929 resultados para Vitamin d


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Regular exercise and adequate nutrition, particularly dietary calcium, vitamin D, and protein, are prescribed as strategies to optimize peak bone mass and maintain bone and muscle health throughout life. Although the mechanism of action of exercise and nutrition on bone and muscle health are different-exercise has a site-specific modifying effect, whereas nutrition has a permissive generalized effect-there is evidence that combining calcium (or calcium rich dairy foods) or dietary protein with exercise can have a synergetic effect on bone mass and muscle health, respectively. However, many questions still remain as to whether there is a threshold level for these nutrients to optimize the exercise-induced gains. Further studies are also needed to investigate whether other dietary factors, such as vitamin D, soy isoflavones or omega-3 fatty acids, or a multinutrient supplement, can enhance the effects of exercise on bone and muscle health.

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We investigated the association between undercarboxylated osteocalcin (ucOC) and lower-limb muscle strength in women over the age of 70years. The study also aims to confirm the association between bone turnover markers and heel ultrasound measures. A post-hoc analysis using data collected as part of a randomized placebo-controlled trial of vitamin D supplementation. An immunoassay was used to quantify total OC (tOC), with hydroxyapatite pre-treatment for ucOC. We determined associations of absolute and relative (ucOC/tOC; ucOC%) measures of ucOC with lower-limb muscle strength, heel ultrasound measures of speed of sound (SOS) and broadband ultrasound attenuation (BUA), bone turnover markers (BTMs; P1NP and CTx) and the acute phase protein alpha-1-antichymotrypsin (α-ACT). ucOC%, but not absolute ucOC concentration, was positively associated with hip flexor, hip abductor and quadriceps muscle strength (all p<0.05). ucOC% was negatively associated with α-ACT (β-coefficient=-0.24, p=0.02). tOC was positively associated with both P1NP and CTx (p<0.001). For each per unit increase in tOC (μg/L) there was a corresponding lower BUA, SOS and SI (β-coefficient = -0.28; -0.23 and -0.23, respectively; all p<0.04). In conclusion, ucOC% is positively associated with muscle strength and negatively associated with α-ACT. These data support a role for ucOC in musculoskeletal interactions in humans. Whilst tOC is associated with bone health, ucOC% and ucOC may also be linked to falls and fracture risk by influencing muscle function.

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It has previously been shown that irradiation with UV light increases the vitamin D content of certain mushroom species, but the effect on other nutrients is unknown, and is difficult to assess due to the complexity of the sample matrix. Here, an offline reversed phase × reversed phase two-dimensional liquid chromatography methodology was developed and applied to Agaricus bisporus mushrooms in order to demonstrate the potential of the technique and assess the effect of UV irradiation on the mushroom’s metabolic profile. The method allowed the detection of 158 peaks in a single analytical run. A total of 51 compounds including sugars, amino acids, organic and fatty acids and phenolic compounds were identified using certified reference standards. After irradiation of the mushrooms with UV for 30 s the number of peaks detected decreased from 158 to 150; 47 compounds increased in concentration while 72 substances decreased. This is the first time that two-dimensional liquid chromatography has been carried out for the metabolomic analysis of mushrooms. The data provide an overview of the gain/loss of nutritional value of the mushrooms following UV irradiation and demonstrate that the increased peak capacity and separation space of two-dimensional liquid chromatography has great potential in metabolomics.

