Vitamin D receptor expression and associated function have been reported in various muscle models, including C2C12, L6 cell lines and primary human skeletal muscle cells. It is believed that 1,25-hydroxyvitamin D3 (1,25(OH)2D3), the active form of vitamin D, has a direct regulatory role in skeletal muscle function, where it participates in myogenesis, cell proliferation, differentiation, regulation of protein synthesis and mitochondrial metabolism through activation of various cellular signalling cascades, including the mitogen-activated protein kinase pathway(s). It has also been suggested that 1,25(OH)2D3 and its associated receptor have genomic targets, resulting in regulation of gene expression, as well as non-genomic functions that can alter cellular behaviour through binding and modification of targets not directly associated with transcriptional regulation. The molecular mechanisms of vitamin D signalling, however, have not been fully clarified. Vitamin D inadequacy or deficiency is associated with muscle fibre atrophy, increased risk of chronic musculoskeletal pain, sarcopenia and associated falls, and may also decrease RMR. The main purpose of the present review is to describe the molecular role of vitamin D in skeletal muscle tissue function and metabolism, specifically in relation to proliferation, differentiation and protein synthesis processes. In addition, the present review also includes discussion of possible genomic and non-genomic pathways of vitamin D action.

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Objective: To evaluate the reproducibility and validity of a previously constructed FFQ to assess the usual diet of patients with type 2 diabetes mellitus (T2DM). Design: Cross-sectional survey using two quantitative FFQ (1-month interval) supported by a food photograph portfolio, a 3 d weighed diet record (WDR) and urinary N output measurement (as a biomarker of protein intake). Setting: Group of Nutrition in Endocrinology, southern Brazil. Subjects: Out-patients with T2DM. Results: From a total of 104 eligible T2DM patients, eighty-eight were included in the evaluation of FFQ reproducibility and seventy-two provided data for the validity study. The intakes estimated from the two FFQ did not differ (P . 0?05) and the correlation coefficients were significant (P , 0?01) for energy and nutrients, ranging from 0?451 (soluble fibre) to 0?936 (PUFA). Regarding the validity evaluation, data from the FFQ were higher than those from the WDR for total (28?3 %), soluble (27?4 %) and insoluble fibres (29?1 %), and SFA (13?5 %), MUFA (11?1 %) and total lipids (9?2 %; all P , 0?05). There were significant correlation coefficients between the FFQ and WDR for most nutrients, when adjusted for energy intake and de-attenuated. Also, the Bland-Altman plots between the FFQ and WDR for energy and macronutrient intakes showed that the FFQ may be used as alternative method to the WDR. The validity coefficient (using the method of triads) for the FFQ protein intake was 0?522 (95 % CI 0?414, 0?597). Conclusions: This quantitative FFQ was valid and precise to assess the usual diet of patients with T2DM, according to its validity and reproducibility.

Aging is associated with impairment in skeletal muscle mass and contractile function, predisposing to fat mass gain, insulin resistance and diabetes. The impact of Vitamin D (VitD) supplementation on skeletal muscle mass and function in older adults is still controversial. The aim of this review was to summarize data from randomized clinical trials, animal dietary intervention and cell studies in order to clarify current knowledge on the effects of VitD on skeletal muscle as reported for these three types of experiments. A structured research of the literature in Medline via PubMed was conducted and a total of 43 articles were analysed (cells n = 18, animals n = 13 and humans n = 13). The results as described by these key studies demonstrate, overall, at cell and animal levels, that VitD treatments had positive effects on the development of muscle fibres in cells in culture, skeletal muscle force and hypertrophy. Vitamin D supplementation appears to regulate not only lipid and mitochondrial muscle metabolism but also to have a direct effect on glucose metabolism and insulin driven signalling. However, considering the human perspective, results revealed a predominance of null effects of the vitamin on muscle in the ageing population, but experimental design may have influenced the study outcome in humans. Well-designed long duration double-blinded trials, standardised VitD dosing regimen, larger sample sized studies and standardised measurements may be helpful tools to accurately determine results and compare to those observed in cells and animal dietary intervention models.