RESUMO
BACKGROUND: Despite daily vitamin D recommendations, women with osteoporosis may not achieve optimal 25-hydroxy-vitamin D (25[OH]D) levels. We retrospectively evaluated the effect of education and vitamin D supplementation (1,000 IU/day) in Korean women with osteoporosis. METHODS: Sixty-one women with osteoporosis who were taking cholecalciferol (800-1,000 IU/day) were enrolled during 2011 to 2012. Forty patients (education only, Edu group) were educated on the importance of >30 min sunlight exposure daily while taking vitamin D. Twenty-one patients (education with vitamin D supplementation, Add group) were prescribed 1,000 IU/day cholecalciferol (total 1,800-2,000 IU/day) plus education. Patients were divided into 3 groups according to serum 25(OH)D status: deficiency (<20 ng/mL), insufficiency (20-30 ng/mL), and sufficiency (≥30 ng/mL). Furthermore, 25(OH)D levels were compared at baseline and after intervention for 3 months. RESULTS: The median (interquartile range) serum 25(OH)D concentration at baseline was 25.10 (18.95-33.60) ng/mL. The mean (±standard error) differences in 25(OH)D levels from baseline to post-intervention were 19.85±3.86 and 31.73±4.82 ng/mL in the Edu group and Add group, respectively. Eighteen patients (29.5%) had vitamin D deficiency, 25 (41.0%) had insufficiency, and 18 (29.5%) had sufficient levels. Optimal 25(OH)D (30 ng/mL or more) was achieved in 54.5% and 95.2% patients in the Edu group and Add group, respectively (P=0.003). CONCLUSIONS: We consider that vitamin D concentration should be measured on a regular basis in order to maintain an optimal level of vitamin D concentration, and education and supplementation is needed if not sufficient.
RESUMO
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of nigral dopaminergic neurons and a reduction in striatal dopaminergic fibers, which result in tremors, rigidity, bradykinesia and gait disturbance. In addition to motor dysfunction, dementia is a widely recognized symptom of patients with PD. Berberine, an isoquinoline alkaloid isolated from Berberis vulgaris L., is known to exert anxiolytic, analgesic, anti-inflammatory, antipsychotic, antidepressant and anti-amnesic effects. In the present study, we investigated the effects of berberine on short-term memory in relation to dopamine depletion and hippocampal neurogenesis using a mouse model of PD, induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid (MPTP/P) treatment. Mice in the berberine-treated groups were orally administered berberine once a day for a total of 5 weeks. Our results revealed that the injection of MPTP/P induced dopaminergic neuronal death in the substantia nigra and fiber loss in the striatum. This resulted in impaired motor balance and coordination, as assessed by the beam walking test. We further demonstrated that MPTP/P-induced apoptosis in the hippocampus deteriorated short-term memory, as shown by the step-down avoidance task. By contrast, neurogenesis in the hippocampal dentate gyrus, which is a compensatory adaptive response to excessive apoptosis, was increased upon PD induction. However, treatment with berberine enhanced motor balance and coordination by preventing dopaminergic neuronal damage. Treatment with berberine also improved short-term memory by inhibiting apoptosis in the hippocampus. Berberine demonstrated maximal potency at 50 mg/kg. Based on these data, treatment with berberine may serve as a potential therapeutic strategy for the alleviation of memory impairment and motor dysfunction in patients with PD.