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Prospective observational studies uniformly link vitamin D deficiency with the incidence of type 2 diabetes mellitus (T2DM), yet trials supplementing participants at risk of T2DM with vitamin D to reduce progression to T2DM have yielded inconsistent results. Inconsistencies between supplementation trials may be due to insufficient dosing or small sample sizes. Observational studies may also have reported spurious associations due to uncontrolled confounding by lifestyle or genetic factors. Alternatively, observational and intervention studies may not be entirely comparable. Observational studies show an association between higher vitamin D status, which is predominantly derived from sun exposure, and decreased incidence of T2DM. Trials intervene with vitamin D supplementation, and therefore may be missing alternate causes of the effect of sun exposure, as seen in observational studies. We propose that sun exposure may be the driving force behind the associations seen in observational studies; sun exposure may have additional benefits beyond increasing serum 25-hydroxyvitamin D (25OHD) levels. We performed an electronic literature search to identify articles that examined associations between sun exposure and T2DM and/or glucose metabolism. A best evidence synthesis was then conducted using outcomes from analyses deemed to have high methodological quality. Ten eligible full-text articles were identified, yielding 19 T2DM-related outcomes. The best evidence analysis considered 11 outcomes which were grouped into six outcome types: T2DM, fasting glucose, glucose tolerance, fasting insulin, insulin secretion and insulin sensitivity. There was moderate evidence to support a role of recreational sun exposure in reducing odds of T2DM incidence. High-level evidence was lacking; evidence presented for other outcomes was of low or insufficient level. This review highlights significant gaps in research pertaining to sun exposure and T2DM-related outcomes. Further research is encouraged as we aim to identify novel preventative strategies for T2DM.

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BACKGROUND: Environmental conditions early in life may imprint the circadian system and influence response to environmental signals later in life. We previously determined that a large springtime increase in solar insolation at the onset location was associated with a younger age of onset of bipolar disorder, especially with a family history of mood disorders. This study investigated whether the hours of daylight at the birth location affected this association. METHODS: Data collected previously at 36 collection sites from 23 countries were available for 3896 patients with bipolar I disorder, born between latitudes of 1.4 N and 70.7 N, and 1.2 S and 41.3 S. Hours of daylight variables for the birth location were added to a base model to assess the relation between the age of onset and solar insolation. RESULTS: More hours of daylight at the birth location during early life was associated with an older age of onset, suggesting reduced vulnerability to the future circadian challenge of the springtime increase in solar insolation at the onset location. Addition of the minimum of the average monthly hours of daylight during the first 3 months of life improved the base model, with a significant positive relationship to age of onset. Coefficients for all other variables remained stable, significant and consistent with the base model. CONCLUSIONS: Light exposure during early life may have important consequences for those who are susceptible to bipolar disorder, especially at latitudes with little natural light in winter. This study indirectly supports the concept that early life exposure to light may affect the long term adaptability to respond to a circadian challenge later in life.

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Due to their differing etiologies and consequences, it has been proposed that the term "sarcopenia" should revert to its original definition of age-related muscle mass declines, with a separate term, "dynapenia", describing muscle strength and function declines. There is increasing interest in the interactions of sarcopenia and dynapenia with obesity. Despite an apparent protective effect of obesity on fracture, increased adiposity may compromise bone health, and the presence of sarcopenia and/or dynapenia ("sarcopenic obesity" and "dynapenic obesity") may exacerbate the risk of falls and fracture in obese older adults. Weight loss interventions are likely to be beneficial for older adults with sarcopenic and dynapenic obesity but may result in further reductions in muscle and bone health. The addition of exercise including progressive resistance training and nutritional strategies, including protein and vitamin D supplementation, may optimise body composition and muscle function outcomes thereby reducing falls and fracture risk in this population.

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Schizophrenia risk has often been conceptualized using a model which requires two hits in order to generate the clinical phenotype-the first as an early priming in a genetically predisposed individual and the second a likely environmental insult. The aim of this paper was to review the literature and reformulate this binary risk-vulnerability model. We sourced the data for this narrative review from the electronic database PUBMED. Our search terms were not limited by language or date of publication. The development of schizophrenia may be driven by genetic vulnerability interacting with multiple vulnerability factors including lowered prenatal vitamin D exposure, viral infections, smoking intelligence quotient, social cognition cannabis use, social defeat, nutrition and childhood trauma. It is likely that these genetic risks, environmental risks and vulnerability factors are cumulative and interactive with each other and with critical periods of neurodevelopmental vulnerability. The development of schizophrenia is likely to be more complex and nuanced than the binary two hit model originally proposed nearly thirty years ago. Risk appears influenced by a more complex process involving genetic risk interfacing with multiple potentially interacting hits and vulnerability factors occurring at key periods of neurodevelopmental activity, which culminate in the expression of disease state. These risks are common across a number of neuropsychiatric and medical disorders, which might inform common preventive and intervention strategies across non-communicable disorders.

