to the reference category, IPIs of 18–23 months), IPIs of <6 months were associated with an increased risk of children being classified as DV1 (adjusted OR (aOR) 1.17, 95% CI 1.08 to 1.34), DV2 (aOR 1.31, 95% CI 1.10 to 1.54) and an increased risk of developmental vulnerability for the domains of Physical Health and Wellbeing (aOR 1.25, 95% CI 1.06 to 1.48) and Emotional Maturity (aOR 1.36, 95% CI 1.12 to 1.66). All IPIs longer than the reference category were associated with and increased risk of children being classified as DV1 and DV2 (aOR >1.15). IPIs of 60–119 months and ≥120 months, were associated with an increased risk of developmental vulnerability on each of the five AEDC domains, with greater odds for each domain for the longer IPI category.ConclusionsIPIs showed independent J-shaped relationships with developmental vulnerability, with short (<6 months) and longer (≥24 months) associated with increased risks of developmental vulnerability.

No abstract