Daily 2000 IU vitamin D supplementation may be effective in optimizing vitamin D status and counteracting the progression of aortic stiffness in black youth. Plasma 25(OH)D concentrations in response to the 2000 IU/d supplementation are negatively modulated by adiposity.

Adipose tissue is a known source of proinflammatory cytokines in obese humans and animal models, including the db/db mouse, in which obesity arises as a result of leptin receptor insensitivity. Inflammatory cytokines induce cognitive deficits across numerous conditions, but no studies have determined whether obesity-induced inflammation mediates synaptic dysfunction. To address this question, we used a treadmill training paradigm in which mice were exposed to daily training sessions or an immobile belt, with motivation achieved by delivery of compressed air on noncompliance. Treadmill training prevented hippocampal microgliosis, abolished expression of microglial activation markers, and also blocked the functional sensitization observed in isolated cells after ex vivo exposure to lipopolysaccharide. Reduced microglial reactivity with exercise was associated with reinstatement of hippocampus-dependent memory, reversal of deficits in long-term potentiation, and normalization of hippocampal dendritic spine density. Because treadmill training evokes broad responses not limited to the immune system, we next assessed whether directly manipulating adiposity through lipectomy and fat transplantation influences inflammation, cognition, and synaptic plasticity. Lipectomy prevents and fat transplantation promotes systemic and central inflammation, with associated alterations in cognitive and synaptic function. Levels of interleukin 1␤ (IL1␤) emerged as a correlate of adiposity and cognitive impairment across both the treadmill and lipectomy studies, so we manipulated hippocampal IL1 signaling using intrahippocampal delivery of IL1 receptor antagonist (IL1ra). Intrahippocampal IL1ra prevented synaptic dysfunction, proinflammatory priming, and cognitive impairment. This pattern supports a central role for IL1-mediated neuroinflammation as a mechanism for cognitive deficits in obesity and diabetes.

Objective The objectives were to characterize the vitamin D status of black and white adolescents residing in the southeastern United States (latitude: 33°N) and to investigate relationships with adiposity. Methods Plasma 25-hydroxyvitamin D levels were measured with liquid chromatography-tandem mass spectroscopy for 559 adolescents 14 to 18 years of age (45% black and 49% female). Fat tissues, physical activity, and cardiovascular fitness also were measured. Results The overall prevalences of vitamin D insufficiency (<75nmol/L) and deficiency (≤50 nmol/L) were 56.4% and 28.8%, respectively. Black versus white subjects had significantly lower plasma 25-hydroxyvitamin D levels in every season (winter, 35.9±2.5 vs 77.4±2.7 nmol/L; spring, 46.4±3.5 vs 101.3±3.5 nmol/L; summer, 50.7±4.0 vs 104.3±4.0 nmol/L; autumn, 54.4± 4.0 vs 96.8±2.7 nmol/L). With adjustment for age, gender, race, season, height, and sexual maturation, there were significant inverse correlations between 25-hydroxyvitamin D levels and all adiposity measurements, including BMI percentile (P=.02), waist circumference (P<.01), total fat mass (P<.01), percentage of body fat (P <.01), visceral adipose tissue (P <.015), and subcutaneous abdominal adipose tissue (P<.039). There were significant positive associations between 25-hydroxyvitamin D levels and vigorous physical activity (P <.01) and cardiovascular fitness (P =.025). Conclusions Low vitamin D status is prevalent among adolescents living in a year-round sunny climate, particularly among black youths. The relationships between 25-hydroxyvitamin D levels, adiposity, physical activity, and fitness seem to be present in adolescence.