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Leprosy is a complex infectious disease influenced by genetic and environmental factors. The genetic contributing factors are considered heterogeneous and several genes have been consistently associated with susceptibility like PARK2, tumor necrosis factor (TNF), lymphotoxin-alpha (LTA) and vitamin-D receptor (VDR). Here, we combined a case-control study (374 patients and 380 controls), with meta-analysis (5 studies; 2702 individuals) and biological study to test the epidemiological and physiological relevance of the interleukin-10 (IL-10) genetic markers in leprosy. We observed that the -819T allele is associated with leprosy susceptibility either in the case-control or in the meta-analysis studies. Haplotypes combining promoter single-nucleotide polymorphisms also implicated a haplotype carrying the -819T allele in leprosy susceptibility (odds ratio (OR) = 1.40; P = 0.01). Finally, we tested IL-10 production in peripheral blood mononuclear cells stimulated with Mycobacterium leprae antigens and found that -819T carriers produced lower levels of IL-10 when compared with noncarriers. Taken together, these data suggest that low levels of IL-10 during the disease outcome can drive patients to a chronic and unprotective response that culminates with leprosy.

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To study the 'in vivo' importance of vitamin D on the natural killer (NK) activity, rats were submitted to privational rickets induced by a diet deficient in vitamin D and phosphorus (D-P-). Thirty days after the beginning of treatment the animals showed low body weight, changes in the bone development, and decreased levels of 25-hydroxyvitamin D-3 (25-OH D-3). NK activity, evaluated using a cytotoxicity assay against Cr-51-labeled Yac.1 target cells, was not modified by the rickets-inducing treatment during the first 30 days. Following a long-term treatment (60 days) the rachitic rats (D-P-) exhibited higher NK activity than control animals (D + P +) (P < 0.05). on the other hand, D - P + animals showed higher cytotoxic activity than D - P - and D + P + groups. Feed replacement to the rachitic rats by a complete diet (D - P - /D + P +) led to a partial recuperation of growth, bone development, and 25-OH D-3 scrum. levels. The NK activity was also influenced by vitamin D intake, decreasing after treatment. (C) 2002 Elsevier B.V. B.V. All rights reserved.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Zinc is known to play a relevant role in growth and development. The basic mechanisms of action of this trace element are intimately linked to the structure and action of countless enzymes involved in many different metabolic processes. In this respect, when zinc specifically acts on cartilage growth it is involved in multiple enzymatic reactions which make this a multifactorial event. Thus, we may divide the actions of zinc into three distinct types: 1) action on taste and smell acuity, appetite regulation, and food consumption and regulation; 2) action on DNA and RNA synthesis stimulating a) cell replication and differentiation of chondrocytes, osteoblasts and fibroblasts; b) cell transcription culminating in the synthesis of somatomedin-C (liver), alkaline phosphatase, collagen and osteocalcin (bone), and c) protein, carbohydrate and lipid metabolism, that is intimately related to the mechanisms of smell, taste, appetite, and food consumption and utilization; 3) action on hormonal mediation by participating in a) GH synthesis and secretion in somatomammotroph cells, b) the action of GH on liver somatomedin-C production, and c) somatomedin-C activation in bone cartilage. In addition to these multiple functions, zinc also interacts with other hormones somehow related to bone growth such as testosterone, thyroid hormones, insulin, and vitamin D-3.On the basis of the above considerations, we conclude that the integration of these mechanisms contributes to the perfect physiological functioning of bone. Tn the presence of zinc deficiency, this homeostasis is impaired, causing the weight-height deficiency detected in several species studied, the human species in particular.